McQuiston A R, Madison D V
Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California 94305, USA.
J Neurosci. 1999 Jul 15;19(14):5693-702. doi: 10.1523/JNEUROSCI.19-14-05693.1999.
Inhibitory interneurons appear to be an important target for the muscarinic actions of cholinergic inputs to the hippocampus. We investigated the effect of muscarinic receptor activity on the membrane potential (V(m)) and currents of rat hippocampal CA1 interneurons using whole-cell recording from visually identified CA1 interneurons. The predominant response observed was a muscarinic depolarization that was detected in interneurons from all layers of CA1. This depolarization was mediated by at least two mechanisms: a reduction in a potassium current and a mechanism that depended on extracellular sodium. Other interneurons responded to muscarinic agonists with a hyperpolarization or a biphasic response (hyperpolarization followed by depolarization). Hyperpolarizations and biphasic responses were found in all layers of CA1 but more frequently in stratum radiatum and stratum lacunosum moleculare. Muscarinic hyperpolarization was caused by the activation of a barium- and cesium-sensitive inwardly rectifying potassium channel. A small number of interneurons, primarily in or bordering the stratum pyramidale, produced slow membrane potential (0.04 Hz) oscillations. Many interneurons did not respond to muscarinic activity at all; half of these were in the stratum oriens. There was no strong correlation between any changes in V(m) response to muscarine and morphology, as determined by reconstruction of the interneurons. It was not possible to predict the morphology or the layer distribution of an interneuron based on the type of muscarinic membrane potential response it had. This lack of correlation between muscarinic function and morphology implies a greater complexity of interneuron function than has been realized previously.
抑制性中间神经元似乎是胆碱能输入至海马体的毒蕈碱样作用的一个重要靶点。我们使用全细胞膜片钳记录技术，从视觉识别的大鼠海马体CA1区中间神经元，研究了毒蕈碱受体活性对其膜电位（V(m)）和电流的影响。观察到的主要反应是毒蕈碱样去极化，在CA1区所有层的中间神经元中均可检测到。这种去极化至少由两种机制介导：一种是钾电流的减少，另一种是依赖细胞外钠离子的机制。其他中间神经元对毒蕈碱激动剂的反应是超极化或双相反应（超极化后去极化）。超极化和双相反应在CA1区所有层均有发现，但在辐射层和分子层隙状层中更为常见。毒蕈碱样超极化是由钡离子和铯离子敏感的内向整流钾通道的激活引起的。少数中间神经元，主要位于锥体层内或其边界，产生缓慢的膜电位（0.04 Hz）振荡。许多中间神经元对毒蕈碱活性根本没有反应；其中一半位于海马体的原层。通过中间神经元的重建确定，对毒蕈碱的V(m)反应的任何变化与形态之间均无强相关性。根据中间神经元的毒蕈碱样膜电位反应类型，无法预测其形态或层分布。毒蕈碱功能与形态之间缺乏这种相关性意味着中间神经元功能比以前认识到的更为复杂。
