PRESYNAPTIC CELL TYPE-DEPENDENT REGULATION OF GABAERGIC SYNAPTIC TRANSMISSION BY NITRIC OXIDE IN RAT INSULAR CORTEX
PRESYNAPTIC CELL TYPE-DEPENDENT REGULATION OF GABAERGIC SYNAPTIC TRANSMISSION BY NITRIC OXIDE IN RAT INSULAR CORTEX
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DOI：
10.1016/j.neuroscience.2014.09.062
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发表时间：
2015-01-22
期刊：
影响因子：
3.3
通讯作者：
Kobayashi, M.
中科院分区：
文献类型：
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作者：
Yamamoto, K.;Takei, H.;Kobayashi, M.
一氧化氮（NO）是调节大脑皮层突触传递的关键逆行信使。然而，很少有人知道NO诱导的调制作用及其机制相对于抑制性突触传递。本研究旨在研究NO对单一抑制性突触后电流（uIPSC）的影响，并推测NO作用的突触位置。我们进行了多次全细胞膜片钳记录从大鼠岛叶皮层和记录的细胞分为三个亚型：锥体细胞（Pyr），快速尖峰中间神经元（FS），和非FS GABA能中间神经元。在从FS到Pyr（FS -> Pyr）的连接中，应用NO供体S-亚硝基-N-乙酰基-DL-青霉胺（SNAP，100 μ M）抑制了31%的连接中的uIPSC振幅，而39%的连接显示uIPSC易化。剩余的FS -> Pyr连接显示SNAP对uIPSC的影响很小。配对脉冲比（PPR）的分析暗示了突触前机制参与SNAP诱导的对uIPSC的影响。在FS -> FS/非FS连接中观察到SNAP的类似作用;分别有33%、54%和13%的连接被促进、抑制和不变。相比之下，non-FS -> Pyr或FS/non-FS显示出通过SNAP的恒定uIPSC抑制。PPR分析支持以下假设：这些SNAP诱导的效应是由FS -> FS/非FS和非FS-> Pyr/FS/非FS连接中的突触前机制介导的。NO清除剂2-苯基-4，4，5，5-四甲基咪唑啉氧基-1-氧基-3-氧化物（PTIO）或鸟苷酸环化酶抑制剂1H-[1，2，4]恶二唑并[4，3-a]喹喔啉-1-酮（ODQ）可阻断SNAP对uIPSC的调节作用。这些结果表明，抑制性突触传递的NO调节依赖于突触前细胞亚型，并且至少部分地由突触前机制介导。(C)2014年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Nitric oxide (NO) is a key retrograde messenger that regulates synaptic transmission in the cerebral cortex. However, little is known about NO-induced modulatory effects and their mechanisms relative to inhibitory synaptic transmission. The present study aimed to examine the effects of NO on unitary inhibitory postsynaptic currents (uIPSCs) and to postulate the synaptic location of NO action. We performed multiple whole-cell patch-clamp recordings from rat insular cortex and divided recorded cells into three subtypes: pyramidal cells (Pyr), fast-spiking interneurons (FS), and non-FS GABAergic interneurons. In the connections from FS to Pyr (FS -> Pyr), the application of S-nitroso-N-acetyl-DL-penicillamine (SNAP, 100 mu M), an NO donor, suppressed uIPSC amplitudes in 31% of the connections, whereas 39% of the connections showed uIPSC facilitation. The remaining FS -> Pyr connections showed little effect of SNAP on uIPSCs. An analysis of paired-pulse ratio (PPR) implied the involvement of presynaptic mechanisms in SNAP-induced effects on uIPSCs. Similar effects of SNAP were observed in FS -> FS/non-FS connections; 33%, 54%, and 13% of the connections were facilitated, suppressed, and unchanged, respectively. In contrast, non-FS -> Pyr or FS/non-FS showed constant uIPSC suppression by SNAP. PPR analysis supports the hypothesis that these SNAP-induced effects are mediated by presynaptic mechanisms in FS -> FS/non-FS and non-FS -> Pyr/FS/non-FS connections. The NO scavenger, 2-phenyl-4,4,5,5-tetramethylimidazolineoxyl-1-oxyl-3-oxide (PTIO), or the inhibitor of guanylate cyclase, 1H-[1,2,4]oxadiazolo[4,3-a] quinoxalin-1-one (ODQ), abolished the SNAP-induced uIPSC modulation. These results suggest that NO regulation of inhibitory synaptic transmission is dependent on presynaptic cell subtypes and that, at least in part, the effects are mediated by presynaptic mechanisms. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.