Electrophysiological studies of synaptic transmission in the central and peripheral autonomic neurons.

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1. Presynaptic regulation of sympathetic preganglionic neurons (SPN) : Noradrenaline (NA) inhibits the fast EPSP presynaptically This inhibiton appeared to be due to activation of alpha_2 receptors on the gultaminergic presynaptic nerve terminals that might cause hyperpolarization and/or reduction of Ca conductance of the terminal membrane.2. The receptor and signal transduction mechanisms underlying the catecholaminergic transmission in SPNs : The alpha_1 and alpha_2 receptors on SPNs, respectively, mediate the slow EPSP and the slow IPSP.The alpha_1 receptors are endowed mainly on the dendrites and the alpha_2 receptors on the soma. The former produces the slow response via G-protein and proteinkinase C and the latter via G-protein alone.3. The indolaminergic and peptidergic transmissions in SPNs : Both serotonin (5-HT) and tachykinins cause reduction of the Ca-dependent K conductance that results in a slow depolarization and the inhibition of the slow afterhyperpolarization of SPNs. The 5-HT action is mediated by 5-HT_2 receptors.4. Intracellular signal transduction that mediates the slow IPSP in submucous neurons of the guinea-pig caecum : The mechanisms underlying intracellular signal transduction of the slow IPSP mediated by NA appeared to be following : i) the increased K conductance was mediated by the activation of pertussis toxin-sensitive G protein and the corresponding accumulation of intracellular Ca^<2+> released from the internal stores by IP_3. The binding of the released Ca^<2+> to calmoduline might result in an increase in potassium conductance.