Regulation of exocytotic release of neurotransmitters by Ca^<2+> and associated proteins.

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The giant presynaptic terminal of chick ciliary ganglion was used to examine how noradrenaline (NA) modulates neurotransmitter release. The cholinergic excitatory synaptic currents (EPSCs) were recorded under whole-cell voltage clamp of the postsynaptic neuron. Although the EPSC was potentiated by NA,the current directly activated by acetylcholine (I_<ACh>) was unaffected. NA also increased the quantal contents without changing the quantal size. The NA-dependent potentiation was antagonized by neither phentolamine nor propranolol. The EPSC was also potentiated by adrenaline and dopamine but not by normetanephrine, phenylephrine or isoproterenol. The EPSC was attenuated by clonidine. Therefore, NA potentiated the transmitter release through a receptor pharmacologically different from both alpha- or beta- adrenergic receptors. The Ca^<2+> increment produced by an action potential (DELTA[Ca^<2+>]_<pre>) was reduced by NA through an alpha_2-adrenergic receptor. However, when alpha_<2+>-adrenergic receptors were blocked, neither DELTA[Ca^<2+>]_<pre> nor resting Ca^<2+> were changed by NA.The [Ca^<2+>]_o-EPSC relation was shifted by NA, decreasing the half saturating [Ca^<2+>]_o, without changing the maximum. It is concluded that NA-dependent potentiation of transmitter release was due to an increase in the Ca^<2+> sensitivity of the exocytotic process. The enhancement of the fusion probability is suggested.