Abstract
Rapid solution exchange techniques were used to characterize 5-hydroxytryptamine type 3A (5-HT3A) receptor function. The 5-HT3A receptor agonists 5-HT and dopamine were found to have distinct effects on activation, deactivation, and desensitization. Although isoflurane does not enhance submaximal 5-HT-evoked currents or reduce the receptor's agonist EC50 for current activation, it significantly accelerates the rates of activation, deactivation, and desensitization. This acceleration may produce important changes in 5-HT3A receptor-mediated currents in synapses where agonist exposure is brief.
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