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大鼠下丘脑切片中室旁核神经元的局部抑制性突触输入。

Local inhibitory synaptic inputs to neurones of the paraventricular nucleus in slices of rat hypothalamus.

作者信息

Tasker J G, Dudek F E

机构信息

Mental Retardation Research Center, University of California Los Angeles 90024.

出版信息

J Physiol. 1993 Sep;469:179-92. doi: 10.1113/jphysiol.1993.sp019810.

Abstract
  1. Intracellular recordings were obtained from neurones in the region of the paraventricular nucleus in slices of rat hypothalamus. Glutamate microdrops were applied to the surface of the slices at sites dorsal, lateral and ventral to the paraventricular nucleus to selectively activate local presynaptic neurones. The gamma-aminobutyric acidA (GABAA)-receptor antagonists picrotoxin or bicuculline were bath-applied to block synaptic inhibition. 2. Glutamate microapplication caused a tonic depolarization and often repetitive action potentials in twenty of forty-seven recorded cells. This was probably caused by the direct exposure of the dendrites of the recorded cells to the glutamate microdrops. 3. Glutamate microstimulation elicited inhibitory synaptic responses in nine of forty-seven neurones tested. Glutamate microdrops caused discrete, hyperpolarizing postsynaptic potentials (PSPs) in four cells recorded with microelectrodes containing potassium acetate and evoked depolarizing PSPs in four cells recorded with KCl-filled microelectrodes. Glutamate microapplication inhibited spontaneous spike firing in another cell recorded with a potassium acetate microelectrode. 4. Bath application of GABAA-receptor antagonists completely blocked the hyperpolarizing PSPs elicited by glutamate microstimulation in three of three cells recorded with potassium acetate electrodes and the depolarizing PSPs in two of two cells recorded with KCl electrodes, indicating they were inhibitory PSPs caused by the release of GABA. Suppression of GABAA-mediated synaptic inhibition did not reveal any glutamate-evoked excitatory PSPs. 5. Recorded cells were identified as magnocellular, parvocellular or non-paraventricular bursting neurones on the basis of their electrophysiological properties. Direct depolarization and local inhibitory synaptic responses were observed in all three cell types. 6. Several conclusions can be drawn from these data: (1) functional glutamate receptors are distributed throughout neuronal populations in the paraventricular region of the hypothalamus, confirming and extending previous observations; (2) local synaptic inputs to neurones in the paraventricular nucleus are primarily inhibitory, supplied by perinuclear GABAergic neurones; (3) both magnocellular and parvocellular subpopulations receive local inhibitory synaptic inputs. The possibility that these local GABAergic circuits mediate inhibitory inputs to paraventricular neurones from limbic structures is discussed.
摘要
  1. 采用细胞内记录法,从大鼠下丘脑切片室旁核区域的神经元获取电信号。将谷氨酸微滴施加于室旁核背侧、外侧和腹侧的切片表面,以选择性激活局部突触前神经元。将γ-氨基丁酸A(GABAA)受体拮抗剂印防己毒素或荷包牡丹碱浴槽给药,以阻断突触抑制。2. 对47个记录细胞中的20个施加谷氨酸微滴,引发了持续性去极化,并常常伴有重复动作电位。这可能是由于记录细胞的树突直接暴露于谷氨酸微滴所致。3. 对47个测试神经元中的9个进行谷氨酸微刺激,引发了抑制性突触反应。谷氨酸微滴在4个用含醋酸钾微电极记录的细胞中引起离散的超极化突触后电位(PSP),在4个用充满氯化钾的微电极记录的细胞中引发去极化PSP。对另一个用醋酸钾微电极记录的细胞施加谷氨酸微滴,抑制了其自发放电。4. 对用醋酸钾电极记录的3个细胞中的3个以及用氯化钾电极记录的2个细胞中的2个,浴槽施加GABAA受体拮抗剂完全阻断了谷氨酸微刺激引发的超极化PSP和去极化PSP,表明它们是由GABA释放引起的抑制性PSP。抑制GABAA介导的突触抑制未揭示任何谷氨酸诱发的兴奋性PSP。5. 根据记录细胞的电生理特性,将其鉴定为大细胞、小细胞或非室旁爆发性神经元。在所有三种细胞类型中均观察到直接去极化和局部抑制性突触反应。6. 从这些数据可以得出几个结论:(1)功能性谷氨酸受体分布于下丘脑室旁区域的整个神经元群体中,证实并扩展了先前的观察结果;(2)室旁核中神经元的局部突触输入主要是抑制性的,由核周GABA能神经元提供;(3)大细胞和小细胞亚群均接受局部抑制性突触输入。讨论了这些局部GABA能回路介导来自边缘结构对室旁神经元抑制性输入的可能性。

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