Loss of striatal somatostatin neurons following prenatal methylazoxymethanol.
Prenatal administration of methylazoxymethanol acetate (MAM), which kills neuroblasts undergoing mitosis, was used to lesion striatal somatostatin neurons. Previous [3H]thymidine autoradiographic studies had indicated that striatal somatostatin neurons undergo their final mitotic division at Gestational Days (G) 15 and 16. Therefore, pregnant Sprague-Dawley rats received an intraperitoneal injection of MAM (25 mg/kg) on G15. Neurochemical and histological examination of the mature offspring indicated the loss of half the striatal aspiny interneurons in which somatostatin, neuropeptide Y, and NADPH diaphorase coexist, with relative sparing of the cholinergic interneurons and medium spiny projection cells. This prenatal MAM treatment was without apparent effect on the patch-matrix organization of the striatum.
Vincent
S R
SR
Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Semba
K
K
Radke
J M
JM
Jakubovic
A
A
Fibiger
H C
HC
D000818:Animals; D001835:Body Weight; D002395:Catecholamines / Q000378:metabolism*; D003342:Corpus Striatum / Q000166:cytology / Q000378:metabolism*; D005260:Female; D005333:Fetus / Q000187:drug effects / Q000378:metabolism*; D008746:Methylazoxymethanol Acetate / Q000031:analogs & derivatives* / Q000494:pharmacology; D008938:Mitosis / Q000187:drug effects; D009474:Neurons / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000378:metabolism*
D002395:Catecholamines; D013004:Somatostatin; D008746:Methylazoxymethanol Acetate; C030667:methylazoxymethanol