ABSTRACT
Bilateral injections of 30 mug of 6-hydroxydopamine (6-OHDA, as base) into the anterolateral hypothalamic area induced constant vaginal cornification (CVC), polyfollicular ovaries and uterine hypertrophy in cyclic adult female rats. There were no important changes in the vaginal patterns or ovarian and uterine morphology in animals given injections in the same area with the solvent only and in animals given injections with 6-OHDA in the anterior amygdaloid area. It is suggested that the persistent estrus after anterolateral hypothalamic injections of 6-OHDA results from lesions of central catecholaminergic pathways, which are probably involved in gonadotropin secretion.
Subject(s)
Estrus , Hydroxydopamines/pharmacology , Hypothalamus/drug effects , Animals , Brain Mapping , Female , Organ Size , Ovary/anatomy & histology , Pituitary Gland/anatomy & histology , Pregnancy , Rats , Uterus/anatomy & histologySubject(s)
Castration , Ovary/physiology , Water Deprivation , Animals , Dehydration , Estrogens/metabolism , Female , Hypertrophy , Organ Size , Ovary/metabolism , Ovary/pathology , Ovary/surgery , RatsSubject(s)
Estrus , Water Deprivation , Animals , Body Weight , Circadian Rhythm , Female , Pregnancy , RatsABSTRACT
PIP: The participation of a central cholinergic system in the control of hypophysial folliculotrophin release was confirmed in an experiment in which 250 gm of atropine sulfate, a blocking agent, was implanted in the anterior and lateral hypothalamic areas of rate; 22 rats were killed after 15 days, 24 after 30 days, and 10 were hemicastrated the same day of implantation and sacrificed 15 days later. A significantly prolonged diestrous phase from 4-12 days were observed in 43 of 46 intact rats implanted with atropine, suggesting an inhibition in the ovulatory discharge of gonadotrophins; lowered ovarian weight after 15 days due to a decrease in number and diameter of corpora lutea indicated that the drug may mainly affect the release of luteinizing hormone. Normal ovarian weight, morphology, and ovulatory activity was resumed after 30 days indicating that the blockade of ovulation was a transient consequence of the neural action of atropine. Ovarian compensatory hypertrophy in hemicastrated rats was prevented by the same dose of atropine but without disturbance in the estrous cycle, indicating incomplete inhibition of folliculotrophin release.^ieng
