Electrophysiological aspects of 5-HT receptor-mediated adenylyl cyclase activation

Abstract

Stimulation of adenylyl cyclase by 5-hydroxytryptamine increases the excitability of central neurones through several ionic mechanisms. Prominent among these is enhancement of the hyperpolarization-activated inward rectifier, I_lv and inhibition of a calcium-sensitive potassium current responsible for the slow afterhyperpolarization following action potential discharge. Increased excitability results from a small depolarization coupled with more subtle effects on the integrative properties of neurones. Interestingly, pharmacologically distinct 5-HT receptors mediate these responses. In addition, the mechanisms by which cAMP modulates the target ion channels may also be different.