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首页> 外文期刊>CNS neuroscience & therapeutics. >Transient Receptor Potential Vanilloid 4 Mediates Hypotonicity‐Induced Enhancement of Synaptic Transmission in Hippocampal Slices
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Transient Receptor Potential Vanilloid 4 Mediates Hypotonicity‐Induced Enhancement of Synaptic Transmission in Hippocampal Slices

机译：瞬态受体电位香草酸4介导低渗诱导的海马片突触传递增强。

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Summary Aim and methods Changes in cerebrospinal fluid osmotic pressure modulate brain excitability. Transient receptor potential vanilloid 4 ( TRPV 4), which is sensitive to hypotonic stimulation, is expressed in hippocampus. The present study investigated the effect of hypotonic stimulation on hippocampal synaptic transmission and the role of TRPV 4 in hypotonicity‐action using electrophysiological recording and pharmacological technique. Results Accompanied with the decrease in paired pulse facilitation, field excitatory postsynaptic potential (f EPSP ) was enhanced by hypotonicity and TRPV 4 agonist 4α‐ PDD in hippocampal slices, which was sensitive to TRPV 4 antagonist HC ‐067047. Hypotonicity‐induced increase in f EPSP was blocked by α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid ( AMPA ) receptor antagonist, but not N ‐methyl‐ d ‐aspartate receptor or N‐ or P/Q‐type voltage‐gated calcium channel antagonist. High voltage‐gated calcium current ( I Ca) in hippocampal CA 3 pyramidal neurons was not affected by hypotonicity. AMPA ‐activated current ( I AMPA) in hippocampal CA 1 pyramidal neurons was increased by hypotonicity and 4α‐ PDD , which was attenuated by HC ‐067047. Inhibition of protein kinase C or protein kinase A markedly attenuated hypotonicity‐increased I AMPA, whereas antagonism of calcium/calmodulin‐dependent protein kinase II had no such effect. Conclusion TRPV 4 is involved in hypotonicity‐induced enhancement of hippocampal synaptic transmission, which may be mediated through promoting presynaptic glutamate release and increasing postsynaptic AMPA receptor function.
机译：摘要目的和方法脑脊液渗透压的变化调节大脑的兴奋性。对低渗刺激敏感的瞬时受体电位香草酸4（TRPV 4）在海马中表达。本研究使用电生理记录和药理学技术研究了低渗刺激对海马突触传递的影响以及TRPV 4在低渗作用中的作用。结果伴随着成对脉冲促进作用的降低，低渗性和海马切片中的TRPV 4激动剂4α‐PDD增强了田间兴奋性突触后突触电位（f EPSP），这对TRPV 4拮抗剂HC ‐067047敏感。低渗诱导的f EPSP的增加被α‐氨基‐3‐羟基‐5‐甲基‐4‐异恶唑丙酸（AMPA）受体拮抗剂阻止，但未被N‐甲基d天冬氨酸受体或N‐或P / Q‐阻止型电压门控钙通道拮抗剂。海马CA 3锥体神经元的高压门控钙电流（I Ca）不受低渗性的影响。低渗和4α-PDD增加了海马CA 1锥体神经元的AMPA激活电流（I AMPA），而HC-067047减弱了该作用。抑制蛋白激酶C或蛋白激酶A可以显着减弱低渗性增加的I AMPA，而对钙/钙调蛋白依赖性蛋白激酶II的拮抗作用则没有这种作用。结论TRPV 4参与低渗诱导的海马突触传递的增强，其可能通过促进突触前谷氨酸释放和增加突触后AMPA受体功能来介导。

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