Voltage-dependent calcium current induced by serotonin.

Abstract

CALCIUM ions have a central role in the regulation of neural activity1,2. Changes in intracellular calcium concentration affect membrane permeability to other ions and thereby alter membrane excitability3. Furthermore, calcium is required for transmitter release from nerve terminals4. A neurotransmitter that specifically induces an inward calcium current might have profound effects. We report here that in some neurones of Aplysia, serotonin can induce such a calcium current. A previous investigation5 revealed that iontophoretically applied serotonin elicited an unusual excitatory response in some neurones of Aplysia. At hyperpolarised potentials the neurotransmitter produced a slow excitation (component 1) that behaved simply as an increase in sodium conductance, similar to the A′ response of Gerschenfeld and Paupardin–Tritsch6. At depolarised potentials (>−30 mV), the response was voltage dependent and behaved as a regenerative inward current (component 2). At all potentials, the slow excitatory response to serotonin was insensitive to changes in extracellular chloride or potassium concentration. However, in sucrose-substituted sodium-free solutions, the response was greatly attenuated. Although a calcium current was not excluded, it was tentatively suggested that sodium was responsible for the regenerative inward current as well as for component 1. Further study has now shown that the regenerative inward current component is carried by calcium ions.