缺氧性前脑胆碱能神经元损伤：葡萄糖、兴奋性氨基酸受体及一氧化氮的作用

Hypoxic forebrain cholinergic neuron injury: role of glucose, excitatory amino acid receptors and nitric oxide.

作者信息

Flavin M P, Yang Y, Ho G

机构信息

Department of Pediatrics, Kingston General Hospital, Queen's University, Ont., Canada.

出版信息

Neurosci Lett. 1993 Dec 24;164(1-2):5-8. doi: 10.1016/0304-3940(93)90843-a.

DOI:10.1016/0304-3940(93)90843-a

PMID:7908728

Abstract

Glucose depletion increased sensitivity to hypoxic insult in basal forebrain forebrain cultures in a dose-dependent manner as indicated by reduction of choline acetyltransferase (ChAT) activity, increased lactate dehydrogenase (LDH) release and disrupted morphology. The glutamate receptor antagonists 2-amino-5-phosphonovaleric acid (APV) and 6-cyano-2,3-nitroquinoxoline (CNQX) limited the degree of injury in combination and individually. The nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine (NNLA) also either completely protected against mild injury or attenuated severe injury.

摘要

葡萄糖耗竭以剂量依赖的方式增加了基底前脑培养物对缺氧损伤的敏感性，这表现为胆碱乙酰转移酶（ChAT）活性降低、乳酸脱氢酶（LDH）释放增加以及形态破坏。谷氨酸受体拮抗剂2-氨基-5-磷酸戊酸（APV）和6-氰基-2,3-硝基喹喔啉（CNQX）单独或联合使用均能限制损伤程度。一氧化氮合酶（NOS）抑制剂N-硝基-L-精氨酸（NNLA）要么完全保护细胞免受轻度损伤，要么减轻重度损伤。