Systemic glutamate induces degeneration of a subpopulation of tyrosine hydroxylase-immunoreactive neurons in the rat area postrema.
Neuronal damage in the area postrema (AP) of 12-14-week-old male rats was induced by subcutaneous administration of monosodium glutamate (MSG). An immunocytochemical method was used to visualize catecholaminergic neurons in the AP after MSG-treatment. Some tyrosine hydroxylase-immunoreactive neurons exhibited marked signs of degeneration, while others appeared undamaged. We conclude that catecholamine-synthesizing neurons in the AP are differentially sensitive to the neuroexcitotoxic effect of systemic glutamate.
Phelix
C F
CF
Department of Pharmacology and Toxicology, College of Pharmacy, University of Georgia, Athens 30602.
Hartle
D K
DK
D000818:Animals; D002395:Catecholamines / Q000378:metabolism*; D002552:Cerebral Ventricles / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005971:Glutamates / Q000494:pharmacology*; D007150:Immunohistochemistry; D007279:Injections, Subcutaneous; D008297:Male; D009410:Nerve Degeneration / Q000187:drug effects*; D009498:Neurotoxins / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012970:Sodium Glutamate / Q000494:pharmacology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism*
D002395:Catecholamines; D005971:Glutamates; D009498:Neurotoxins; D014446:Tyrosine 3-Monooxygenase; D012970:Sodium Glutamate