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Biology of Reproduction, Vol 22, 927-934, Copyright © 1980 by Society for the Study of Reproduction
1 Department of Psychology,
University of California,
Los Angeles, California 90024 Adult female rats received bilateral corticomedial amygdala lesions, olfactory bulbectomy,
or sham surgery. Following ovariectomy, luteinizing hormone (LH) responses to estradiol benzoate
(EB) and progesterone (P) treatment were assessed. With 4 weeks separating each injection, each
rat received at 1200 h each of 3 doses of EB: 0.7, 3.5 and 7.0 µg/100 g BW. Oil or 2 mg of P was
administered 72 h after EB treatment. Jugular blood samples (0.5 ml) were taken 5 times for each
dose of EB: 43 h prior to, and 5, 29, 53 and 77 h after EB administration. Five hours after the
0.7 µg/100 g BW dose of EB, and at both 5 and 29 h after the 3.5 µg/100 g BW dose of EB, plasma
LH levels were depressed in all groups, but subsequently recovered to near pre-EB levels. Plasma
LH levels were also depressed 5 and 29 h after the 7 µg EB/100 g BW dose in all groups, but by
53 h LH levels were significantly elevated beyond pre-EB levels when analyzed without regard to
surgical treatment. However, the rats with corticomedial amygdala lesions did not respond to this
high dose of EB; plasma LH titers 53 h post-EB were only equivalent to pre-EB levels. Regardless
of surgical treatment, all rats given P 72 h after EB treatment responded with elevated LH levels
relative to LH levels in oil-treated controls. As the dose of EB increased from 0.7 to 7 µg/100 g BW,
the magnitude of the P-induced rise in LH increased. Thus, although olfactory bulbectomy was
without effect, corticomedial amygdala lesions attenuated LH elevations induced by EB but not
those induced by EB plus P treatment. The corticomedial amygdala may play a role specifically in
the positive feedback action of EB.
2 Department of Anatomy and Brain Research Institute,
University of California,
Los Angeles, California 90024
Accepted on February 6, 1980
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