Extracellular potassium, glial and neuronal potentials in the solitary complex of rat brainstem slices
Extracellular potassium, glial and neuronal potentials in the solitary complex of rat brainstem slices
复制标题
大鼠脑干切片孤立复合体中的细胞外钾、胶质细胞和神经元电位
DOI：
10.1016/0006-8993(93)91493-c
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发表时间：
1993
期刊：
影响因子：
2.9
通讯作者：
J. Velluti
中科院分区：
文献类型：
--
作者：
K. Ballanyi;P. Branchereau;J. Champagnat;G. Fortin;J. Velluti
在大鼠脑干脑片的孤束核(NTS)和迷走神经背侧运动核(DVMN)，记录顺向刺激孤束核(TS)后的细胞外K+活动(AKE)、神经元和神经胶质细胞膜电位。在神经胶质细胞中，重复刺激TS可引起高达30 mV的去极化，然后再极化，并用指数曲线拟合，其时间常数为1.6-5 S。类似刺激引起的KE值最高可达8 mm，恢复可用单指数曲线拟合，时间常数在1.6-4 S之间。在低钙、高镁离子溶液中阻断突触传递时，KE值下降了75%，应用6-氰基-7-硝基-7-硝基-2，3-二酮(CNQX，50μM)后，KE值下降了24%。低镁溶液灌流可增强对刺激TS的反应，这种作用可被加入2-氨基-5-膦-戊酸(AP7，50μM)而减弱。灌流高浓度八肽缩胆囊素(CCK_8，1~5μM)和C端四肽(CCK_4，50~100μM)对KE和神经胶质细胞无明显影响。刺激TS对孤立复合体神经元的影响表明，在突触激活非NMDA或NMDA型离子受体的过程中，细胞外K+浓度升高。相反，在没有可测量的细胞外K+波动或神经胶质细胞去极化的情况下，由重复传入活动或CCK激动剂兴奋引起的缓慢去极化在神经元中发展。
Extracellular K+activities (aKe) and neuronal and glial membrane potentials were recorded in the nucleus tractus solitarius (NTS) and in the dorsal vagal motor nucleus (DVMN) of rat brainstem slices after orthodromic stimulation of the tractus solitarius (TS). In glial cells, repetitive stimulation of the TS induced depolarizations of up to 30 mV followed by repolarizations which were fitted by exponential curves with a time constant of 1.6–5 s. Similar stimulations induced elevations ofaKeof up to 8 mM, the recovery of which was fitted by single exponential curves with a time constant ranging between 1.6 and 4 s. These elevations inaKewere reduced by 75% during blockage of synaptic transmission in low Ca2+, high Mg2+solution, and by 24% with application of 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX, 50 μM). Perfusion with a low Mg2+solution increased theaKeresponse to stimulation of the TS, an effect that was reduced by the addition of 2-amino-5-phosphono-valeric acid (AP7, 50 μM) to the bath. No significant change inaKeand glial potential was seen when superfusing high concentrations of the C-terminal octapeptide of cholecystokinin (CCK8, 1–5 μM) and C-terminal tetrapeptide (CCK4, 50–100 μM). The effect of TS stimulations on solitary complex neurons suggests that extracellular K+concentration is increased during synaptic activation of non-NMDA or NMDA ionotropic receptors. Conversely, slow depolarizations elicited by repetitive afferent activity or excitation by CCK agonists develop in neurons in the absence of measurable extracellular K+fluctuations or glial depolarization.