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缺氧在体外诱导新生呼吸神经元功能失活。

Anoxia induced functional inactivation of neonatal respiratory neurones in vitro.

作者信息

Ballanyi K, Völker A, Richter D W

机构信息

II Physiologisches Institut, Universität Göttingen, Germany.

出版信息

Neuroreport. 1994 Dec 30;6(1):165-8. doi: 10.1097/00001756-199412300-00042.

Abstract

In the isolated brain stem-spinal cord preparation of neonatal rats, respiratory (C4) 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.

摘要

在新生大鼠离体脑干-脊髓标本中,组织缺氧时呼吸(C4)活动以降低的频率持续存在。在用“盲法”膜片钳技术记录的7个双相呼气(Bi-E)神经元和22个吸气(Insp)神经元中的12个中,缺氧诱发了高达16 mV的持续超极化,而其余Insp神经元的膜电位则略有去极化或未受影响。所有Bi-E神经元和大约50%的Insp神经元中与呼吸相关的突触电位和动作电位发放被阻断,而其他细胞中节律性活动持续存在。结果表明,新生儿呼吸神经元的主要群体在缺氧时功能失活。这种机制可能有助于未成熟脑的缺氧耐受性。

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