CB1 modulation of temporally distinct synaptic facilitation among local circuit interneurons mediated by N-type calcium channels in CA1
CB1 modulation of temporally distinct synaptic facilitation among local circuit interneurons mediated by N-type calcium channels in CA1
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DOI：
10.1152/jn.00831.2010
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发表时间：
2011-03-01
影响因子：
2.5
通讯作者：
Ali, Afia B.
中科院分区：
文献类型：
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作者：
Ali, Afia B.
阿里公司CB1对CA1中N型钙通道介导的局部回路中间神经元之间时间上不同的突触易化的调制。J Neurophysiol 105：1051 - 1062，2011.首次发表于2010年12月1日; doi：10.1152/jn.00831.2010. -决定神经元网络行为的关键因素之一是中间神经元之间局部回路连接的影响。采用双全细胞记录结合生物胞素和免疫荧光双标记技术，在P18 - 21 d大鼠放射层（SR）和分子陷窝层（SLM）急性脑片上研究了CA1抑制性中间神经元的短时程突触可塑性和突触前钙通道的亚型。两种形式的时间上不同的突触促进中间神经元之间的连接，涉及突触前胆囊收缩素（CCK）阳性细胞在SR，频率依赖性的促进，和延迟开始释放（45 - 80毫秒）与随后的促进（DORF）。在这两个突触的抑制下，紧张性大麻素1型（CB1）受体活性。DORF突触没有显示传统的释放依赖性的属性，然而，阻断CB1受体拮抗剂AM-251（10 μ M）改变了突触传递的频率依赖性抑郁症的快速启动释放（2 - 4毫秒）。突触前CCK阴性的中间神经元在SLM引起抑制性突触后电位（IPSPs）不敏感的CB1受体药理学表现出频率依赖性抑郁症。GABA的释放在促进突触是唯一介导的N型突触前钙通道，而抑制突触利用P/Q型通道。这些数据揭示了与突触前钙通道亚型相关的中间神经元电路中神经递质释放模式的两种不同模型。这些数据表明，内源性大麻素通过CB1受体选择性地调节N型钙通道来改变信号传递。
Ali AB. CB1 modulation of temporally distinct synaptic facilitation among local circuit interneurons mediated by N-type calcium channels in CA1. J Neurophysiol 105: 1051-1062, 2011. First published December 1, 2010; doi: 10.1152/jn.00831.2010.-One of the critical factors in determining network behavior of neurons is the influence of local circuit connections among interneurons. The short-term synaptic plasticity and the subtype of presynaptic calcium channels used at local circuit connections of inhibitory interneurons in CA1 were investigated using dual whole-cell recordings combined with biocytin and double immunofluorescence labeling in acute slices of P18- to 21-day-old rat stratum radiatum (SR) and stratum lacunosum moleculare (SLM). Two forms of temporally distinct synaptic facilitation were observed among interneuron connections involving presynaptic cholecystokinin (CCK)-positive cells in SR, frequency-dependent facilitation, and a delayed onset of release (45-80 ms) with subsequent facilitation (DORF). Inhibition at both these synapses was under tonic cannabinoid-type 1 (CB1) receptor activity. DORF synapses did not display conventional release-dependent properties; however, blocking CB1 receptors with antagonist AM-251 (10 mu M) altered the synaptic transmission to frequency-dependent depression with a fast onset of release (2-4 ms). Presynaptic CCK-negative interneurons in SLM elicited inhibitory postsynaptic potentials (IPSPs) insensitive to CB1 receptor pharmacology displayed frequency-dependent depression. Release of GABA at facilitating synapses was solely mediated via N-type presynaptic calcium channels, whereas depressing synapses utilized P/Q-type channels. These data reveal two distinct models of neurotransmitter release patterns among interneuron circuits that correlate with the subtype of presynaptic calcium channel. These data suggest that endocannabinoids act via CB1 receptors to selectively modulate N-type calcium channels to alter signal transmission.