Testosterone regulates substance P within neurons of the medial nucleus of the amygdala, the bed nucleus of the stria terminalis and the medial preoptic area of the male golden hamster.

Abstract:

:The medial nucleus of the amygdala, bed nucleus of the stria terminalis, and medial preoptic area appear to mediate steroidal regulation of mating behavior in male rodents. The mechanism of action has not been determined. One way testosterone could enhance neuronal function is by increasing neurotransmitter levels, thus altering neuronal transmission. To assess this hypothesis, we examined the effect of castration and testosterone treatment on substance P levels in the neurons of these three brain regions. Brains from male Syrian hamsters that were (1) gonadally intact, (2) castrated for 13 weeks, or (3) castrated for 9 weeks and treated with testosterone for 4 weeks, were processed for substance P, and the numbers of substance P immunoreactive neurons in the medial nucleus of the amygdala, bed nucleus of the stria terminalis, and medial preoptic area were determined. Castration reduced the number of substance P neurons in the bed nucleus of the stria terminalis and medial preoptic area relative to those in intact hamsters; the number of substance P neurons in these regions was restored by testosterone treatment. Castration did not reduce the number of substance P neurons in the medial nucleus of the amygdala; however, testosterone treatment increased the numbers of these neurons when compared to intacts. Thus, testosterone regulates substance P levels in areas that regulate mating behavior. As substance P enhances male copulatory behavior our results suggest that testosterone may regulate copulatory behavior by enhancing substance P levels in medial nucleus of the amygdala, bed nucleus of the stria terminalis and medial preoptic area.

journal_name

Brain Res

journal_title

Brain research

authors

Swann JM,Newman SW

doi

10.1016/0006-8993(92)91077-r

subject

Has Abstract

pub_date

1992-09-11 00:00:00

pages

18-28

issue

1-2

eissn

0006-8993

issn

1872-6240

pii

0006-8993(92)91077-R

journal_volume

590

pub_type

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