Zhu J J, Uhlrich D J
Department of Anatomy and Neuroscience Training Program, University of Wisconsin Medical School, Madison 53706, U.S.A.
Neuroscience. 1997 Sep;80(1):191-202. doi: 10.1016/s0306-4522(97)00095-x.
We used the in vitro whole-cell recording technique to study the nicotinic responses of relay cells and interneurons in the adult rat dorsal lateral geniculate nucleus, the thalamic nucleus that conveys visual signals from the retina to the cortex. These geniculate relay cells and interneurons were identified by their physiological and morphological properties. We found that, in the presence of a muscarinic antagonist, atropine, acetylcholine induced a depolarization in relay cells. A similar depolarization was induced by application of nicotine. These depolarizations were completely blocked by a nicotinic antagonist, hexamethonium, but were little affected by bath solution that contained tetrodotoxin and/or low calcium concentration to block synaptic transmission. This suggests that the depolarization is mediated directly by nicotinic receptors in relay cells. Application of nicotine also induced a depolarization in geniculate interneurons. The interneurons continued to exhibit a response to nicotine in the presence of synaptic blockade, although the time-course of the response was altered. The nicotinic responses in relay cells and interneurons shared many similar properties. Both exhibited desensitization, although this characteristic was much more pronounced in the interneurons. In both cell types, the nicotinic response activated a relatively linear conductance with a slight inward rectification. The reversal potential for the conductance was about - 33 mV, which is consistent with a permeability to sodium and potassium ions. The reversal potential shifted negatively by 5-6 mV when the bath solution contained low calcium, which further suggests a permeability to calcium ions. Our results indicate that nicotinic receptors are present in both geniculate relay cells and interneurons. The nicotinic depolarization in relay cells may serve to enhance transmission of visual signals through the lateral geniculate nucleus as well as to contribute to a voltage-dependent shift in the response mode of geniculate relay cells from burst to tonic (single-spike) firing. The nicotinic depolarization in interneurons may provide an explanation for reports that activation of the cholinergic system can enhance inhibitory tuning in the lateral geniculate nucleus.
我们运用体外全细胞记录技术，研究成年大鼠背外侧膝状核中继细胞和中间神经元的烟碱反应，该丘脑核将视觉信号从视网膜传导至皮层。这些膝状中继细胞和中间神经元通过其生理和形态学特性得以识别。我们发现，在存在毒蕈碱拮抗剂阿托品的情况下，乙酰胆碱可诱导中继细胞发生去极化。应用尼古丁也可诱导类似的去极化。这些去极化可被烟碱拮抗剂六甲铵完全阻断，但含有河豚毒素和/或低钙浓度以阻断突触传递的浴液对其影响甚微。这表明该去极化是由中继细胞中的烟碱受体直接介导的。应用尼古丁也可诱导膝状中间神经元发生去极化。尽管反应的时间进程发生了改变，但在存在突触阻断的情况下，中间神经元仍继续对尼古丁表现出反应。中继细胞和中间神经元中的烟碱反应具有许多相似特性。两者均表现出脱敏现象，尽管这一特征在中间神经元中更为明显。在这两种细胞类型中，烟碱反应均激活了一种具有轻微内向整流的相对线性电导。该电导的反转电位约为 -33 mV，这与对钠离子和钾离子的通透性一致。当浴液含有低钙时，反转电位向负向移动5 - 6 mV，这进一步表明对钙离子具有通透性。我们的结果表明，烟碱受体同时存在于膝状中继细胞和中间神经元中。中继细胞中的烟碱去极化可能有助于增强视觉信号通过外侧膝状核的传递，以及促成膝状中继细胞反应模式从爆发式放电向紧张式（单峰）放电的电压依赖性转变。中间神经元中的烟碱去极化可能为胆碱能系统激活可增强外侧膝状核抑制性调谐的报道提供一种解释。
