The excitability of various neurones in the mammalian central nervous system (CNS), ranging from motoneurones to serotonergic neurones, is enhanced by α1-adrenoceptor agonists1. Excitations mediated via α1-adrenoceptors are associated with a slow depolarization and an increase in input resistance, probably resulting from a decrease in resting potassium conductance1,2. However, the involvement of voltage-dependent transient currents in mediating α1 excitatory effects has not been evaluated. An early transient outward current has been described which is important in regulating the frequency of repetitive firing; it is activated by depolarizing voltage steps from potentials more negative than rest and blocked by 4-aminopyridine3,4. This current, which has been termed ‘IA’, was found originally in invertebrates3,4 and subsequently in various vertebrate neurones5–8. The present single-electrode voltage-clamp study demonstrates an early transient outward current (IA) in serotonergic neurones which is suppressed by noradrenaline and the α1-agonist phenylephrine; a suppression of IA may account in part for the acceleration of pacemaker activity induced by α1-agonists in serotonergic neurones.
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Aghajanian, G. Modulation of a transient outward current in serotonergic neurones by α1-adrenoceptors. Nature 315, 501–503 (1985). https://doi.org/10.1038/315501a0
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