GABAergic hippocampal neurons resistant to ischemia-induced neuronal death contain the Ca2(+)-binding protein parvalbumin.
Bilateral transient occlusion of carotid arteries in gerbils for 7 min results in delayed neuronal cell death in hippocampal field CA1. Local gamma-aminobutyric acid (GABA)ergic neurons survive the ischemic insult. Here we show that interneurons in gerbil hippocampus are parvalbumin-immunoreactive, that they contain the GABA-synthetizing enzyme glutamic acid decarboxylase (GAD), and that they are resistant to the effects of ischemia, being present up to 28 days after the insult. It might be concluded that the presence of the Ca2+-binding protein parvalbumin protects the GABAergic neurons from the deleterious consequences of ischemia-induced excitotoxin-mediated Ca2+-influx.
Nitsch
C
C
Neuroanatomical Department, University in Basel, Switzerland.
Scotti
A
A
Sommacal
A
A
Kalt
G
G
D000818:Animals; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D002470:Cell Survival; D005849:Gerbillinae; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006624:Hippocampus / Q000098:blood supply* / Q000201:enzymology / Q000473:pathology; D007150:Immunohistochemistry; D007511:Ischemia / Q000473:pathology*; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D010320:Parvalbumins / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D002135:Calcium-Binding Proteins; D009124:Muscle Proteins; D010320:Parvalbumins; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase