AP Psychology FRQs | Free Practice Question with Answer

Unit 1: Biological Bases of Behavior

FRQ 1: Discuss the influence of both nature (heredity) and nurture (environment) on the development of intelligence. In your answer, define these concepts and provide evidence (for example, from twin or adoption studies) illustrating how genetic and environmental factors contribute to a person’s IQ.

Thesis/Main Argument: Intelligence is the result of an interaction between genetic factors (“nature”) and environmental influences (“nurture”); a strong answer will assert that both heredity and environment significantly shape IQ, rather than one alone being responsible.

Key Points:

Definition of “nature” (genetic heredity) vs. “nurture” (environment and experience).
Evidence for genetic contributions to intelligence (e.g., high IQ correlation in identical twins).
Evidence for environmental contributions (e.g., improved IQ with enriched education or the Flynn effect of rising IQ scores over time).
The idea of gene-environment interaction (genes may set a potential range, environment determines where within that range one falls).

Supporting Evidence & Examples:

Twin Studies: Research with identical twins reared apart (Bouchard et al.) found their IQ scores to be strongly correlated, suggesting a genetic influence. For example, identical twins often have more similar IQs than fraternal twins or non-siblings, indicating heredity plays a significant role.
Adoption Studies: Adopted children’s IQs can resemble their biological parents’ (genetics) but also increase when raised in stimulating homes, showing environment matters. Children adopted from deprived orphanages into enriched families often show IQ gains, underscoring nurture’s impact.
Flynn Effect: Over the past decades, average IQ scores have risen worldwide, too rapidly to be explained by genetics. This improvement is attributed to environmental factors like better nutrition, education, and complexity of modern environments, highlighting how nurture influences measured intelligence.
Reaction Range: A theoretical concept where genetics give a range for potential IQ, but environmental quality determines where an individual lands in that range. For instance, a child with a high genetic potential for IQ might only reach a lower end of that potential if malnourished or poorly educated, whereas a rich learning environment could help them reach the upper end of their genetic potential.

Organization: Begin by clearly stating that both heredity and environment contribute to intelligence. Then define “nature” and “nurture.” The body should present evidence for nature (e.g., twin and adoption study findings) and evidence for nurture (environmental influences, Flynn effect). Finally, conclude by explaining that nature and nurture work together (interaction), rather than one outweighing the other. Each paragraph should directly tie evidence back to how it supports either genetic or environmental influence on IQ.

Depth & Rigor: A thorough answer not only cites studies (like twin/adoption research) but also explains what those studies mean (e.g., why twin similarities point to genes). It addresses potential misconceptions (such as interpreting a high heritability of IQ to mean environment doesn’t matter) by noting the interplay of factors. The response could mention concepts like heritability (the proportion of variation in intelligence in a population attributable to genes) and clarify that a high heritability does not mean intelligence is fixed or unaffected by environment. This demonstrates a nuanced understanding of the complexity of the nature-nurture issue.

Relevance: Every part of the answer is focused on intelligence and the roles of genes and environment. Definitions ensure the terms are directly addressed, research evidence is explicitly connected to either genetic or environmental factors in IQ, and the conclusion reinforces how both sets of factors are relevant. There are no off-topic digressions; all examples (twins, adoption, Flynn effect) directly support the argument about nature and nurture in intelligence.

FRQ 2: Explain the different functions of the sympathetic and parasympathetic divisions of the nervous system by describing what would happen in a scenario where a person encounters a sudden threat (like a snake) and then recovers after the danger passes.

Thesis/Main Argument: The sympathetic and parasympathetic divisions of the autonomic nervous system have opposite effects: the sympathetic system mobilizes the body’s energy in a “fight-or-flight” response to emergencies, while the parasympathetic system calms the body down, promoting “rest-and-digest” functions once the threat is gone.

Key Points:

Identification of the sympathetic nervous system as activating/arousing (fight-or-flight) and the parasympathetic nervous system as calming (restoring homeostasis).
Sympathetic responses to a threat (e.g., increased heart rate, dilated pupils, adrenaline release).
Parasympathetic responses during recovery (e.g., slowed heart rate, resumed digestion, relaxation).
The complementary nature of these systems in maintaining body balance (homeostasis).

Supporting Evidence & Examples:

Sympathetic Activation: Upon seeing a snake, the sympathetic division triggers the adrenal glands to release adrenaline (epinephrine). This leads to rapid heartbeat, increased breathing rate, blood being redirected to muscles, pupils dilating, and digestion pausing. For example, the person might immediately feel their heart pounding and palms sweating – physiological changes preparing them to run away or fight the snake. They may experience a surge of energy and alertness (heightened awareness) as part of this fight-or-flight reaction.
Parasympathetic Activation: After the snake slithers away and the danger is over, the parasympathetic division takes over. It releases neurotransmitters (like acetylcholine) that slow the heart rate and breathing, constrict pupils back to normal, and resume digestive processes. The person begins to calm down – their trembling subsides, and they might notice they’re catching their breath and feeling exhaustion as the body tries to return to its resting state.
Illustration of Opposite Effects: If we measured the person’s vital signs, during the threat their blood pressure and heart rate would spike (sympathetic action), and a few minutes after the threat, those measures would drop back toward baseline (parasympathetic action). The sympathetic system acting like a gas pedal (accelerating bodily functions) and the parasympathetic like a brake (slowing things down) ensures the body can handle emergencies and then recover.
Additional Example: Consider stage fright: right before stepping on stage, sympathetic responses (butterflies in stomach, dry mouth due to inhibited salivation) kick in. After leaving the stage, parasympathetic responses bring the person back to a relaxed state (salivation returns, heart rate normalizes). This everyday example reinforces how these systems manifest in real-life stress and relief situations.

Organization: The answer should first define or identify the sympathetic vs. parasympathetic systems. Then it should organize the scenario chronologically: describe what the sympathetic does during the snake encounter, and then what the parasympathetic does after the threat. Each system’s effects can be grouped in its own paragraph or clearly separated set of sentences. The conclusion can note that these two systems work in tandem to keep the body’s internal state balanced, referencing the initial definitions.

Depth & Rigor: A comprehensive answer mentions multiple physiological changes (heart rate, respiration, pupil size, digestion, etc.) and correctly links them to the appropriate system. It demonstrates understanding by possibly naming the autonomic nervous system as the overarching system containing both divisions, and by using terms like “homeostasis” or “arousal.” It could also mention that these responses are automatic (not under conscious control). For full rigor, the answer might note that the sympathetic response releases glucose for energy and inhibits non-urgent processes (like digestion), which is adaptive, and that the parasympathetic response involves processes like acetylcholine release to relax the body. Including such details shows a strong grasp of the physiological mechanisms.

Relevance: The response stays on the functions of the sympathetic and parasympathetic systems, anchored by the threat scenario. Every described effect (e.g., heart racing, heart slowing) is clearly tied to one of the two systems as asked. The scenario of encountering a snake and calming down is used effectively to illustrate the systems’ roles, fulfilling the prompt. No extraneous information (like unrelated brain parts or cognitive responses) is introduced, ensuring the answer remains focused on the autonomic nervous system divisions.

FRQ 3: Describe how a neural impulse (action potential) travels through a neuron and is then transmitted to another neuron. In your answer, explain the roles of the action potential, the synapse, and neurotransmitters in this process, and how this neural communication can influence behavior.

Thesis/Main Argument: Neurons communicate via an electrochemical process: an action potential (electrical impulse) travels down the neuron’s axon, leading to the release of neurotransmitters across the synapse (the gap between neurons). These neurotransmitters carry the signal to the next neuron, which can trigger a new impulse. This sequence underlies all of our behaviors, as it is the fundamental way information is transmitted in the nervous system.

Key Points:

The generation of an action potential (brief electrical charge) along a neuron’s axon (all-or-none firing).
The presence of a synapse, the gap between the sending neuron’s axon terminal and the receiving neuron’s dendrite.
Release of neurotransmitters from the axon terminals into the synapse when the action potential arrives.
Neurotransmitters binding to receptors on the next neuron, influencing it to either fire (if excitatory) or not fire (if inhibitory).
This neural communication as the basis for behavior (e.g., muscle contraction, sensation, thought all depend on these neural signals).

Supporting Evidence & Examples:

Action Potential Propagation: When a neuron is sufficiently stimulated (exceeds threshold), an action potential is generated at the cell body and travels down the axon. This involves a wave of depolarization – positively charged ions (sodium) rushing into the axon membrane – moving in a chain reaction. The action potential obeys the all-or-none law, meaning it either fires at full strength or not at all. For example, if you prick your finger, sensory neurons undergo action potentials that carry the pain signal toward your spinal cord/brain. The intensity of a stimulus (like a strong pinch versus a light touch) is coded by the frequency of action potentials and the number of neurons firing, not by the strength of a single impulse (all impulses have the same magnitude).
Synaptic Transmission: When the action potential reaches the axon terminals (the end of the neuron), it triggers vesicles containing neurotransmitters to fuse with the cell membrane and release these chemical messengers into the synaptic cleft. For instance, a motor neuron’s axon terminals release the neurotransmitter acetylcholine into the synapse at a muscle fiber. This acetylcholine then binds to the muscle’s receptors, causing the muscle to contract – a direct link from neural impulse to behavior (movement).
Neurotransmitter Binding: On the receiving neuron’s side (often the dendrite or cell body), neurotransmitters bind to specific receptors like a key in a lock. Depending on the neurotransmitter and receptor, the effect can be excitatory (making the next neuron more likely to fire its own action potential) or inhibitory (making it less likely to fire). For example, dopamine released in a brain synapse might excite the next neuron if it binds to excitatory receptors, influencing feelings of pleasure or movement initiation. Conversely, GABA (an inhibitory neurotransmitter) binding might prevent an action potential, leading to calming effects.
Reset and Reuptake: After neurotransmitters have done their job, they are often taken back up by the sending neuron in a process called reuptake (or broken down by enzymes). This clearing of the synapse ensures the signal is brief and allows the sending neuron to recycle neurotransmitter molecules. Many psychoactive drugs influence this step (for instance, SSRIs block the reuptake of serotonin, leaving more serotonin in the synapse to continue affecting the next neuron).
Behavioral Impact: This whole process—from action potential to synaptic transmission—underlies everything from reflexes to complex thoughts. For example, when you decide to answer a question verbally, motor neurons fire action potentials to release neurotransmitters onto muscle cells in your larynx and tongue, causing them to contract and produce speech. If neural transmission is disrupted (say by a toxin that blocks neurotransmitter release), behavior is affected (paralysis, numbness, etc.). In diseases like multiple sclerosis, where myelin sheaths on axons degenerate and slow/stop action potentials, people experience muscle weakness or loss of coordination, directly showing how impaired neural impulses alter behavior.

Organization: The response should follow the sequence of neural communication: start with a neuron at rest and then stimulation causing an action potential; next, cover what happens when that impulse reaches the synapse (release of neurotransmitters); then describe the effect on the next neuron. It helps to explicitly mention the roles of the three key terms in order: action potential (within one neuron), neurotransmitters (chemical messengers), synapse (the site of transmission between neurons). A concluding sentence can tie this back to behavior, reinforcing that this process is the basic mechanism for all neural control of actions and mental processes.

Depth & Rigor: A strong answer will correctly use terms like depolarization, all-or-none principle, synaptic cleft, receptors, and reuptake, showing a detailed understanding of the steps involved. It might mention the refractory period (brief period after an action potential when the neuron cannot fire again) to emphasize how signals are discrete. It could also differentiate between electrical communication (within a neuron via action potentials) and chemical communication (between neurons via neurotransmitters). By including an example (like muscle contraction or reflex or drug effect), it demonstrates the student can apply the concept to real situations, which shows depth. Mentioning a specific neurotransmitter and its role (acetylcholine for movement, serotonin for mood, etc.) adds rigor by connecting the abstract process to concrete outcomes.

Relevance: The answer stays focused on neural communication, specifically highlighting action potentials, synapses, and neurotransmitters exactly as the question asks. Each part of the explanation (generation of the impulse, chemical transmission, effect on next neuron) directly addresses how signals are carried forward. The inclusion of behavioral examples (movement, drug effect) is relevant because it ties the mechanism to its psychological significance, reinforcing why this process matters. The response does not stray into unrelated topics (e.g., it wouldn’t discuss brain lobes or unrelated endocrine functions), keeping it on-point.

FRQ 4: Explain how neurotransmitters influence human behavior by providing specific examples. In your answer, describe the role of dopamine in Parkinson’s disease and the role of serotonin in depression, indicating how imbalances in these neurotransmitters are linked to the disorders.

Thesis/Main Argument: Neurotransmitters are chemical messengers that play a crucial role in regulating behavior and mental processes. Imbalances or disruptions in neurotransmitter systems can lead to noticeable changes in behavior and are associated with various disorders. For example, a deficiency of dopamine is linked to the movement problems seen in Parkinson’s disease, while low levels of serotonin are associated with the mood disturbances of depression. Restating this in the thesis: different neurotransmitters (like dopamine and serotonin) have specific effects on behavior, and when their levels are abnormal, characteristic symptoms or disorders can result.

Key Points:

General role of neurotransmitters in transmitting signals and affecting behavior (neurotransmitters regulate mood, movement, arousal, etc.).
Dopamine: functions in movement control, motivation, and reward; how too little dopamine is related to Parkinson’s disease symptoms (tremors, rigidity).
Serotonin: functions in mood regulation, appetite, sleep; how too little serotonin is linked to depression (sad mood, low energy).
The concept that restoring neurotransmitter balance (through medication or other means) can ameliorate these conditions, supporting the idea that the neurotransmitter imbalance was causal in the behavioral symptoms.

Supporting Evidence & Examples:

Dopamine and Parkinson’s: Dopamine is produced in the substantia nigra region of the brain and is critical for smooth, coordinated muscle movements. In Parkinson’s disease, those dopamine-producing neurons degenerate, causing dopamine levels to drop. As a result, patients exhibit motor symptoms such as tremors at rest, muscle stiffness, bradykinesia (slowness of movement), and postural instability. For instance, a person with Parkinson’s may have a characteristic shaking hand and struggle to initiate movements like walking or writing, illustrating dopamine’s role in enabling normal movement. A key piece of evidence is that treatments for Parkinson’s often aim to increase dopamine levels – L-Dopa, a medication that the brain converts to dopamine, can temporarily improve motor function in Parkinson’s patients, which underscores that lack of dopamine was contributing to their impaired behavior.
Serotonin and Depression: Serotonin is involved in regulating mood, appetite, and sleep. Low serotonin activity in certain brain circuits is strongly associated with clinical depression, which is characterized by persistent sadness, lack of interest or pleasure, changes in weight and sleep, and sometimes suicidal thoughts. Supporting evidence comes from antidepressant medications: Selective Serotonin Reuptake Inhibitors (SSRIs), like Prozac or Zoloft, work by preventing the reuptake of serotonin in synapses, thereby increasing the amount of serotonin available to stimulate neurons. These medications often alleviate depressive symptoms, suggesting that insufficient serotonin was a factor in causing those symptoms. For example, before medication, a depressed individual might experience hopeless mood and lethargy; after SSRIs raise serotonin levels, they often report improved mood and energy, highlighting serotonin’s influence on emotion.
Additional Context: While the question specifically asks for dopamine/Parkinson’s and serotonin/depression, it’s notable that neurotransmitter imbalances are implicated in many other behaviors and disorders. For instance, an excess of dopamine in certain brain pathways is linked to symptoms of schizophrenia (e.g., hallucinations), and low acetylcholine is associated with memory problems in Alzheimer’s disease. Also, neurotransmitters like endorphins can affect pain perception and mood (runners feel euphoria, “runner’s high,” due to endorphin release). These examples reinforce the general principle that neurotransmitters critically influence behavior.
In both examples provided: when neurotransmitter levels are brought closer to normal (through L-Dopa for dopamine in Parkinson’s or SSRIs for serotonin in depression), the behavioral symptoms improve (motor function or mood), strongly suggesting a causal link. Conversely, if one were to block dopamine in a healthy person (as some antipsychotic drugs do), that person might develop Parkinson-like side effects (tremors, etc.), further illustrating dopamine’s role in movement.

Organization: Begin with a general statement linking neurotransmitters to behavior. Then devote one paragraph or set of sentences to dopamine – describe its normal function and what happens in Parkinson’s disease when it’s lacking (with evidence). Next, have a paragraph or section on serotonin – its normal role and what happens in depression when it’s low (with evidence). It’s effective to clearly separate the two examples for clarity. Finally, a concluding sentence can tie back to the broader theme: these examples show how crucial neurotransmitter balance is for normal behavior and how disturbances can lead to serious disorders.

Depth & Rigor: A strong answer will correctly identify the neurotransmitter and disorder pairs and elaborate on how the imbalance leads to symptoms. It will use proper terminology (e.g., “dopamine-producing neurons in the substantia nigra degenerate” or “low serotonin levels in synapses”). Mentioning treatment (L-Dopa, SSRIs) as evidence of the neurotransmitter’s role adds depth, as does noting specifics like the basal ganglia involvement in Parkinson’s or the limbic system/frontal lobe involvement in depression. The answer might also acknowledge that these disorders are complex (for instance, depression can have multiple causes, not just serotonin, but serotonin is a key biological factor), showing critical thinking. However, since the question directs focus to neurotransmitters, maintaining that focus while acknowledging complexity shows rigor.

Relevance: The answer stays directly on the influence of neurotransmitters on behavior, exactly as asked. It specifically addresses dopamine/Parkinson’s and serotonin/depression, which were explicitly requested. Each example is clearly explained in terms of behavioral effect (motor behavior for dopamine, mood for serotonin). The answer doesn’t stray into other unrelated aspects of Parkinson’s or depression (like psychological therapies or non-neurotransmitter causes); it sticks to neurotransmitters’ roles, which keeps it relevant to the question.

FRQ 5: Explain how psychoactive drugs can alter neurotransmission in the brain. In your answer, define the terms agonist and antagonist and provide an example of each (for instance, how an SSRI medication affects serotonin as an agonist mechanism, and how a drug like naloxone acts as an antagonist).

Thesis/Main Argument: Psychoactive drugs affect brain function and behavior by interfering with neurotransmitter systems. They can act as agonists, enhancing or mimicking the effect of a neurotransmitter, or as antagonists, reducing or blocking the effect of a neurotransmitter. A solid thesis will state that agonists increase neurotransmitter activity (either by imitating the neurotransmitter or increasing its availability), whereas antagonists decrease neurotransmitter activity (by blocking receptors or reducing release), and these actions explain how drugs influence mood, perception, and behavior.

Key Points:

Definition of an agonist: a substance that mimics or enhances the action of a neurotransmitter.
Definition of an antagonist: a substance that blocks or inhibits the action of a neurotransmitter.
Example of an agonist: SSRIs (Selective Serotonin Reuptake Inhibitors) as indirect serotonin agonists, or morphine mimicking endorphins.
Example of an antagonist: Naloxone as an opioid antagonist, or antipsychotic drugs blocking dopamine receptors.
How these drug actions translate to effects on behavior (e.g., relief of depression with SSRIs, reversal of overdose with naloxone).

Supporting Evidence & Examples:

Agonist Example (SSRI): SSRIs, such as Prozac or Zoloft, are used to treat depression by acting as serotonin agonists. They don’t add more serotonin directly, but they block the reuptake of serotonin into the presynaptic neuron, which means more serotonin remains available in the synapse to bind to receptors on the next neuron. By enhancing serotonin’s action, SSRIs improve mood and anxiety symptoms in many depressed patients. This illustrates an agonist effect because the drug increases the neurotransmitter’s impact. Another agonist example is morphine (or heroin), which structurally resembles endorphins (the brain’s natural painkillers) and binds to endorphin receptors in the brain. Morphine mimics endorphins, leading to pain relief and euphoria, much like high levels of endorphins would. This mimicry classifies morphine as an endorphin agonist.
Agonist Example (continued): A more direct agonist example is nicotine. Nicotine acts as an acetylcholine agonist by binding to nicotinic acetylcholine receptors and activating them. Smokers experience increased arousal or pleasure partly because nicotine is stimulating these neurotransmitter pathways (it essentially “stands in” for acetylcholine on certain receptors).
Antagonist Example (Naloxone): Naloxone (brand name Narcan) is an opioid antagonist. In cases of opioid overdose, naloxone can be injected to literally block opioid (endorphin) receptors. Naloxone molecules attach to the same receptors that opioids like heroin or morphine would bind to, but naloxone does not activate those receptors. By occupying the receptor, it prevents the opioid from binding and exerting its effect. This can rapidly reverse life-threatening effects of an overdose (like respiratory depression) because it stops the opioid from acting – a clear demonstration of antagonist action. Similarly, antipsychotic medications for schizophrenia (e.g., Haloperidol) act as dopamine antagonists; they block dopamine receptors in certain brain pathways, thereby reducing dopamine activity and alleviating hallucinations or delusions that are linked to excess dopamine.
Another Antagonist Example: Curare, a toxin used on arrow tips by some indigenous South American groups, is an acetylcholine antagonist. It blocks acetylcholine receptors at the neuromuscular junction (where nerves stimulate muscles). When curare enters the bloodstream, it causes paralysis because motor neurons’ acetylcholine can no longer activate muscles. This is a classic illustration: curare occupies the receptor but doesn’t activate the muscle – it just prevents acetylcholine from triggering muscle contraction.
Behavioral Effects: By understanding agonists and antagonists, we can explain many drug effects. For instance, benzodiazepines like Valium are GABA agonists – they enhance the inhibitory effects of GABA, leading to sedation and anxiety reduction. On the other hand, a drug like caffeine is an antagonist for adenosine (a neurotransmitter that promotes sleepiness); by blocking adenosine receptors, caffeine reduces the feeling of fatigue and keeps someone alert. Each drug’s behavioral outcome (pain relief, alertness, mood elevation, etc.) ties back to whether it’s boosting or blocking a neurotransmitter’s natural action.

Organization: The answer should clearly define and differentiate agonist vs antagonist at the start. Then it should present one specific example of each, in separate paragraphs or clearly separate parts, explaining how that example works in terms of neurotransmitter interaction and what effect it has. The examples given in the prompt (SSRI and naloxone) can be a good structure: one paragraph on SSRIs as agonists, another on naloxone as antagonist. Additional examples (like morphine or antipsychotics) can be mentioned to reinforce understanding. Finally, a summary sentence might emphasize how these interactions account for the drug’s influence on behavior.

Depth & Rigor: A thorough answer doesn’t just name “agonist = helper, antagonist = blocker,” but specifically explains mechanisms: e.g., an agonist might mimic a neurotransmitter by binding to the same receptor (like morphine) or might increase the neurotransmitter’s availability (like SSRIs or MAO inhibitors). It should also clarify that an antagonist typically binds to receptors without activating them (often called a “receptor blocker”). Using correct vocabulary (reuptake, receptors, activate vs. inhibit, etc.) shows precision. The answer might note that some drugs can also cause increased neurotransmitter release or prevent breakdown (another agonist method), demonstrating deeper insight. Also, acknowledging that the brain maintains balance and that chronic use of agonists/antagonists can lead to tolerance (the brain adjusting by reducing receptor sensitivity or number) would show sophisticated understanding, though this is not strictly required by the prompt.

Relevance: The response stays focused on drug actions at the neurotransmitter level, as required. The definitions of agonist and antagonist directly answer the question, and the examples (SSRI, naloxone, etc.) illustrate those definitions in the context of real drugs. The answer doesn’t stray into unrelated territory (e.g., it doesn’t discuss purely behavioral aspects of drugs without linking to neurotransmitters, nor does it get into peripheral effects unrelated to brain neurotransmission). Each example is explicitly tied back to being either an agonist or antagonist, keeping the answer squarely on what the prompt is asking.

FRQ 6: After a head injury, a patient is unable to form new long-term memories but can still recall events from before the accident. Explain which brain structure was most likely damaged and why. In your answer, describe the role of that brain region in memory and how its damage leads to the patient’s symptoms.

Thesis/Main Argument: The patient’s symptoms – an inability to form new long-term memories while retaining old memories – suggest damage to the hippocampus (likely in the medial temporal lobe). The hippocampus is critical for encoding and consolidating new explicit memories (facts and events) into long-term storage. If the hippocampus is damaged (a condition famously exemplified by anterograde amnesia), a person can no longer effectively create new memories, although memories established before the injury (stored elsewhere in the cortex) remain intact. Thus, the hippocampal damage explanation directly addresses why the patient can remember the past but not form new memories.

Key Points:

Identification of the hippocampus as the key brain structure for forming new explicit long-term memories.
Description of the hippocampus’s role: it encodes new declarative memories (episodic and semantic) and is involved in the consolidation process (transferring information from short-term/working memory to long-term storage in the cortex).
Definition of anterograde amnesia (inability to form new memories) versus retrograde amnesia (inability to recall old memories). Noting that this patient has anterograde amnesia, which is consistent with hippocampal damage.
Explanation that previously formed memories are stored in distributed cortical areas, so they can still be retrieved without the hippocampus (explaining why old memories remain).
Possibly mention famous case studies (like patient H.M.) as evidence linking hippocampal damage to this pattern of memory loss.

Supporting Evidence & Examples:

Role of the Hippocampus: The hippocampus acts somewhat like a “save button” for new experiences – it helps stabilize and store the memory trace of events as long-term memories. When someone experiences an event (say a birthday party), the hippocampus helps link all the pieces of that memory (sights, sounds, emotions) and consolidate them so that later the person can recall the party. If the hippocampus is damaged on both sides of the brain, new events cannot be properly recorded, leading to anterograde amnesia.
Patient H.M. (Henry Molaison): A classic example reinforcing this is Henry Molaison, who had both hippocampi surgically removed to treat epilepsy. After the surgery, H.M. could recall his childhood and events from years before (his surgery didn’t erase old memories), but he was unable to form new explicit memories. He could meet someone and then a half-hour later not recognize that he had just met them. This is essentially the same profile as described in the question, and it pinpointed the hippocampus as crucial for new memory formation. H.M. could still learn new motor skills (like drawing a star in the mirror) without remembering doing the task before – illustrating that his procedural memory (which doesn’t rely on the hippocampus) was intact, whereas conscious recall (declarative memory) was not, due to hippocampal loss.
Clive Wearing: Another real-world example is Clive Wearing, a man who had hippocampal damage due to encephalitis. He has only moment-to-moment memory; he can’t form new lasting memories and repeatedly feels like he’s “just awoken.” However, he remembers his wife and how to play piano pieces learned long ago (old memories and skills). This aligns with hippocampal damage: he lives in a constant present (anterograde amnesia) but his older knowledge remains.
Anatomy and Specifics: The hippocampus is located in the temporal lobe. Often, head injuries that damage the hippocampus (or related structures like nearby medial temporal lobe regions) result in this exact condition. If the injury is unilateral (one side), memory impairment might be less severe, but bilateral hippocampal damage (both sides) typically causes profound anterograde amnesia. The fact that the patient in the question can recall earlier events (meaning retrieval from long-term memory is possible) yet cannot encode new ones is a hallmark sign pointing to the hippocampus, rather than other memory-related areas. For example, damage to parts of the frontal lobe might impair working memory or retrieval strategies, but wouldn’t produce the clean “no new memories” profile described. Damage to areas of the cortex could cause specific retrograde amnesia (loss of certain old memories), but this case’s preservation of old memories means cortical storage is fine. It specifically implicates the region responsible for new input—again, the hippocampus.
Conclusion Evidence: Neuroscientific studies (using fMRI) show the hippocampus lights up when people are learning new information or navigating new environments (it’s also important for spatial memory). And when the hippocampus is injured or deteriorates (like in early Alzheimer’s disease), one of the first symptoms is difficulty forming new memories while older memories might be retrieved longer. All these points support the answer that the hippocampus is the structure at play.

Organization: The answer should start by naming the hippocampus as the likely damaged structure. It should then explain what the hippocampus normally does in terms of memory formation. Next, directly connect that function to the symptom: without a functioning hippocampus, new memories cannot be stored (causing anterograde amnesia), but recall of pre-existing memories (already stored in the cortex) is unaffected. It would help to mention the term “anterograde amnesia” to categorize the patient’s condition. Incorporating an example or case study (like H.M.) in a separate sentence or two reinforces the explanation. Finally, sum up that hippocampal damage perfectly accounts for the described scenario.

Depth & Rigor: A high-quality answer will include the correct terminology (hippocampus, anterograde amnesia, memory consolidation). It might clarify that the hippocampus is particularly involved in explicit memory (facts and events) and not necessary for implicit memory (skills, conditioning), which is why the patient might still learn new skills or exhibit conditioning even if they can’t recall experiences. Mentioning that older memories are stored in the cerebral cortex (like visual aspects in occipital, auditory in temporal, etc., with the hippocampus serving as an index or hub initially) shows a sophisticated understanding of memory systems. By referencing well-known evidence (H.M., Clive Wearing), the answer demonstrates that this is a well-documented phenomenon.

Relevance: The response zeroes in on explaining the patient’s symptoms via hippocampal damage, just as the question asks. It doesn’t drift into unrelated memory topics (for example, it wouldn’t start discussing short-term memory capacity or the cerebellum’s role in procedural memory except insofar as it contrasts with hippocampal function). The inclusion of examples and terms like “anterograde amnesia” are directly relevant to linking brain structure to behavior here. Every part of the answer is aimed at answering “which structure and why,” making it entirely pertinent to the question.

FRQ 7: A split-brain patient (someone who had their corpus callosum severed) is shown an image of a key in their left visual field and a cup in their right visual field. Describe how the patient will verbally report what they saw and how they can demonstrate recognition of the other object, explaining the roles of the left and right hemispheres in this situation.

Thesis/Main Argument: In a split-brain patient, the left and right hemispheres of the brain cannot communicate directly due to the cut corpus callosum. Because the left hemisphere (which receives information from the right visual field) is typically dominant for language and speech, the patient will verbally report seeing the object that was in the right visual field (the cup). The right hemisphere (receiving information from the left visual field) cannot produce speech, so the patient will not verbally name the object on the left (the key). However, the patient can still demonstrate that the right hemisphere saw the key by using non-verbal means, such as drawing the key with the left hand or selecting the key by touch with the left hand, since the right hemisphere controls the left hand.

Key Points:

In split-brain patients, visual information from the left visual field goes to the right hemisphere, and information from the right visual field goes to the left hemisphere, with no cross-talk between hemispheres.
The left hemisphere typically contains the language centers (Broca’s and Wernicke’s areas in most right-handed individuals), enabling spoken language.
The right hemisphere is largely nonverbal but can process spatial information and control the left side of the body.
Expected outcome: The patient will say they saw the “cup” (right visual field -> left hemisphere speech), but they won’t initially report the “key” (left visual field -> right hemisphere, no speech). They can indicate the key nonverbally (e.g., by picking up a key or drawing a key with their left hand).

Supporting Evidence & Examples:

Verbal Report (Left Hemisphere): When the cup is shown in the right visual field, the image is processed by the visual cortex in the left hemisphere. Because the left hemisphere can formulate speech, the patient will be able to name the cup. If asked “What did you see?” the split-brain patient will likely respond, “I saw a cup.” This is because the left hemisphere “saw” the cup and it also controls language output; it has no awareness of the key on the left side because the corpus callosum is cut and the right hemisphere’s information isn’t shared.
Nonverbal Recognition (Right Hemisphere): The key shown in the left visual field is processed in the right hemisphere, which is mute (cannot produce language). Therefore, the patient cannot say “key” because the left hemisphere (which speaks) never got the information about the key. However, the right hemisphere does know a key is there – it has perceived it. The right hemisphere controls the left hand. So, if the patient is asked to use their left hand to pick up or point to the object they just saw (from a selection of objects), the left hand can correctly choose the key. For example, if several items are on a table out of sight, the patient’s left hand might feel around and pick up a key, demonstrating that the right hemisphere “remembers” seeing the key and guides the left hand to select it. Similarly, the patient could draw a key with their left hand without verbally acknowledging it.
Detailed Example: In classic split-brain experiments by Roger Sperry and Michael Gazzaniga, patients were shown, say, a snow scene to the right hemisphere and a chicken claw to the left hemisphere. The patient verbally said they saw a chicken claw (left hemisphere speaking) and might pick a related image (a chicken) with the right hand. But when asked to point to a related image with the left hand (controlled by right hemisphere), the patient might point to a shovel (to clean snow, related to the snow scene that only the right hemisphere saw). When asked why they pointed to a shovel, the verbal left hemisphere confabulates (e.g., “Oh, the shovel is to clean out the chicken coop”) because it doesn’t truly know what the right hemisphere saw. This anecdote underscores how each hemisphere acts separately when the connection is severed. In our scenario, the same principle applies: the left hemisphere can articulate only what it knows (the cup), and the right hemisphere can act (via left hand) on what it knows (the key) even though it can’t speak.
Roles of Hemispheres: The left hemisphere’s specialization in language means it’s the one saying “cup.” The right hemisphere, while it cannot speak, has other abilities (like spatial processing, simple language comprehension, facial recognition). It “knows” about the key but can’t verbalize it. However, it can use alternative methods to communicate that knowledge, such as guiding motor actions of the left hand. This phenomenon shows the lateralization of brain function: certain cognitive functions are dominated by one side. In most people, speech is lateralized to the left hemisphere. The split-brain condition is a dramatic demonstration of this, as it isolates the two sides.

Organization: The answer should be organized by first explaining the setup: in split-brain patients, each half of the visual field is processed by the opposite hemisphere and the hemispheres cannot share information due to the severed corpus callosum. Then clearly state what happens with the right visual field (cup -> left hemisphere -> speech) and what happens with the left visual field (key -> right hemisphere -> no speech). After describing the verbal report, describe the nonverbal demonstration. It’s helpful to explicitly mention the left and right hemisphere roles. Finally, tie it together by noting this shows how the hemispheres specialize (left in speech, right in nonverbal tasks).

Depth & Rigor: An excellent answer might mention terms like corpus callosum (the bundle of neural fibers that is cut in split-brain patients, normally responsible for interhemispheric communication). It would likely mention that the left hemisphere is typically where Broca’s area and Wernicke’s area reside (language production and comprehension). It could also mention that the right hemisphere can comprehend simple language (it might understand “key” but not be able to say it) – for instance, a split-brain patient’s right hemisphere can follow simple instructions given to the left visual field, like “point to the object you saw.” Citing the well-known split-brain experiment results (like the chicken claw vs snow scene story, or the ability to draw two different shapes with each hand simultaneously) would add rigor. Discussing the contralateral control (each hemisphere controlling opposite hand/visual field) by name shows technical accuracy. The key to rigor here is correctly explaining why the patient behaves that way neurologically, not just stating the outcome.

Relevance: The response directly answers both parts of the question: what the patient will verbally report (and why), and how they can indicate the other object (and why). It stays focused on the roles of the hemispheres in a split-brain context. There’s no unnecessary information about other brain parts or unrelated symptoms. The scenario of key vs cup is explicitly addressed, ensuring the answer is tailored to the question’s specifics. The explanation of hemisphere roles (left for speech, right for spatial/visual recognition) is exactly relevant to understanding the patient’s behavior.

FRQ 8: Explain the concept of brain plasticity and how it enables recovery of function after brain injury. Provide an example or research finding that illustrates the brain’s ability to reorganize (such as how a child’s brain adapts after a hemispherectomy or how cortical areas can change after practice or injury).

Thesis/Main Argument: Brain plasticity refers to the brain’s ability to change its structure and function in response to experience, learning, or damage. This malleability allows the brain to reorganize itself – for example, if one part is injured, other parts may adapt to take over its functions, especially in children or through therapy. A strong thesis might state: “The brain is not a static organ; it exhibits plasticity, meaning that through rerouting neural connections and even growing new ones, it can compensate for injuries and adapt to new circumstances, as evidenced by cases where individuals regain abilities due to neural reorganization.”

Key Points:

Definition of brain plasticity (also known as neuroplasticity): the ability of the brain to modify its connections or reassign functions to different areas as needed.
Plasticity is generally higher in childhood but exists throughout life (though to a lesser degree in adults).
After a brain injury, intact areas can sometimes assume functions of damaged areas, especially if prompted by rehabilitation (e.g., therapy encouraging use of an affected limb).
Examples of plasticity: hemispherectomy in children (removal of one cerebral hemisphere) with surprisingly minimal long-term deficits due to the remaining hemisphere adapting; motor cortex reorganization after limb amputation (neighboring areas take over, leading to phenomena like phantom limb sensations or improved use of remaining limbs); changes in cortical maps with practice (e.g., musicians have enlarged representation for finger control).

Supporting Evidence & Examples:

Childhood Hemispherectomy Example: In extreme cases of epilepsy, surgeons have removed an entire hemisphere in a young child (hemispherectomy) to stop seizures. Astonishingly, many of these children go on to lead relatively normal lives with near-typical cognitive function. If a right hemisphere is removed in a 5-year-old, for instance, functions we normally associate with the right hemisphere (like spatial abilities or even left-side motor control) can often be taken over by the remaining left hemisphere. These children might have a slight limp or weaker use of one hand, but they can walk, run, speak, and even eventually go to school like other kids. This dramatic example shows the brain’s capacity to rewire – the intact hemisphere forms new connections to control both sides of the body and cover for the lost tissue. The younger the patient, the more complete the recovery, illustrating that plasticity is greatest early in life.
Stroke Recovery and Therapy: In adults, if one area of the brain is damaged by a stroke (say the area controlling the right arm movement in the left motor cortex), often the patient cannot initially use that arm. However, through rehabilitation and the brain’s plasticity, other nearby networks or the corresponding region in the opposite hemisphere can sometimes partially take over control. Therapies like constraint-induced movement therapy (where the good arm is restrained to force use of the impaired arm) are effective because they drive plastic changes: the brain reorganizes by strengthening alternative pathways for moving the impaired arm. Over time, patients can regain significant function, demonstrating plasticity in action. Brain scans before and after therapy show that new areas light up when using the previously paralyzed limb, indicating that the brain has reassigned functions.
Sensory Reorganization Example: If someone loses their sight, the visual cortex doesn’t just sit idle. Research using fMRI and PET scans has found that in blind individuals, the occipital lobe (which normally processes vision) can become responsive to auditory or tactile tasks (like Braille reading). This cross-modal plasticity means the brain is reallocating resources – the visual cortex in a blind person might help with hearing distinctions or touch, improving those senses. In one study, temporarily blindfolded sighted individuals for a few days started to show visual cortex activity when using touch to read Braille patterns, and their ability to discern the patterns improved. Once the blindfold was removed, the visual cortex returned to its normal function. This illustrates rapid, reversible plastic changes in adults.
Musician’s Brain: On the structural side, MRI studies show that people who practice a skill intensively have slight brain anatomy changes. For example, violinists (who use their left fingers extensively on the strings) have a larger somatosensory cortex area devoted to those left hand fingers compared to non-musicians. London taxi drivers, who undergo extensive navigation training, have been found to have an enlarged posterior hippocampus (involved in spatial memory). These examples show that the brain’s structure can change (growing certain areas or increasing synaptic density) in response to repeated practice – a form of plasticity related to learning.
Phantom Limb and Reorganization: In cases of amputation, patients often experience a “phantom limb” sensation (feeling the missing limb). A classic explanation for this is cortical reorganization: for example, in the sensory cortex, the area that used to receive input from the amputated hand might get taken over by inputs from the face or arm. So when the face is touched, it invades the “hand” area and the person might feel it in the phantom hand. Over time, with therapy (like mirror therapy where they watch a reflection of their intact hand moving), the brain can adjust and reduce the phantom pain. This shows both maladaptive plasticity (initially causing confusing sensations) and adaptive plasticity (reducing pain through reorganization).

Organization: The answer should begin by defining brain plasticity in clear terms. Then, it should provide at least one illustrative example of plasticity aiding recovery – explaining the scenario and how the brain adapts. The example could be structured as: situation -> what changed in the brain -> resulting recovery/improvement. It might be beneficial to contrast recovery potential in children vs adults to emphasize plasticity’s variability. A concluding remark could generalize that plasticity is the reason learning and recovery are possible, tying together the concept and example(s).

Depth & Rigor: A thorough answer might mention terms like “reorganization of cortical maps”, “neuronal sprouting” (neurons growing new dendrites/axons to form new connections), or “synaptic plasticity”. It would make clear that plasticity can involve forming new connections or strengthening existing weaker connections. If discussing childhood vs adult, it could reference “critical periods” when plasticity is highest. Using the term “neuroplasticity” is appropriate as a synonym. The best answers will not only give an example but explicitly link it back to the concept: e.g., “This recovery was possible because of the brain’s plasticity – the ability of other neurons to change their function or make new connections to compensate for the loss.” If referencing research, naming known scientists (like Michael Merzenich for cortical map plasticity in animals, or Eleanor Maguire for the taxi driver study) can add credibility, though not necessary. The key is showing understanding that the brain’s wiring is not fixed and can be reshaped by experience or injury.

Relevance: The answer squarely addresses brain plasticity and recovery after injury, exactly as asked. The example provided (be it a hemispherectomy case, stroke rehab, or a learning-induced change) directly illustrates plasticity rather than something tangential (it avoids unrelated facts like memory storage or reflexes that don’t involve reorganization). The discussion clearly connects the example to the broader concept of plasticity, ensuring that the example isn’t just a story but proof of the concept in action. All parts of the explanation serve to underscore how plasticity works and why it’s important, keeping it highly relevant.

FRQ 9: Compare and contrast two techniques for studying brain structure and function: for example, MRI (magnetic resonance imaging) and fMRI (functional MRI). In your answer, describe how each technique works and what type of information it provides to researchers, highlighting their differences and uses.

Thesis/Main Argument: MRI and fMRI are non-invasive imaging tools used in neuroscience, but they serve different purposes. An MRI scan provides a detailed static image of the brain’s structure (anatomy), whereas an fMRI scan measures brain function by detecting changes associated with blood flow, thus showing which parts of the brain are active during certain tasks. The thesis should emphasize that MRI is about anatomy (what the brain looks like), and fMRI is about physiology in action (what the brain is doing).

Key Points:

MRI (Structural MRI): Uses strong magnetic fields and radio waves to produce high-resolution images of brain structures. Shows the size, shape, and integrity of brain tissues (gray matter, white matter, fluid, etc.). Useful for detecting tumors, brain damage, or anatomical differences.
fMRI (Functional MRI): Builds on MRI technology to measure changes in blood oxygenation (the BOLD signal – Blood Oxygen Level Dependent signal) over time. Highlights active brain regions by detecting where blood flow (oxygen use) increases when a person performs a task. Produces maps of brain function or activation.
How each works: MRI measures signals from hydrogen atoms in water of different tissues (structure), fMRI measures changes in magnetic properties of blood as oxygen is used (function).
Information provided: MRI provides a snapshot of structure (e.g., can see a lesion or the volume of the hippocampus), fMRI provides a dynamic view of functional activity (e.g., which areas light up when someone is solving a math problem).
Differences: MRI = one-time static image (spatial resolution is very high, a few millimeters), fMRI = series of images over time (temporal resolution a couple seconds, showing changes). MRI can’t tell you what the brain is doing at that moment, fMRI can but with less fine structural detail.
Uses: MRI for clinical diagnosis (tumors, stroke, anatomical research); fMRI for experimental cognitive neuroscience (identifying brain regions involved in specific tasks, understanding functional connectivity).

Supporting Evidence & Examples:

MRI Example: If a patient has chronic seizures, a doctor might order an MRI of the brain to check for structural causes such as a tumor, scar tissue, or developmental malformation. The MRI might reveal a benign tumor in the temporal lobe, clearly delineating its boundaries and its impact on surrounding tissue. This shows MRI’s strength in anatomical detail – you can see differences between gray matter (neuronal cell bodies), white matter (myelinated axons), and cerebrospinal fluid. For researchers, an MRI can allow measurement of brain regions; for example, comparing hippocampal volume in people with Alzheimer’s vs. healthy controls. MRI uses magnetic fields – a person lies in a tube, radio waves excite hydrogen nuclei, and as they return to alignment, the machine detects signals to build a picture. It’s excellent for seeing structure but it’s just a picture at one point in time.
fMRI Example: A cognitive psychologist might use fMRI to study which parts of the brain activate when a person memorizes a list of words versus when they rest. During the memory task, fMRI could show increased blood flow in the left prefrontal cortex and hippocampus, indicating these areas are active in encoding new memories. Each image is like a map highlighting regions of greater oxygenated blood. Over the duration of the scan, the researcher can generate a video or statistical map of activity changes. For instance, fMRI has been used to show that when people look at faces, the fusiform face area in the temporal lobe shows heightened activation, whereas it doesn’t when they look at non-face objects – evidence of a specialized face-processing region. This illustrates how fMRI provides functional information that an MRI alone would not reveal (an MRI would show the fusiform area’s structure but not that it’s specifically active for faces).
Comparative Points: Both MRI and fMRI involve lying in a large magnetic scanner and have no radiation exposure (unlike CT or PET). MRI typically takes a few minutes for a scan; fMRI experiments involve scanning the brain over a period (often many minutes, broken into trial blocks) to observe changes. MRI resolution might allow you to see a 2mm tumor; fMRI spatial resolution is also quite good (3-4mm typically), but its time resolution is slower – there’s a lag of a couple seconds as blood flow changes. Another difference: MRI can be used on unconscious or immobile subjects (even post-mortem for structure), fMRI requires a cooperative subject performing tasks in the scanner to generate meaningful functional data.
Other Methods Mention (if contrasting): If discussing differences, one might also briefly contrast these with other imaging: e.g., PET scans also show function by using radioactive glucose metabolism imaging but have lower resolution than fMRI, and EEG shows electrical activity (function) with great time resolution but poor spatial resolution. This can underscore that MRI = structure, fMRI = function, with each having a niche.

Organization: The response should first introduce both techniques. A good approach is one paragraph focusing on MRI (what it is, how it works, what it shows) and another on fMRI (what it is, how it works, what it shows). Then a concluding comparison noting differences and perhaps complementary uses. Alternatively, it could be structured feature-by-feature: e.g., “Technique, What it measures, How it works, Use cases” comparing MRI vs fMRI along each feature. The key is that both similarities (both use magnetic technology, both give insight into the brain, non-invasive) and differences (structure vs function, static vs dynamic) are highlighted. The question specifically says “compare and contrast” – so explicitly stating at least one similarity and several differences is important.

Depth & Rigor: A thorough answer will mention the BOLD signal for fMRI (even if not by acronym, at least saying fMRI detects oxygenated blood flow changes), and will correctly note that neither MRI nor fMRI uses X-rays (unlike CT) or requires radioactive tracers (unlike PET). It might mention spatial resolution and temporal resolution as factors in comparing. It should avoid common misconceptions, like thinking fMRI directly measures neural activity (it measures a proxy – blood flow). It might also mention that MRI can be adapted for other structural measures like DTI (Diffusion Tensor Imaging) for white matter, whereas fMRI is specifically functional. Including who uses them (clinicians vs researchers) adds context. Using the full names (magnetic resonance imaging, functional magnetic resonance imaging) at least once shows clarity.

Relevance: The answer directly addresses MRI and fMRI as requested (assuming those were chosen; if others, similarly, it stays on the chosen two techniques). It describes how each works and what information each provides, which is exactly what the question calls for. The comparison is made clear with phrases like “in contrast” or “whereas” to explicitly highlight differences. It doesn’t wander off into, say, how to interpret brain scans clinically or other methods not asked about (unless briefly to contextualize differences). Everything included serves to explain MRI vs fMRI, making the answer squarely relevant to the question.

FRQ 10: Identify two hormones from the endocrine system and describe their effects on human behavior. For each hormone, specify where it is produced and give an example of how an imbalance or surge of that hormone might influence a person’s mood, energy, or behavior (for instance, adrenaline in a fight-or-flight situation and cortisol under chronic stress).

Thesis/Main Argument: Hormones are chemical messengers released by endocrine glands that travel through the bloodstream and affect various bodily functions and behaviors. Two important examples are adrenaline (epinephrine) and cortisol, both produced by the adrenal glands. Adrenaline triggers immediate fight-or-flight arousal affecting energy and alertness, while cortisol governs longer-term stress responses and energy regulation, affecting mood and health especially when chronically elevated. The thesis might summarize: “Hormones like adrenaline and cortisol can powerfully influence behavior – adrenaline causes acute excitement and physiological arousal in emergencies, and cortisol, when persistently high due to chronic stress, can lead to fatigue, anxiety, or other health issues – illustrating how the endocrine system affects our mood and actions.”

Key Points:

Definition of hormones and how they differ from neurotransmitters (hormones travel through blood, generally slower, widespread effects).
Adrenaline (Epinephrine): Produced by the adrenal medulla (inner part of adrenal glands, which sit atop the kidneys). Effects: increases heart rate, blood pressure, blood flow to muscles, and alertness; part of the immediate fight-or-flight response. Behavioral impact: heightened alertness, possible feelings of fear/excitement, and mobilization for action (e.g., can make someone jump out of danger or feel “amped up”). Example of surge: riding a roller coaster or facing an sudden stressor releases adrenaline, causing a burst of energy and rapid heartbeat.
Cortisol: Produced by the adrenal cortex (outer part of adrenal glands). It’s a stress hormone that helps regulate metabolism, blood sugar, and the body’s response to long-term stress. Behavioral/mood impact: in short term, it provides energy (by increasing glucose) and can enhance memory of stressful events, but chronically high cortisol is linked to anxiety, depression, concentration problems, and suppressed immune function. Example of imbalance: people under chronic stress (like caregiving for an ill family member) may have consistently elevated cortisol, leading to symptoms like fatigue, irritability, and increased illness (cortisol weakens the immune response).
(Optional additional hormone if needed to reach two distinct ones: could stick with adrenaline and cortisol, or mention others such as thyroxine from the thyroid or oxytocin from the pituitary for more variety, but question suggests adrenaline and cortisol example.)
Tie back: These hormonal changes show how the endocrine system can ramp us up (adrenaline: acute stress, excitement) or wear us down (cortisol: chronic stress), thereby influencing our behavior and emotional state.

Supporting Evidence & Examples:

Adrenaline Example: Imagine nearly getting into a car accident: your adrenal medulla instantly pumps adrenaline into your bloodstream. Within seconds, you feel your heart pounding, you’re breathing faster, and you might even tremble afterward. Behaviorally, you become extremely alert (maybe time “feels slower” in the moment due to heightened arousal) and you may either hit the brakes or swerve quickly (enhanced reaction speed and strength). After the incident, you might feel jittery or excited – that’s the adrenaline rush. This hormone’s surge is adaptive for survival, giving you the immediate energy and focus to deal with emergencies. If someone has an overactive adrenal gland or a tumor (pheochromocytoma), they may experience random adrenaline surges: panic-like symptoms, sweating, rapid heartbeat even without an obvious trigger, showing how too much adrenaline can cause persistent anxiety or panic sensations.
Cortisol Example: Think of a student during final exam week. Their adrenal cortex is likely secreting extra cortisol each day in response to the psychological stress. This cortisol helps keep them going – it raises blood sugar (so they have energy even if they skip a meal), and it initially might help them remain alert. However, if cortisol remains high over many weeks, the student might start feeling run-down: common signs of chronic high cortisol include difficulty sleeping (cortisol disrupts sleep patterns), a tendency to gain weight especially around the abdomen (cortisol affects metabolism and appetite), and mood disturbances (they might feel more anxious or emotionally fragile). Another example: in Cushing’s syndrome, where cortisol levels are abnormally high (either due to medication or a tumor), patients often experience mood swings, irritability or depression, and cognitive difficulties, alongside physical changes like fat redistribution and high blood pressure. On the flip side, too low cortisol (as in Addison’s disease) causes fatigue, low blood pressure, and can lead to depressive moods – showing that balance is key.
Other Hormone Example (if given): Thyroid Hormone (Thyroxine): Produced by the thyroid gland in the neck, it regulates metabolism. Imbalance effects: hyperthyroidism (too much thyroxine) can cause nervousness, restlessness, hyperactivity, insomnia, and weight loss – behaviorally, the person might feel overly anxious or jittery. Hypothyroidism (too little) leads to fatigue, sluggishness, depression, and weight gain. So, a thyroid hormone imbalance can mimic or contribute to psychological conditions – for instance, someone with undiagnosed hypothyroidism might feel depressed and low-energy until treated.
Oxytocin: Produced by the hypothalamus and released by the pituitary gland, oxytocin is often dubbed the “love” or “bonding” hormone. For example, oxytocin surges during hugging, orgasm, and especially childbirth and breastfeeding, promoting bonding between mother and infant. Behaviorally, higher oxytocin is associated with increased trust and social bonding. If an experimenter administers oxytocin via nasal spray, people might show greater tendency to trust others in a monetary exchange game (research supports this). While not typically “imbalanced” in the same way as others, it illustrates how a hormone can modulate social behavior and emotional feelings.
Integration: These examples underscore that hormones can have very broad effects (unlike localized neurotransmitters, hormones reach many organs). Adrenaline’s effect is short-lived, preparing for immediate action, whereas cortisol’s effect is more prolonged, influencing longer-term mood and health. Both are critical to how we respond to stress. Thyroid hormones set our baseline energy and mood; oxytocin influences social interactions. The endocrine system, through these hormones, interacts closely with the nervous system – for instance, the hypothalamus in the brain controls the pituitary (the master gland), which then controls other glands like the adrenals and thyroid. This brain-body connection means our psychological state can alter hormone levels and vice versa.

Organization: The answer should introduce the idea that hormones affect behavior, then clearly take one hormone at a time. A good structure is: Name Hormone 1, state gland and primary effects, give example of its surge or deficit and how that changes behavior/mood. Then Name Hormone 2, do the same. Ensure the examples are specific and illustrate the hormone’s role. A concluding line might generalize how these two examples show the endocrine system’s influence on behavior in both acute and chronic ways.

Depth & Rigor: Using correct hormone names and sources (e.g., adrenaline = epinephrine from adrenal medulla, cortisol from adrenal cortex, etc.) demonstrates precision. Including the alternate name epinephrine for adrenaline shows awareness of terminology. The answer should make clear the difference between immediate stress responses (adrenaline) and sustained stress (cortisol) if using those two, which shows understanding of the body’s stress system (the SAM axis for adrenaline, HPA axis for cortisol). If adding other hormones, correctly stating their source (pituitary releases oxytocin but it’s made in hypothalamus; thyroid hormones from thyroid; etc.) is important. Also, noting that hormones work via bloodstream and can have system-wide effects (thus affecting multiple behaviors or organs) contrasts them with the nervous system’s localized signals, adding depth. Avoiding confusion between hormones and neurotransmitters (e.g., not calling dopamine a hormone – it’s a neurotransmitter, except in certain contexts) will keep the answer accurate.

Relevance: The answer directly identifies two hormones and ties each to behavior, just as asked. The examples (fight-or-flight for adrenaline, chronic stress for cortisol) are clearly relevant to mood/energy/behavior changes. The structure ensures each hormone’s effects are explained. There’s no drift into discussing neural processes or unrelated hormones – everything focuses on endocrine outputs and behavior. The explicit link of hormone -> behavioral outcome keeps the response on target.