What the exam asks
- Multiple-choice questions (Section I): Expect scenarios describing an unfamiliar medication or toxin at the synapse; you must identify whether it acts as an agonist, an antagonist, or a reuptake inhibitor for one of the eight CED neurotransmitters (dopamine, serotonin, norepinephrine, glutamate, GABA, endorphins, substance P, or acetylcholine). You will also match physiological or psychological symptoms to drug classes or distinguish between tolerance and withdrawal.
- Free-response questions (Section II): An AAQ or EBQ may feature a peer-reviewed clinical trial testing a pharmacological treatment or studying substance use. In an EBQ, correctly applying concepts like reuptake inhibition, neuroadaptation, or withdrawal as external psychological knowledge in parts B(ii) or C(ii) to explain how the evidence supports your claim can earn the second reasoning point.
Core ideas
Synaptic mechanisms: Agonists, antagonists, and reuptake inhibitors
Psychoactive drugs alter neural communication by increasing or decreasing the effectiveness of neurotransmitters across the synaptic gap:
- Agonists increase the effectiveness of a neurotransmitter. They may mimic the neurotransmitter by binding to and activating postsynaptic receptor sites, stimulate the presynaptic neuron to release more of the neurotransmitter, or prevent its breakdown in the synapse.
- Reuptake inhibitors are a specific mechanism that blocks the presynaptic neuron’s transporter proteins from reabsorbing excess neurotransmitter molecules from the synaptic cleft. Because the neurotransmitter remains in the synapse longer, it continues to bind to postsynaptic receptors, amplifying its signal (an agonistic effect). For example, cocaine blocks the reuptake of dopamine, serotonin, and norepinephrine, and SSRIs block the reuptake of serotonin.
- Antagonists decrease or block the effectiveness of a neurotransmitter. Most commonly, an antagonist binds to postsynaptic receptor sites without activating them, acting like a key that fits into a lock but will not turn, thereby blocking the endogenous neurotransmitter from binding. Antagonists can also inhibit neurotransmitter synthesis or release (e.g., botulinum toxin blocks acetylcholine release, causing paralysis).