首页> 外文期刊>The Journal of Physiology >Postsynaptic origin of CB1-dependent tonic inhibition of GABA release at cholecystokinin-positive basket cell to pyramidal cell synapses in the CA1 region of the rat hippocampus.
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Postsynaptic origin of CB1-dependent tonic inhibition of GABA release at cholecystokinin-positive basket cell to pyramidal cell synapses in the CA1 region of the rat hippocampus.

机译:突触后起源于大鼠海马CA1区胆囊收缩素阳性篮子细胞对锥体细胞突触的GABA释放的CB1依赖性强直抑制。

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摘要

Cholecystokinin-positive (CCK+) basket cells are a major source of perisomatic GABAergic inputs to CA1 pyramidal cells. These interneurons express high levels of presynaptic cannabinoid type 1 (CB1) receptors that mediate short-term depression of GABA release following depolarization of postsynaptic cells. However, it is not known whether GABA release from CA1 CCK+ basket cells is under tonic endocannabinoid inhibition. In paired patch-clamp recordings, action potentials in presynaptic CCK+ basket cells evoked large IPSCs with fast kinetics in pyramidal cells. The proportion of action potentials that failed to evoke GABA release varied markedly between pairs, from highly reliable to virtually silent connections. Application of the CB1 receptor antagonist AM251 (10 microm) decreased the proportion of failures, revealing a persistent suppression of synaptic transmission by CB1 receptors. However, AM251 had no significant effect on the failure rate when the calcium chelator BAPTA (10 mm) was introduced into the postsynaptic cell, indicating that the tonic inhibition of GABA release by CB1 receptors is homosynaptically controlled by the postsynaptic cell, and that it is not due to constitutive CB1 receptor activity. Application of muscarinic or metabotropic glutamate receptor agonists inhibited synaptic transmission exclusively through the release of endocannabinoids from postsynaptic cells in a manner that could not be blocked by postsynaptic BAPTA, and had no direct effect on transmission. In contrast, GABA(B) receptor activation directly blocked GABA release, but there was no evidence for tonic inhibition of GABA release by GABA(B) receptors. Neither serotonergic nor mu-opioid agonists had significant influence on GABA release from CCK+ axon terminals. These results reveal that GABA release from CA1 CCK+ basket cells is under homosynaptic tonic inhibition by endocannabinoids, and it is subject to both direct and indirect modulation by various G-protein-dependent neuromodulators.
机译:胆囊收缩素阳性(CCK +)篮状细胞是CA1锥体细胞过异型GABA能输入的主要来源。这些中间神经元表达高水平的突触前大麻素1型(CB1)受体,介导突触后细胞去极化后GABA释放的短期抑制。但是,尚不知道CA1 CCK +篮细胞中GABA的释放是否受到强直性内源性大麻素的抑制。在成对的膜片钳记录中,突触前CCK +篮状细胞的动作电位诱发了大型IPSC,而锥体细胞具有快速的动力学。未能引起GABA释放的动作电位比例在各对之间显着不同,从高度可靠的连接到几乎无声的连接。 CB1受体拮抗剂AM251(10微米)的应用降低了失败的比例,揭示了CB1受体对突触传递的持续抑制。然而,当将钙螯合剂BAPTA(10 mm)引入突触后细胞时,AM251对失败率没有显着影响,表明CB1受体对GABA释放的补品抑制作用是由突触后细胞同型突触控制的,并且并非由于本构CB1受体的活性。毒蕈碱或代谢型谷氨酸受体激动剂的应用完全通过突触后BAPTA不能阻断的方式从突触后细胞释放内源性大麻素来抑制突触传递,并且对传递没有直接影响。相反,GABA(B)受体的活化直接阻止了GABA的释放,但是没有证据表明GABA(B)受体能强直抑制GABA的释放。血清素能和类阿片受体激动剂均未对CCK +轴突末端的GABA释放产生显着影响。这些结果表明,CA1 CCK +篮细胞释放的GABA受内源性大麻素的突触性强直抑制,并且受到各种G蛋白依赖性神经调节剂的直接和间接调节。

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