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首页> 美国卫生研究院文献>other >The Cholinergic Agonist Carbachol Increases the Frequency of Spontaneous GABAergic Synaptic Currents in Dorsal Raphe Serotonergic Neurons in the Mouse
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The Cholinergic Agonist Carbachol Increases the Frequency of Spontaneous GABAergic Synaptic Currents in Dorsal Raphe Serotonergic Neurons in the Mouse

机译：胆碱能激动剂卡巴胆碱增加小鼠背缝拉弗血清素能神经元中自发的GABA能突触电流的频率。

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Dorsal raphe nucleus (DRN) serotonin (5-HT) neurons play an important role in feeding, mood control and stress responses. One important feature of their activity across the sleep-wake cycle is their reduced firing during rapid-eye-movement (REM) sleep which stands in stark contrast to the wake/REM-on discharge pattern of brainstem cholinergic neurons. A prominent model of REM sleep control posits a reciprocal interaction between these cell groups. 5-HT inhibits cholinergic neurons, and activation of nicotinic receptors can excite DRN 5-HT neurons but the cholinergic effect on inhibitory inputs is incompletely understood. Here, in vitro, in DRN brain slices prepared from GAD67-GFP knock-in mice, a brief (3 min) bath application of carbachol (50 μM) increased the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) in GFP-negative, putative serotonin neurons but did not affect miniature (tetrodotoxin-insensitive) IPSCs. Carbachol had no direct postsynaptic effect. Thus, carbachol likely increases the activity of local GABAergic neurons which synapse on 5-HT neurons. Removal of dorsal regions of the slice including the ventrolateral periaqueductal gray (vlPAG) region where GABAergic neurons projecting to the DRN have been identified, abolished the effect of carbachol on sIPSCs whereas removal of ventral regions containing the oral region of the pontine reticular nucleus (PnO) did not. In addition, carbachol directly excited GFP-positive, GABAergic vlPAG neurons. Antagonism of both muscarinic and nicotinic receptors completely abolished the effects of carbachol. We suggest cholinergic neurons inhibit DRN 5-HT neurons when acetylcholine levels are lower i.e. during quiet wakefulness and the beginning of REM sleep periods, in part via excitation of muscarinic and nicotinic receptors located on local vlPAG and DRN GABAergic neurons. Higher firing rates or burst firing of cholinergic neurons associated with attentive wakefulness or phasic REM sleep periods leads to excitation of 5-HT neurons via activation of nicotinic receptors located postsynaptically and presynaptically on excitatory afferents.
机译：背沟纹核（DRN）5-羟色胺（5-HT）神经元在进食，情绪控制和应激反应中起重要作用。它们在整个睡眠-觉醒周期中的活动的重要特征之一是，它们在快速眼动（REM）睡眠期间的放电减少，这与脑干胆碱能神经元的觉醒/ REM放电模式形成鲜明对比。 REM睡眠控制的一个杰出模型在这些细胞群之间存在相互作用。 5-HT抑制胆碱能神经元，烟碱样受体的激活可激发DRN 5-HT神经元，但对抑制性输入的胆碱能作用尚不完全清楚。在这里，在体外，在从GAD67-GFP敲入小鼠制备的DRN脑切片中，短暂（3分钟）的卡巴胆碱（50μM）浴应用增加了GFP阴性，推定的自发抑制突触后电流（sIPSC）的频率血清素神经元，但不影响微型（对河豚毒素不敏感的）IPSC。卡巴胆碱没有直接的突触后作用。因此，卡巴胆碱可能增加突触在5-HT神经元上的局部GABA能神经元的活性。切片的背侧区域被去除，包括已经确定了投射到DRN的GABA能神经元的腹外侧导水管周围灰色（vlPAG）区域，消除了卡巴胆碱对sIPSC的影响，而去除了包含桥脑网状核（PnO）口腔区域的腹侧区域） 没有。此外，卡巴胆碱直接激发GFP阳性的GABA能vlPAG神经元。毒蕈碱和烟碱样受体的拮抗作用完全消除了卡巴胆碱的作用。我们建议胆碱能神经元在乙酰胆碱水平较低时（即安静的清醒和REM睡眠期开始时）抑制DRN 5-HT神经元，部分原因是通过激发位于局部vlPAG和DRN GABA能神经元上的毒蕈碱和烟碱样受体激发。与注意力清醒或阶段性REM睡眠期相关的胆碱能神经元的较高放电速率或突发放电可通过激活位于突触后突触和突触前的烟碱样受体激活5-HT神经元。

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