Extracellular pH changes may constitute significant signals for neuronal communication. During synaptic transmission, changes in pH in the synaptic cleft take place. Its role in the regulation of presynaptic Ca2+ currents through multivesicular release in ribbon-type synapses is a proven phenomenon. In recent years, protons have been recognized as neurotransmitters that participate in neuronal communication in synapses of several regions of the CNS such as amygdala, nucleus accumbens, and brainstem. Protons are released by nerve stimulation and activate postsynaptic acid-sensing ion channels (ASICs). Several types of ASIC channels are expressed in the peripheral and central nervous system. The influx of Ca2+ through some subtypes of ASICs, as a result of synaptic transmission, agrees with the participation of ASICs in synaptic plasticity. Pharmacological and genetical inhibition of ASIC1a results in alterations in learning, memory, and phenomena like fear and cocaine-seeking behavior. The recognition of endogenous molecules, such as arachidonic acid, cytokines, histamine, spermine, lactate, and neuropeptides, capable of inhibiting or potentiating ASICs suggests the existence of mechanisms of synaptic modulation that have not yet been fully identified and that could be tuned by new emerging pharmacological compounds with potential therapeutic benefits.

中文翻译：

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质子和酸敏感离子通道介导的突触信号。

细胞外pH变化可能构成神经元交流的重要信号。在突触传递过程中，突触裂中的pH值发生变化。它通过带状突触中的多囊泡释放在突触前Ca2 +电流调节中的作用已被证实。近年来，质子已被认为是在中枢神经系统的多个区域（如杏仁核，伏隔核和脑干）的突触中参与神经元通讯的神经递质。质子通过神经刺激释放并激活突触后酸敏感离子通道（ASICs）。在外围和中枢神经系统中表达了几种类型的ASIC通道。由于突触传递，Ca2 +通过某些亚型的ASIC流入，这与ASIC参与突触可塑性一致。ASIC1a的药理和遗传抑制作用导致学习，记忆和恐惧和可卡因寻求行为等现象的改变。能够抑制或增强ASIC的内源性分子（如花生四烯酸，细胞因子，组胺，精胺，乳酸和神经肽）的识别表明，突触调节机制的存在尚未完全确定，可以通过新的方法进行调节具有潜在治疗益处的新兴药理化合物。