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Multiple Choice

Which stimulant blocks reuptake of dopamine, serotonin, and norepinephrine and is associated with a risk of stroke or seizures within about two hours of use?

Blocking the reuptake of dopamine, serotonin, and norepinephrine is a hallmark of cocaine’s action. By inhibiting the transporters for these monoamines (DAT, SERT, and NET), cocaine floods the synapse with each neurotransmitter, driving intense sympathetic arousal, vasoconstriction, and elevated blood pressure. This combination can rapidly disrupt cerebral blood flow and neuron firing, increasing the risk of stroke and seizures within a short window after use, often within a couple of hours. MDMA does elevate serotonin and other monoamines but its primary effect is serotonin release with reuptake inhibition not as uniform across all three transmitters. Methamphetamine boosts monoamines mainly by triggering release and reversing transporters rather than simply blocking reuptake of all three to the same extent. Opioids don’t block monoamine reuptake at all and act mainly on opioid receptors, so they don’t fit the described mechanism or the associated acute cerebrovascular risk profile.

Blocking the reuptake of dopamine, serotonin, and norepinephrine is a hallmark of cocaine’s action. By inhibiting the transporters for these monoamines (DAT, SERT, and NET), cocaine floods the synapse with each neurotransmitter, driving intense sympathetic arousal, vasoconstriction, and elevated blood pressure. This combination can rapidly disrupt cerebral blood flow and neuron firing, increasing the risk of stroke and seizures within a short window after use, often within a couple of hours.

MDMA does elevate serotonin and other monoamines but its primary effect is serotonin release with reuptake inhibition not as uniform across all three transmitters. Methamphetamine boosts monoamines mainly by triggering release and reversing transporters rather than simply blocking reuptake of all three to the same extent. Opioids don’t block monoamine reuptake at all and act mainly on opioid receptors, so they don’t fit the described mechanism or the associated acute cerebrovascular risk profile.