Hypoxic forebrain cholinergic neuron injury: role of glucose, excitatory amino acid receptors and nitric oxide.
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.
Flavin
M P
MP
Department of Pediatrics, Kingston General Hospital, Queen's University, Ont., Canada.
Yang
Y
Y
Ho
G
G
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D002478:Cells, Cultured; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D005947:Glucose / Q000502:physiology*; D002534:Hypoxia, Brain / Q000201:enzymology / Q000473:pathology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009474:Neurons / Q000201:enzymology / Q000502:physiology* / Q000648:ultrastructure; D009569:Nitric Oxide / Q000502:physiology*; D019335:Nitroarginine; D010275:Parasympathetic Nervous System / Q000201:enzymology / Q000473:pathology*; D016548:Prosencephalon / Q000201:enzymology / Q000473:pathology*; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017459:Receptors, Amino Acid / Q000037:antagonists & inhibitors / Q000502:physiology*
D011810:Quinoxalines; D017459:Receptors, Amino Acid; D019335:Nitroarginine; D009569:Nitric Oxide; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D015763:2-Amino-5-phosphonovalerate; D001120:Arginine; D007770:L-Lactate Dehydrogenase; D002795:Choline O-Acetyltransferase; D005947:Glucose