Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark.
J Neurophysiol. 2012 Nov;108(10):2751-66. doi: 10.1152/jn.01120.2011. Epub 2012 Sep 5.
Cholinergic neurons in the laterodorsal tegmental (LDT) and peduncolopontine tegmental (PPT) nuclei regulate reward, arousal, and sensory gating via major projections to midbrain dopamine regions, the thalamus, and pontine targets. Muscarinic acetylcholine receptors (mAChRs) on LDT neurons produce a membrane hyperpolarization and inhibit spike-evoked Ca(2+) transients. Pharmacological studies suggest M(2) mAChRs are involved, but the role of these and other localized mAChRs (M(1-)-M(4)) has not been definitively tested. To identify the underlying receptors and to circumvent the limited receptor selectivity of available mAChR ligands, we used light- and electron-immunomicroscopy and whole cell recording with Ca(2+) imaging in brain slices from knockout mice constitutively lacking either M(2), M(4), or both mAChRs. Immunomicroscopy findings support a role for M(2) mAChRs, since cholinergic and noncholinergic LDT and pedunculopontine tegmental neurons contain M(2)-specific immunoreactivity. However, whole cell recording revealed that the presence of either M(2) or M(4) mAChRs was sufficient, and that the presence of at least one of these receptors was required for these carbachol actions. Moreover, in the absence of M(2) and M(4) mAChRs, carbachol elicited both direct excitation and barrages of spontaneous excitatory postsynaptic potentials (sEPSPs) in cholinergic LDT neurons mediated by M(1) and/or M(3) mAChRs. Focal carbachol application to surgically reduced slices suggest that local glutamatergic neurons are a source of these sEPSPs. Finally, neither direct nor indirect excitation were knockout artifacts, since each was detected in wild-type slices, although sEPSP barrages were delayed, suggesting M(2) and M(4) receptors normally delay excitation of glutamatergic inputs. Collectively, our findings indicate that multiple mAChRs coordinate cholinergic outflow from the LDT in an unexpectedly complex manner. An intriguing possibility is that a local circuit transforms LDT muscarinic inputs from a negative feedback signal for transient inputs into positive feedback for persistent inputs to facilitate different firing patterns across behavioral states.
背外侧脑桥核(LDT)和脚桥被盖核(PPT)中的胆碱能神经元通过主要投射到中脑多巴胺区域、丘脑和脑桥靶点来调节奖励、觉醒和感觉门控。LDT 神经元上的毒蕈碱乙酰胆碱受体(mAChR)产生膜超极化并抑制刺激诱发的 Ca(2+)瞬变。药理学研究表明 M(2)mAChR 参与其中,但这些和其他局部 mAChR(M(1-)-M(4))的作用尚未得到明确测试。为了确定潜在的受体并避免可用 mAChR 配体的有限受体选择性,我们使用光和电子免疫显微镜以及脑切片中的全细胞记录和 Ca(2+)成像,这些脑切片来自持续缺乏 M(2)、M(4)或两者 mAChR 的基因敲除小鼠。免疫显微镜研究结果支持 M(2)mAChR 的作用,因为胆碱能和非胆碱能 LDT 和脑桥被盖核神经元含有 M(2)-特异性免疫反应性。然而,全细胞记录显示,存在 M(2)或 M(4)mAChR 就足够了,并且这些 carbachol 作用需要至少存在一种这些受体。此外,在缺乏 M(2)和 M(4)mAChR 的情况下,carbachol 在胆碱能 LDT 神经元中引发直接兴奋和自发兴奋性突触后电位 (sEPSP) 的弹幕,这些 sEPSP 由 M(1)和/或 M(3)mAChR 介导。手术减少切片中的焦点 carbachol 应用表明,局部谷氨酸能神经元是这些 sEPSP 的来源。最后,直接或间接兴奋都不是基因敲除的假象,因为在野生型切片中都检测到了这两种兴奋,尽管 sEPSP 弹幕延迟,表明 M(2)和 M(4)受体通常延迟谷氨酸能传入的兴奋。总的来说,我们的研究结果表明,多种 mAChR 以一种出人意料的复杂方式协调 LDT 中的胆碱能输出。一个有趣的可能性是,局部回路将 LDT 毒蕈碱输入从瞬态输入的负反馈信号转换为持续输入的正反馈,以促进不同行为状态下的不同放电模式。