Effect of testosterone and the oestrous cycle on neuronal refractory periods and firing rates of stria terminalis neurones in the female rat
- 1 November 1981
- journal article
- research article
- Published by Springer Nature in Experimental Brain Research
- Vol. 44 (3) , 331-336
- https://doi.org/10.1007/bf00236571
Abstract
Absolute refractory periods of a subpopulation of corticomedial amygdala (CMA) neurones which project to the medial preoptic/ anterior hypothalamic junction (MPH) via the stria terminalis were recorded in the female rat. Previous experiments have shown that this sub-population of CMA neurones is testosterone-sensitive in the male rat. In the ovariectomised female testosterone propionate (TP, 200 μg/day for 18–22 days) significantly reduced the mean absolute refractory period of these CMA neurones compared to oil treated controls (from 1.34 ms to 0.87 ms). In a second experiment the absolute refractory periods of these CMA neurones were measured during the pro-oestrus and di-oestrus stages of the oestrous cycle as well as in ovariectomised controls. The mean absolute refractory period of these neurones was significantly shortened at pro-oestrus (0.99 ms) compared both to animals in di-oestrus 1 (1.45 ms) and ovariectomised controls (1.42 ms). The median firing rate of these CMA neurones was also significantly increased at pro-oestrus (1.24 Hz) compared to di-oestrus 1 (0.13 Hz) and ovariectomised controls (0.09 Hz). No firing rate increase was observed after TP treatment of ovariectomised animals in the first experiment. Results show that the testosterone-sensitive CMA neurones originally discovered in the male rat have a similar sensitivity in the female rat. They also show that the refractory periods of these neurones are shortened at pro-oestrus. Further, these same neurones also show firing rate increases at this time, although such an increase has not been observed in gonadally intact male rats when compared to castrated ones. Results are interpreted in terms of a possible functional sexual dimorphism in the output of these CMA neurones.Keywords
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