Department of Physiology and Pharmacology and Department of Clinical Neurological Sciences, University of Western Ontario, London, ON N6A5C1, Canada.
Cereb Cortex. 2010 Aug;20(8):1865-77. doi: 10.1093/cercor/bhp251. Epub 2009 Nov 19.
We hypothesize that endogenous cholinergic modulation of dendritic processing of hippocampal CA1 is layer specific, and it specifically enhances spike output resulting from basal as compared with the apical dendritic excitation. Laminar profiles of evoked field potentials were recorded in the CA1 area of urethane-anesthetized rats using multichannel silicon probes and analyzed as current source density. High-frequency stimulation of the pontis oralis (PnO) attenuated the midapical more than the basal or distal apical dendritic excitatory sink. Population spike (PS) and excitatory sink-PS potentiation resulting from basal dendritic excitation were facilitated, while the PS evoked by apical dendritic stimulation was attenuated by PnO stimulation. Perfusion of cholinergic agonist carbachol onto hippocampal slices in vitro also attenuated the apical more than the basal dendritic excitatory postsynaptic potentials. Excitatory sink attenuation and PS changes after PnO stimulation were blocked by systemic or local scopolamine and by intracerebroventricular (icv) M1 receptor antagonist pirenzepine but not by icv M2 receptor antagonist AFDX-116 or nicotinic antagonists. However, a hippocampal theta rhythm activated by PnO stimulation was blocked by systemic but not by local scopolamine. We conclude that endogenous acetylcholine mediates a stronger presynaptic inhibition of the midapical than basal and distal apical excitation mainly through M1 receptors.
我们假设内源性胆碱能调制海马 CA1 树突处理是层特异的，并且它特异性地增强了基底而非顶端树突激发引起的尖峰输出。在使用多通道硅探针麻醉的大鼠 CA1 区记录诱发的场电位的层状分布，并作为电流源密度进行分析。桥脑嘴侧部（PnO）的高频刺激减弱了中顶端的兴奋性吸收，而不是基底或远顶端的兴奋性吸收。基底树突激发引起的群体锋电位（PS）和兴奋性吸收-PS 增强被促进，而顶端树突刺激引起的 PS 被 PnO 刺激减弱。体外灌流胆碱能激动剂 carbachol 也减弱了顶端多于基底的树突兴奋性突触后电位。PnO 刺激后的兴奋性吸收减弱和 PS 变化被全身或局部东莨菪碱和脑室内（icv）M1 受体拮抗剂 pirenzepine 阻断，但不受 icv M2 受体拮抗剂 AFDX-116 或烟碱受体拮抗剂阻断。然而，PnO 刺激激活的海马θ节律被全身而非局部东莨菪碱阻断。我们得出结论，内源性乙酰胆碱通过 M1 受体介导对中顶端的突触前抑制作用强于基底和远顶端的兴奋作用。
