Abstract

Short- and long-term influences of various neonatal hormonal manipulations were assessed in the mouse amygdala with respect to α-bungarotoxin binding capacity, a possible parameter for cholinergic receptor integrity and function. To estimate the short-term effects, [ 125I]α-bungarotoxin binding to the tissue homogenate obtained from the posterior corticomedial amygdala was determined by a filtration assay using mice killed at 14 days post partum. The amygdaloid tissue from the normal male had a greater binding capacity for [ 125I]α-bungarotoxin than that from the normal female. However, castration of the male on the day of birth decreased the binding down to the female's level. A treatment of the female with either 250 μg testosterone propionate or 10 μg estradiol benzoate on days 1, 3, 5 and 7 increased the binding up to the male's level, although similar neonatal administration of 250 μg 5α-dihydrotestosterone was ineffective. The long-term effects of neonatal hormonal manipulations were examined with 77-day-old mice which had been gonadectomized for 49 days. A quantitative light-microscopic autoradiography for [ 125I]α bungarotoxin binding showed that specific grain density over the nucleus amygdaloideus medialis posterior of the androgenized female exceeded that of the female without neonatal hormone treatment. These observations provide further evidence that neonatal sex steroids play a determinate role in the sexual differentiation of the brain by exerting an organizational influence on developing cholinergic binding sites in the amygdala.

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