ANOXIA-INDUCED FUNCTIONAL INACTIVATION OF NEONATAL RESPIRATORY NEURONS IN-VITRO

被引:41
作者
BALLANYI, K
VOLKER, A
RICHTER, DW
机构
[1] II Physiologisches Institute, Universitat Gottingen, Gottingen, D37073
关键词
METABOLISM; EPSPS; GLYCOLYSIS; HYPOXIA; IPSPS; POTASSIUM CHANNELS; RHYTHM GENERATION; VENTRAL RESPIRATORY GROUP;
D O I
10.1097/00001756-199412300-00042
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
IN the isolated brain stem-spinal cord preparation of neonatal rats, respiratory (C-4) activity persisted at reduced frequency during tissue anoxia. In seven biphasic expiratory (Bi-E) and in 12 of 22 inspiratory (Insp) neurones, recorded with the 'blind' patch-clamp technique, anoxia evoked a persistent hyperpolarization by up to 16 mV whereas membrane potential of the remaining Insp neurones depolarized slightly or remained unaffected. Respiration-related synaptic potentials and action potential discharges were blocked in all Bi-E and in about 50% of the Insp neurones, whereas rhythmic activity persisted in the other cells. The results indicate that a major population of neonatal respiratory neurones is functionally inactivated during anoxia. This mechanism might contribute to the anoxia tolerance of the immature brain.
引用
收藏
页码:165 / 168
页数:4
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