Sexual dimorphism in alpha-bungarotoxin binding capacity in the mouse amygdala.
A sex difference in alpha-bungarotoxin binding capacity in the mouse amygdala has been demonstrated by quantitative light microscopic autoradiography. The difference persisted even under widely different steroid-hormonal environment. In addition, it was observed that the binding capacities in both sexes were reversibly activated by administration of either testosterone or estradiol. Neonatal castration, on the other hand, permanently altered the toxin binding capacity in the adult male mouse. These data suggest the possibility that neonatal sex steroids irreversibly modify the cholinergic nicotinic mechanism in the developing mouse amygdala, while the hormones reversibly modulate the mechanism when applied in adulthood.
D000679:Amygdala / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001345:Autoradiography; D002038:Bungarotoxins / Q000378:metabolism*; D002369:Castration; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D006801:Humans; D007457:Iodine Radioisotopes; D051379:Mice; D008810:Mice, Inbred C57BL; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000378:metabolism*; D011978:Receptors, Nicotinic; D012737:Sex Factors; D013739:Testosterone / Q000494:pharmacology; D064569:alpha7 Nicotinic Acetylcholine Receptor
D002038:Bungarotoxins; C579167:Chrna7 protein, human; C579166:Chrna7 protein, mouse; D007457:Iodine Radioisotopes; D011950:Receptors, Cholinergic; D011978:Receptors, Nicotinic; D064569:alpha7 Nicotinic Acetylcholine Receptor; D013739:Testosterone; D004958:Estradiol