关键词: insular cortex kainate receptor nitric oxide presynaptic long-term potentiation

Mesh : Long-Term Potentiation / physiology Nitric Oxide / metabolism Animals Cerebral Cortex / physiology Presynaptic Terminals / physiology Receptors, Kainic Acid / metabolism Patch-Clamp Techniques Rats Pyramidal Cells / physiology Nitric Oxide Synthase / metabolism Mice

来  源:   DOI:10.1098/rstb.2023.0475

Abstract:
Nitric oxide (NO) is a key diffusible messenger in the mammalian brain. It has been proposed that NO may diffuse retrogradely into presynaptic terminals, contributing to the induction of hippocampal long-term potentiation (LTP). Here, we present novel evidence that NO is required for kainate receptor (KAR)-dependent presynaptic form of LTP (pre-LTP) in the adult insular cortex (IC). In the IC, we found that inhibition of NO synthase erased the maintenance of pre-LTP, while the induction of pre-LTP required the activation of KAR. Furthermore, NO is essential for pre-LTP induced between two pyramidal cells in the IC using the double patch-clamp recording. These results suggest that NO is required for homosynaptic pre-LTP in the IC. Our results present strong evidence for the critical roles of NO in pre-LTP in the IC. This article is part of a discussion meeting issue \'Long-term potentiation: 50 years on\'.
摘要:
一氧化氮(NO)是哺乳动物大脑中的关键可扩散信使。有人提出NO可能逆行扩散到突触前末端,有助于诱导海马长时程增强(LTP)。这里,我们提供了新的证据,表明NO是成年岛叶皮质(IC)中红藻氨酸受体(KAR)依赖性LTP突触前形式(Pre-LTP)所必需的。在IC中,我们发现抑制NO合成酶消除了前LTP的维持,而pre-LTP的诱导需要KAR的激活。此外,NO对于使用双膜片钳记录在IC中的两个锥体细胞之间诱导的前LTP是必需的。这些结果表明,IC中的同质突触前LTP需要NO。我们的研究结果为NO在IC前LTP中的关键作用提供了强有力的证据。本文是讨论会议问题“长期增强:50年后”的一部分。
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