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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Synapse number and synaptic efficacy are regulated by presynaptic cAMP and protein kinase A.
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Synapse number and synaptic efficacy are regulated by presynaptic cAMP and protein kinase A.

机译：突触数量和突触功效受突触前cAMP和蛋白激酶A的调节。

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摘要

The mechanisms by which neurons regulate the number and strength of synapses during development and synaptic plasticity have not yet been defined fully. This lack of fundamental knowledge in the fields of neurodevelopment and synaptic plasticity can be attributed, in part, to compensatory mechanisms by which neurons accommodate for the loss of function in their synaptic partners. This is generally achieved either by scaling up neuronal transmitter release capabilities or by enhancing the postsynaptic responsiveness. Here, we demonstrate that regulation of synaptic strength and number between identified Lymnaea neurons visceral dorsal 4 (VD4, the presynaptic cell) and left pedal dorsal 1 (LPeD1, the postsynaptic cell) requires presynaptic activation of a cAMP-PKA-dependent signal. Experimental activation of the cAMP-PKA pathway resulted in reduced synaptic efficacy, whereas inhibition of the cAMP-PKA cascade permitted hyperinnervation and an overall enhancement of synaptic strength. Because synaptic transmission between VD4 and LPeD1 does not require a cAMP-PKA pathway, our data show that these messengers may play a novel role in regulating the synaptic efficacy during early synaptogenesis and plasticity.
机译：神经元在发育和突触可塑性过程中调节突触的数量和强度的机制尚未完全定义。在神经发育和突触可塑性领域缺乏基础知识的部分原因可归因于神经元在其突触伴侣中适应功能丧失的补偿机制。通常通过扩大神经元递质释放能力或增强突触后反应来实现。在这里，我们证明，已确定的Lymnaea神经元内脏背侧4（VD4，突触前细胞）和左踏板背侧1（LPeD1，突触后细胞）之间的突触强度和数量调节需要突触前激活cAMP-PKA依赖性信号。 cAMP-PKA途径的实验激活导致突触效力降低，而对cAMP-PKA级联的抑制则使神经过度兴奋并增强了突触强度。由于VD4和LPeD1之间的突触传递不需要cAMP-PKA途径，因此我们的数据表明，这些信使在早期突触形成和可塑性过程中可能在调节突触功效中发挥了新的作用。

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