The receptor itself can be a drug target. Three categories of receptor-acting drugs cover most of the clinical pharmacology you will encounter: agonists, antagonists, and allosteric modulators.
Agonists mimic the neurotransmitter. They bind the receptor and produce the same effect as the endogenous ligand would. Full agonists produce maximal receptor activation (morphine at the mu-opioid receptor; insulin at the insulin receptor). Partial agonists bind the receptor tightly but produce only a submaximal effect even at full occupancy — they have a built-in ceiling. Buprenorphine is the canonical partial mu-opioid agonist; it occupies the receptor and produces enough effect to suppress withdrawal and craving without the euphoric surge that drives addiction. Aripiprazole is a partial dopamine D2 agonist used in psychotic and bipolar disorders.
Antagonists block the receptor without activating it. They occupy the binding site, so the endogenous neurotransmitter cannot. Examples include haloperidol (D2 antagonist), naloxone and naltrexone (mu-opioid antagonists), prazosin (alpha-1 adrenergic antagonist), diphenhydramine (H1 antihistamine), and most antipsychotics.
Allosteric modulators bind to a different site on the receptor (the allosteric site, distinct from where the neurotransmitter binds) and change how the receptor responds when the neurotransmitter is present. They cannot activate the receptor on their own — they need the endogenous ligand to be there.
Positive allosteric modulators enhance the response. Benzodiazepines are positive allosteric modulators of the GABA-A receptor: they do not bind GABA's binding site, and they cannot activate the GABA-A receptor alone, but when GABA is present they make the receptor open more easily, amplifying inhibition. This is why benzodiazepines are safer than barbiturates in overdose — they cannot drive GABA inhibition past what endogenous GABA can produce, while barbiturates can directly open GABA channels at high doses, producing fatal respiratory depression.
Negative allosteric modulators dampen the response. They reduce the effect of the endogenous neurotransmitter without blocking the binding site directly. There are fewer clinically prominent examples, but the concept matters.
Inverse agonists are a less common but conceptually important category. They bind the receptor and produce the opposite effect of the agonist — they actively reduce the receptor's baseline (constitutive) activity below resting levels. Pimavanserin is a 5-HT2A inverse agonist used for Parkinson's disease psychosis.
Subtype selectivity matters because different receptor subtypes do different things even when they share a neurotransmitter. The dopamine D1 vs D2 distinction we discussed in Stage 5 matters enormously for which clinical effect you get. The 5-HT1A, 5-HT2A, 5-HT2C, and 5-HT3 receptor subtypes for serotonin produce different effects when activated, and selective drugs (buspirone for 5-HT1A; ondansetron for 5-HT3; pimavanserin for 5-HT2A) take advantage of this.
Hold the four categories: full agonist, partial agonist, antagonist, allosteric modulator (positive or negative). Combined with subtype selectivity, these categories let you predict and reason about every receptor-targeted medication in psychiatry and neurology.