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首页> 外文期刊>The European Journal of Neuroscience >Two distinct types of repetitive bursting activity mediated by NMDA in hypothalamic neurons in vitro.
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Two distinct types of repetitive bursting activity mediated by NMDA in hypothalamic neurons in vitro.

机译：NMDA在下丘脑神经元中介导的两种不同类型的重复性爆发活性。

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摘要

Hypothalamic magnocellular dorsal nucleus neurons were recorded from adult guinea pig brain slices with the whole-cell patch-clamp technique to determine the effects of N-methyl-D-aspartate (NMDA) applied in the bath or by iontophoresis. In a majority of cells (59 of 77, 76.6%), rhythmic bursting discharges were evoked by specific activation of NMDA receptors when the membrane was more negative than -60 mV. This endogenous rhythmic activity was resistant to tetrodotoxin. It was suppressed by removal of extracellular Mg2+, indicating the involvement of the voltage-dependent block of the NMDA channel by Mg2+. Application of thapsigargin showed that rhythmic activity did not depend on the release of Ca2+ from reticulum stores. Blockers of Ca2+ conductances Ni2+ and nifedipine had no effects on the bursts. Their repolarization did not involve the activation of a strophantidin- or ouabain-sensitive pump, but partly depended on an apamine-sensitive Ca2+-dependent K+current. In a small subset of cells (9 of 69, 13%), specific activation of NMDA receptors induced another type of bursting activity which consisted of repetitive low-threshold spikes sustaining bursts of action potentials. Rhythmic low-threshold spikes subsisted in the presence of tetrodotoxin but were suppressed by Ni2+. Increasing the amount of NMDA brought about a switch from the rhythmic low-threshold spike burst firing to the rhythmic bursting activity observed for the majority of cells. The present data show for the first time that NMDA receptor activation can induce two independent rhythmic bursting behaviours in the same neuron, probably depending on the strength of the glutamatergic drive.
机译：使用全细胞膜片钳技术从成年豚鼠脑切片记录下丘脑的巨细胞背核神经元，以确定在浴中或通过离子电渗疗法应用的N-甲基-D-天冬氨酸（NMDA）的作用。在大多数细胞中（77个中的59个，占76.6％），当膜的负电性高于-60 mV时，NMDA受体的特异性激活会引起节律性的爆裂放电。这种内在的节律性活动对河豚毒素具有抗性。它被细胞外Mg2 +去除所抑制，表明Mg2 +参与了NMDA通道的电压依赖性传导阻滞。 thapsigargin的应用表明节律性活动不依赖于网状存储中Ca2 +的释放。 Ca2 +电导的阻滞剂Ni2 +和硝苯地平对爆发没有影响。它们的复极化不涉及对链霉抗生物素蛋白或哇巴因敏感的泵的激活，但部分取决于对apamine敏感的Ca2 +依赖性K +电流。在一小部分细胞中（69个细胞中的9个，占13％），NMDA受体的特异性激活诱导了另一种类型的爆发活动，该活动由重复的低阈值尖峰组成，维持动作电位的爆发。在存在河豚毒素的情况下，节律性的低阈值尖峰仍然存在，但被Ni2 +抑制。 NMDA量的增加导致从有节奏的低阈值尖峰爆发触发转变为对大多数细胞观察到的有节奏爆发活性。目前的数据首次表明NMDA受体激活可以在同一神经元中诱导两种独立的有节奏的爆发行为，这可能取决于谷氨酸能驱动的强度。

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