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

用鸡睫状神经节巨大的突触前末梢研究了去甲肾上腺素（NA）对神经递质释放的调节作用。在突触后神经元全细胞电压钳下记录胆碱能兴奋性突触电流（EPSC）。NA可增强EPSC，但对乙酰胆碱直接激活的电流<ACh>无影响。NA也增加了量子含量，而不改变量子大小。NA依赖性增强既不被酚妥拉明也不被普萘洛尔拮抗。肾上腺素和多巴胺也能增强EPSC，但去甲甲肾上腺素、苯肾上腺素或异丙肾上腺素不能增强EPSC。可乐定可使EPSC减弱。因此，NA通过不同于α-或β-肾上腺素能受体的受体β加强递质释放。NA通过α_2-肾上腺素能受体降低动作电位（DELTA[Ca^&lt;2+&gt;]_）产生的Ca^&lt;2 +&gt;增量<pre>。当阻断α_（2+）-肾上腺素能受体时，NA对[Ca^&lt;2+&gt;]_o<pre>和静息Ca^&lt;2+&gt;均无影响，NA使[Ca^&lt;2+&gt;]_o-EPSC关系移动，使半饱和[Ca^&lt;2+]_o降低，但不改变最大值。由此得出结论，NA依赖性增强递质释放是由于胞吐过程中Ca^&lt;2+&gt;敏感性的增加。提出了提高融合概率的建议。

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.