Serotonin-induced modulation of excitability in an identified Helisoma trivolvis neuron.
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abstract
Exogenous serotonin (5-hydroxytryptamine; 5-HT) induced inhibitory effects in Helisoma trivolvis buccal neuron 5 (B5), which included a hyperpolarization of the membrane potential, a reduction in input resistance and a decrease in the stimulus-evoked spiking rate. The reversal potential for the 5-HT-induced hyperpolarization was -88.7 mV, suggesting the involvement of an enhanced K+ conductance. Input/output curves measuring the number of action potentials evoked by current injection demonstrated a 5-HT-induced reduction in B5 neuronal excitability that was dose-dependent with a 50 % inhibitory concentration (IC50) of 1.1 µmol l-1. These inhibitory effects on neuron B5 were in striking contrast to the excitatory effects of this neurotransmitter on the buccal radular tensor motoneuron B19. In this neuron, 5-HT elicited a sustained depolarization and enhanced spiking activity. Previous cell culture studies have demonstrated that 5-HT also inhibits B19 growth cone motility and neurite outgrowth, but has no effect on the extension of neuritic processes from neuron B5. These effects, and the divergent effects of 5-HT on the outgrowth of neurons B5 and B19, probably result from differential effects of 5-HT on neuronal membrane potential and excitability. Modulation of the levels of spiking activity, translated into changes in neuronal Ca2+ levels, would cause alterations in growth cone motility. Previous studies have shown that the effects of 5-HT on B19 membrane potential and neurite extension are cyclic-AMP-dependent. We have used specific activators and inhibitors of signal transduction mechanisms to demonstrate that the 5-HT-induced reductions in B5 neuronal excitability are cyclic-AMP-independent and may involve the lipoxygenase pathway of arachidonic acid metabolism. Our results support the hypothesis that modulatory signals and signal transduction pathways regulating the plasticity of mature neural circuits may also modulate the differentiation of the neurons comprising those networks during development.
