Cocaine causes feelings of happiness and agitation

The argument

Cocaine interferes with the brain's signalling processes by blocking the removal of neurotransmitters from synapses. Ordinarily a neurotransmitter released into a synapse is cleared once it has delivered its signal, which is what allows signalling to be discrete rather than continuous. Cocaine binds with the transport molecules responsible for the uptake of dopamine, so the clearing step does not occur and dopamine accumulates within the synapses instead. The consequences follow from what dopamine does. Because its presence is integral to the brain's reward system, the accumulation amplifies reward signals beyond the level that any ordinary experience would produce, and this amplification is experienced as euphoria. The elevation in mood and alertness associated with stimulants is therefore not the drug supplying a feeling directly; it is the drug interfering with a mechanism the brain already uses, so that existing reward signalling is registered at a greatly increased intensity. The same interference accounts for the effects that appear over a longer period. Sustained disruption of this signalling can lead to abnormalities in the cortex, and cocaine use is associated with impairments to cognition, motor function and reaction time. These are described as changes to the tissue involved rather than as symptoms present only while the drug is active. Dependency can develop from long-term use, and proponents of this account tie it to the same mechanism: a reward system repeatedly driven far beyond its normal range adjusts to that input, so that ordinary sources of reward no longer register as they did. Depression is common when usage stops, which is consistent with a reward system that has adapted to an artificially amplified signal and is left, once the signal is withdrawn, responding weakly to everything else.

Premises

Counter-arguments

The pharmacology is incomplete in a way that matters for the argument's own title. Cocaine blocks the reuptake of serotonin and noradrenaline as well as dopamine, and it is the noradrenergic action that accounts for much of the agitation, raised heart rate and vasoconstriction the title names — so a dopamine-only mechanism explains the euphoria while leaving the second half of the stated effect unexplained. Cocaine is also a sodium-channel blocker and therefore a local anaesthetic, which is why it retains limited clinical use in certain procedures, and that action has nothing to do with reward signalling at all. "Elevates mood" also describes only the acute phase. Tolerance, the dysphoric crash that follows a dose, and sensitisation to agitation and paranoia on repeated use mean the same drug lowers mood over the course of use — as the body's own reference to depression on cessation concedes. Grouping effects at the level of a drug class blurs further differences: amphetamines act largely by promoting transmitter release rather than by blocking reuptake, and act for far longer, while some substances conventionally classed as stimulants raise alertness with little euphoria. A generalisation drawn from cocaine's dopamine transporter blockade describes cocaine better than it describes stimulants.

Rejecting the premises

[Rejecting P1] Cocaine blocks the reuptake of serotonin and noradrenaline as well as dopamine, and separately blocks sodium channels as a local anaesthetic, so a dopamine-only mechanism is incomplete. [Rejecting P2] Euphoria describes the acute phase only — tolerance, the dysphoric crash and sensitisation to agitation and paranoia mean mood falls with continued use, as the premise's own reference to depression concedes — and mechanisms differ across the stimulant class, so cocaine does not stand in for it.