The Yin and Yang of GABAergic and Glutamatergic Synaptic Plasticity: Opposites in Balance by Crosstalking Mechanisms.
The Yin and Yang of GABAergic and Glutamatergic Synaptic Plasticity: Opposites in Balance by Crosstalking Mechanisms.
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GABA 能和谷氨酸能突触可塑性的阴阳：串扰机制的平衡对立。
DOI：
10.3389/fnsyn.2022.911020
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发表时间：
2022
影响因子：
3.7
通讯作者：
Jacob, Tija C.
中科院分区：
文献类型：
--
作者：
Chapman, Caitlyn A.;Nuwer, Jessica L.;Jacob, Tija C.
关键词：
突触可塑性是通过允许神经元响应于活动的变化而调节其突触强度来调节神经元活动的关键过程。尽管兴奋性突触后区和抑制性GABA能突触后区及其在树突状区域内的功能整合高度接近，但历史上并发可塑性一直被低估。越来越多的证据表明，在神经系统和神经发育障碍的兴奋和抑制（E/I）平衡的病理性破坏表明，需要一个改进的，更“整体”的理解突触的相互作用。尽管抑制性长时程增强（iLTP）和抑郁（iLTD）的重要性越来越明显，但长期以来人们一直关注兴奋（兴奋性长时程增强; eLTP）的持续增强及其在学习和记忆中的作用。新出现的证据进一步指出兴奋性和抑制性突触之间的动态对话，但关于这种交换的机制和程度仍有许多有待理解。在这篇简短的综述中，我们探讨了钙信号和突触串扰在调节突触后可塑性和神经元兴奋性中的作用。我们研究目前的知识GABA能和mammatergic突触反应的扰动活动，重点是突触后可塑性诱导的短期药物治疗的行为，以增强或降低神经元兴奋性，通过离子型受体调节神经元培养。为了深入研究突触串扰的潜在机制，我们讨论了突触活动对关键调控蛋白的影响，包括激酶，磷酸酶和突触结构/支架蛋白。最后，我们简要地提出了未来研究的途径，以更好地了解之间的串扰amatergic和GABA能突触。
Synaptic plasticity is a critical process that regulates neuronal activity by allowing neurons to adjust their synaptic strength in response to changes in activity. Despite the high proximity of excitatory glutamatergic and inhibitory GABAergic postsynaptic zones and their functional integration within dendritic regions, concurrent plasticity has historically been underassessed. Growing evidence for pathological disruptions in the excitation and inhibition (E/I) balance in neurological and neurodevelopmental disorders indicates the need for an improved, more “holistic” understanding of synaptic interplay. There continues to be a long-standing focus on the persistent strengthening of excitation (excitatory long-term potentiation; eLTP) and its role in learning and memory, although the importance of inhibitory long-term potentiation (iLTP) and depression (iLTD) has become increasingly apparent. Emerging evidence further points to a dynamic dialogue between excitatory and inhibitory synapses, but much remains to be understood regarding the mechanisms and extent of this exchange. In this mini-review, we explore the role calcium signaling and synaptic crosstalk play in regulating postsynaptic plasticity and neuronal excitability. We examine current knowledge on GABAergic and glutamatergic synapse responses to perturbances in activity, with a focus on postsynaptic plasticity induced by short-term pharmacological treatments which act to either enhance or reduce neuronal excitability via ionotropic receptor regulation in neuronal culture. To delve deeper into potential mechanisms of synaptic crosstalk, we discuss the influence of synaptic activity on key regulatory proteins, including kinases, phosphatases, and synaptic structural/scaffolding proteins. Finally, we briefly suggest avenues for future research to better understand the crosstalk between glutamatergic and GABAergic synapses.
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