Ballanyi K, Branchereau P, Champagnat J, Fortin G, Velluti J
Biologie Fonctionnelle du Neurone, Institut Alfred Fessard, C.N.R.S. Gif-sur-Yvette, France.
Brain Res. 1993 Apr 2;607(1-2):99-107. doi: 10.1016/0006-8993(93)91493-c.
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 of aKe of 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 in aKe were 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 microM). Perfusion with a low Mg2+ solution increased the aKe response to stimulation of the TS, an effect that was reduced by the addition of 2-amino-5-phosphono-valeric acid (AP7, 50 microM) to the bath. No significant change in aKe and glial potential was seen when superfusing high concentrations of the C-terminal octapeptide of cholecystokinin (CCK8, 1-5 microM) and C-terminal tetrapeptide (CCK4, 50-100 microM). 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.
在对大鼠脑干切片的孤束(TS)进行顺向刺激后,记录孤束核(NTS)和迷走神经背运动核(DVMN)中的细胞外钾离子活性(aKe)以及神经元和神经胶质细胞膜电位。在神经胶质细胞中,对TS的重复刺激诱导了高达30 mV的去极化,随后是复极化,其符合时间常数为1.6 - 5 s的指数曲线。类似的刺激诱导aKe升高高达8 mM,其恢复符合时间常数在1.6至4 s之间的单指数曲线。在低钙、高镁溶液中阻断突触传递期间,这些aKe的升高降低了75%,而应用6 - 氰基 - 7 - 硝基喹喔啉 - 2,3 - 二酮(CNQX,50 μM)时降低了24%。用低镁溶液灌注增加了对TS刺激的aKe反应,在浴液中添加2 - 氨基 - 5 - 磷酸戊酸(AP7,50 μM)可减弱这种效应。当灌注高浓度的胆囊收缩素C末端八肽(CCK8,1 - 5 μM)和C末端四肽(CCK4,50 - 100 μM)时,未观察到aKe和神经胶质细胞电位有明显变化。TS刺激对孤束复合神经元的影响表明,在非NMDA或NMDA离子otropic受体的突触激活过程中细胞外钾离子浓度升高。相反,在没有可测量的细胞外钾离子波动或神经胶质细胞去极化的情况下,由重复传入活动引起的缓慢去极化或CCK激动剂引起的兴奋在神经元中产生。