Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion
Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion
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DOI：
10.1113/jphysiol.1996.sp021632
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发表时间：
1996-09-15
影响因子：
5.5
通讯作者：
Brockhaus, J
中科院分区：
文献类型：
--
作者：
Ballanyi, K;Doutheil, J;Brockhaus, J
1.取成年大鼠脑干切片。结果1.在迷走神经背核，代谢紊乱时神经元(DVNs)和神经胶质细胞的膜电位(E(M))，以及细胞外氧、K+和pH(P-O2，AK(0)，pH(0))。重复电刺激孤束(TS)所诱发的DVNs突触后电位，导致次级神经胶质细胞去极化高达25 mV，P-O2下降高达150毫米汞柱，细胞外AK(0)上升高达9 mm，pH(0)下降约0.2pH单位。低氧过灌流引起组织缺氧，导致AK(O)增加不到2 mm，pH(O)下降0.24+/-0.04个pH单位(平均值+/-S.D)。无糖溶液延迟8min后，AK(O)缓慢升高1.9+/-0.8 mm，pH(O)平均升高0.24+/-0.13个pH单位。在无糖溶液中预先孵育后，缺氧使AK(O)升高达15 mM，而缺氧引起的pH(O)下降被完全阻断。在118个DVNs中，有45个在缺氧状态下出现15.6+/-5.0 mV的持续性超极化。在其余的DVNs中，缺氧暴露没有引起E(M)的改变(37%)或导致去极化小于10 mV(25%)。缺氧时，神经胶质细胞的去极化稳定在9+/-3.8 mV。在有氧无葡萄糖溶液中，延迟12-80分钟后也有类似的反应。代谢相关的超极化可被100-500 mU的甲苯磺丁胺或20-100 mU的格列本脲阻断，使自发的(0.5-6赫兹)棘波放电恢复。在这些细胞中，400-500亩M二氮卓可引起自发性活动的超极化和阻断。在DVNs和神经胶质细胞中，在无糖溶液中预先孵育后，在缺氧暴露过程中，逐渐出现幅度高达40 mV的去极化。结果表明，氧气或葡萄糖的耗竭不会损害DVNX细胞的活力。讨论了神经元ATP敏感性K+(K-ATP)通道在这种耐受中的作用。
1. Brainstem slices were taken from mature rats. In the dorsal vagal nucleus (DVNX), membrane potentials (E(m)) of neurons (DVNs) and glia, as well as extracellular oxygen, K+ and pH (P-O2, aK(0), pH(0)), were analysed during metabolic disturbances.2. Postsynaptic potentials of DVNs, elicited by repetitive electrical stimulation of the solitary tract (TS), led to a secondary glial depolarization of up to 25 mV, a fall in P-O2 of up to 150 mmHg, a rise in extracellular aK(0) of up to 9 mM, and a fall in pH(0) of about 0.2 pH units.3. Hypoxic superfusates produced tissue anoxia, leading to an aK(o) increase of less than 2 mM and a pH(o) fall of 0.24 +/- 0.04 pH units (mean +/- S.D). Glucose-free solution evoked, after a delay of more than 8 min, a slow rise in aK(o) of 1.9 +/- 0.8 mM, accompanied by a mean increase in pH(o) of 0.24 +/- 0.13 pH units. After pre-incubation in glucose-free solution, anoxia elevated aK(o) by up to 15 mM, whereas the anoxia-induced pH(o) decrease was completely blocked.4. In 45 of 118 DVNs, anoxia elicited a persistent hyperpolarization of 15.6 +/- 5.0 mV. In the remaining DVNs, anoxic exposure either did not produce a change in E(m) (37 %) or led to a depolarization of less than 10 mV (25 %). A stable depolarization of 9 +/- 3.8 mV was detected in glial cells during anoxia. Similar responses were revealed in oxygenated glucose-free solution after a delay of 12-80 min.5. The metabolism-related hyperpolarizations were blocked by 100-500 mu M tolbutamide or 20-100 mu M glibenclamide, leading to recovery of spontaneous (0.5-6 Hz) spike discharge. In these cells, 400-500 mu M diazoxide evoked hyperpolarizations and blockade of spontaneous activity.6. In DVNs and glial cells, a progressive depolarization of up to 40 mV in amplitude developed during anoxic exposure after pre-incubation in glucose-free solution.7. The results show that oxygen or glucose depletion does not impair the viability of DVNX cells. The contribution of neuronal ATP-sensitive K+ (K-ATP) channels to this tolerance is discussed.