The response of GABAergic and cholinergic neurons to transient cerebral ischemia.
The vulnerability of striatal and hippocampal neurons to ischemia was studied by measuring the activity of neurotransmitter-related enzymes after transient forebrain ischemia in rats. Activities of glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT) were measured 6 h to 8 days after 20, 30 or 40 min of forebrain ischemia, as markers for GABAergic and cholinergic neurons respectively. Transient forebrain ischemia resulted in depression of striatal GAD activity while striatal CAT and hippocampal GAD activities were unaffected. Striatal GAD activity progressively decreased during the first 24 h postischemia and remained depressed 5--8 days later, suggesting irreversible damage to this population of neurons. The stability of striatal CAT and hippocampal GAD activity indicates that these cells were resistant to the present ischemic conditions.
D000109:Acetylcholine / Q000502:physiology; D000818:Animals; D001921:Brain / Q000503:physiopathology*; D002262:Carboxy-Lyases / Q000378:metabolism*; D002795:Choline O-Acetyltransferase / Q000378:metabolism*; D003342:Corpus Striatum / Q000201:enzymology / Q000503:physiopathology*; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D006624:Hippocampus / Q000201:enzymology / Q000503:physiopathology*; D006651:Histocytochemistry; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D009474:Neurons / Q000201:enzymology / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D005680:gamma-Aminobutyric Acid; D002795:Choline O-Acetyltransferase; D002262:Carboxy-Lyases; D005968:Glutamate Decarboxylase; D000109:Acetylcholine