Steroid-induced polycystic ovaries in rats: effect of electro-acupuncture on concentrations of endothelin-1 and nerve growth factor (NGF), and expression of NGF mRNA in the ovaries, the adrenal glands, and the central nervous system.

Previous studies on the effect of repeated electro-acupuncture (EA) treatments in rats with steriod-induced polycystic ovaries (PCO), EA has been shown to modulate nerve growth factor (NGF) concentration in the ovaries as well as corticotropin releasing factor (CRF) in the median eminence (ME). In the present study we tested the hypothesis that repeated EA treatments modulates sympathetic nerve activity in rats with PCO. This was done by analysing endothelin-1 (ET-1), a potent vasoconstrictor involved in ovarian functions, as well as NGF and NGF mRNA expression involved in the pathophysiological process underlying steroid-induced PCO. The main result in the present study was that concentrations of ET-1 in the ovaries were significantly lower in the PCO group receiving EA compared with the healthy control group (p < 0.05). In the hypothalamus, however, ET-1 concentrations were found to be significantly higher in the PCO group receiving EA than in the healthy control group (p < 0.05). Concentrations of ovarian NGF protein were significantly higher in the PCO control group compared with the healthy control group (p < 0.001), and these concentrations decreased significantly after repeated EA treatments compared with those in the PCO control group (p < 0.05) and were found to be the same as those in the healthy control group. In conclusion, these results indicate that EA modulates the neuroendocrinological state of the ovaries, most likely by modulating the sympathetic nerve activity in the ovaries, which may be a factor in the maintenance of steroid-induced PCO.

The regional hypothalamic distribution of type II 5'-monodeiodinase in euthyroid and hypothyroid rats.

The brain topographical distribution of type II 5'-monodeiodinase (5'D-II), which converts thyroxine (T4) to triiodothyronine (T3), was studied in euthyroid and hypothyroid rats. Low levels of 5'D-II activity were detected in the median eminence, but not in any other brain regions of euthyroid rats. The arcuate nucleus and median eminence were also the sites of highest 5'D-II activity in brains of hypothyroid rats. Under these conditions, the paraventricular nucleus contained almost no detectable 5'D-II, while intermediate enzyme activity was present in other medial basal hypothalamic sites.

Alleviation of estrogen-induced hyperprolactinemia through intracerebral transplantation of hypothalamic tissue containing dopaminergic neurons.

Prolactin-secreting pituitary tumors can be induced in young rats through prolonged estrogen treatment. Recent evidence suggests that such tumors are associated with a degeneration of tuberoinfundibular dopaminergic (TI-DA) neurons, which normally inhibit prolactin secretion by the anterior pituitary's lactrophs. For this study, chronic hyperprolactinemia was induced in young, ovariectomized Fisher 344 rats through Silastic capsule implants of 17 beta-estradiol, placed subcutaneously for 1 month prior to removal. Rats with such estrogen-induced hyperprolactinemia then received transplants of neonatal arcuate-median eminence (ME) tissue (containing TI-DA neurons) or amygdala (control) tissue, placed either within the third ventricle or bilaterally within the hypothalamus. Blood samples were obtained 1 month after transplantation and prolactin concentrations measured by radioimmunoassay. Two of 4 animals receiving ventricularly-placed arcuate-ME transplants and 4 of 7 animals receiving bilateral arcuate-ME transplants showed substantial reductions in plasma prolactin levels compared to mean values in control animals. Follow-up catecholamine (CA) histochemistry indicated a bright fluorescence intensity in the median eminence of animals remaining hyperprolactinemic with ineffective transplants. Furthermore, in sharp contrast to the very low, nonpulsatile LH levels found during a second bleeding in recipients bearing ineffective transplants, recipients with effective arcuate-ME transplants had the high, pulsatile levels of LH characteristic of normal, ovariectomized rats. These data suggest that developing TI-DA neurons, within effective arcuate-ME transplants, became functional to reinstate or accentuate DA inhibition of prolactin secretion and, in so doing, indirectly normalized LH secretion as well.

Effect of hypothalamus lesions on the presence of CRF-immunoreactive nerve terminals in the median eminence and on the pituitary-adrenal response to stress.

By use of an antiserum raised against conjugated ovine corticotropin releasing factor (CRF1-41), nerve fibres can be stained immunocytochemically in the external zone of the median eminence of rats. The presence of CRF-immunoreactive (CRFi) nerve fibres and the plasma corticosterone response to ether stress were studied in rats 6-7 days after making various types of lesions in the hypothalamus. Complete anterolateral deafferentation of the mediobasal hypothalamus caused complete disappearance of CRFi fibres from the median eminence and blocked the corticosterone response to stress. Incomplete anterolateral hypothalamic deafferentation did not prevent the stress-induced increase of corticosterone and in these rats, part of the CRFi nerve fibres remained intact. A horizontal cut placed ventral to the paraventricular nuclei, completely prevented the corticosterone response in those rats that showed a complete disappearance of CRFi nerve fibres from the median eminence. Some rats however, still exhibited CRFi nerve fibres and these animals responded to stress with increased corticosterone levels. A similar horizontal cut made just dorsal to the paraventricular nuclei affected neither the corticosterone response to stress nor the appearance of CRFi nerve fibres in the median eminence. We conclude that the presence of CRFi nerve fibres in the median eminence is a prerequisite for rats to show a pituitary-adrenal response to ether stress and therefore represents the first functional evidence for the role of these hypothalamic CRFi-neurons.

Intrahypothalamic terminals of stress conducting fibers.

Surgical stress did not elevate plasma corticosterone level in rats with bilateral surgical transection of the lateral retrochiasmatic area (RCAL). After RCAL transections light and electron microscopic terminal degeneration was observed in both the external and the internal layers of the median eminence as well as in the arcuate and ventromedial nuclei. Incisions lateral to the medial forebrain bundle did not prevent the stress-induced rise in plasma corticosterone level and were not followed by degeneration in the median eminence. Transection of the medial forebrain bundle rostral or caudal to the RCAL caused degeneration in both the median eminence and the arcuate nucleus.

Gonadotrophin release in hypogonadal and normal mice after electrical stimulation of the median eminence or injection of luteinizing hormone releasing hormone.

Electrical stimulation of the median eminence, using parameters known to cause the release of LH in normal male mice, failed to elicit any gonadotrophin response in nypogonadal (hpg) male mice. Administration of 40 ng synthetic LH releasing hormone (LH-RH) resulted in release of LH from the pituitary gland of hpg mice, although the response was significantly lower than that of normal mice. These results were consistent with the hypothesis that the hypogonadal state of the hpg mouse results from a functional basence of LH-RH in the hypothalamus rather than from a lack of response of the pituitary gland to the releasing hormone.