摘要:

The purpose of this study was to examine the role that the dorsal raphe (DR)-median eminence (ME) serotonergic projection may have in the proestrous gonadotropin and prolactin (PRL) release. DR electrolytic lesions were performed in cycling rats during the first day of diestrus. The effect of DR lesions after 48–72 h of survival (short-term lesioned animals) or after 35–40 days of survival (long-term lesioned animals) on estrous cyclicity, preovulatory gonadotropin and PRL releasing pattern, ovulation and serotonin (5-HT) content of the ME were studied. Following DR lesions the estrous cycle became irregular, remaining in the diestrus phase for several days. Preovulatory gonadotropin release in short-term lesioned animals was increased; on the contrary, in long-term lesioned rats a delay in the surge of these two hormones and a decrease in LH secretion were detected. Long-term lesioned animals also showed a diminished secretion of PRL. The number of ova did not differ between control and lesioned animals. DR lesions in both short- and long-term lesioned rats reduced 5-HT levels in the ME by about 50% and nullified the normal 5-HT decline during the afternoon of proestrus. Our results suggest that the DR exerts a stimulatory influence on the provulatory gonadotropin release by means of its 5-HT projection to the ME. As the pattern of hormonal secretion in lesioned animals remains similar to that of controls, it may be suggested that this pathway acts as a fine modulator of the mechanisms involved in the regulation of LH and FSH release in cycling rats. Our results also indicate that the DR plays a role in the release of PRL on proest

ISSN:0028-3835    

DOI:10.1159/000124828

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The facilitation of peptide secretion from the neurohypophysis induced by increasing stimulation frequency is accompanied by action potential (AP) prolongation. One hypothesis argues that inactivation of potassium channels in the neural lobe terminal membranes, under these conditions, is the underlying mechanism which leads to AP prolongation, and, therefore, increased calcium entry and secretion per AP. Therefore, factors which are known to cause AP prolongation, such as stimulus frequency and potassium channel blocking agents, were studied and compared with regard to their ability to augment electrically evoked release of oxytocin (OT) and vasopressin (VP) from isolated rat neurointermediate lobes (s). OT release (to a constant applied stimulus of 600 spikes) was maximally facilitated by increasing frequency up to a rate of 30 Hz, whereas VP release in the same stimulus paradigm was maximal between 12 and 20 Hz. Tetraethylammonium (TEA), 4-aminopyridine (4AP) and barium each caused a significant augmentation of AP-dependent, electrically stimulated hormone release, without affecting basal levels. The magnitude of the effect of the K channel blocking agents was inversely related to the frequency of the applied stimulus. Application of either 4AP or TEA caused a shift in the range of frequency dependence for OT such that maximal release was seen at a stimulus frequency of 12 Hz, but there was no comparable change in the pattern of VP release. The maximal effects of TEA and 4AP were additive indicating that the terminals have two types of K channels which appear to be involved in the regulation of secretion. Addition of the three agents together produced maximal release at a stimulus frequency of 4 Hz, which was not facilitated further by the increase of stimulus frequency to 20 Hz. These data demonstrate the importance of potassium channels in the regulation of VP and OT secretion, and provide indirect support for the spike prolongation hypothesis of frequency facilitated secretion in the neural lobe.

ISSN:0028-3835    

DOI:10.1159/000124829

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Somatostatin-immunoreactive perikarya in the periventricular anterior hypothalamus were demonstrated to be surrounded by gamma aminobutyric acid GABA-immunoreactive nerve terminals, by combining pre-embedding immunocytochemistry for somatostatin and gold labelling post-embedding immunocytochemistry for GABA. Ultrastructural studies revealed that in each 100-nm section, cells immunoreactive for somatostatin (n = 62) were contacted by a mean of 7.6 + 0.4 terminal profiles of which 3.0 + 0.3 (40%) were GABA-immunoreactive. Most GABA-immunoreactive terminals contained clear rounded vesicles and, where synaptic specializations were well demonstrated, appeared to be symmetric. The finding provides evidence that there is a significant GABA input to somatostatin neurons, an observation strengthening the hypothesis that GABA may inhibit somatostatin neurons, thereby causing increased secretion of growth hormone.

ISSN:0028-3835    

DOI:10.1159/000124830

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The juvenile-peripubertal transition period in the female rat is associated with an ovarian-independent afternoon increase in the amplitude of plasma luteinizing hormone (LH) pulses. To determine if the immature pituitary could be activated to cause precocious puberty juvenile female rats were subjected for 4 days to a microprocessor-driven pulsatile intravenous administration of LH-releasing hormone (LHRH) at a dose that produced a peripubertal pattern of LH release. To determine if the LHRH neurons themselves could be prematurely activated to induce such a pattern of plasma LH, and hence lead to precocious puberty, the neuroexcitatory amino acid analog N-methyl-DL-aspartic acid (NMA) was similarly administered. The time of puberty (vaginal opening and first ovulation) was advanced by both the LHRH and NMA treatments, by 5 and 7 days, respectively. Ovarian weight and incidence of corpora lutea at first diestrus were similar in all animals regardless of treatment, but a juvenile body weight was retained by the animals that underwent precocious puberty. Therefore, just as the adenohypophysis can be driven by exogenous LHRH to initiate puberty, the LHRH neuronal system can be precociously activated by the episodic administration of an excitatory amino acid analog that is known to interact with specific brain receptors. It is likely, therefore, that sexual maturation is limited by factors that lie further upstream in the hypothalamo-pituitary axis (e.g., the neuronal circuits that impinge upon LHRH-producing neurons).

ISSN:0028-3835    

DOI:10.1159/000124831

出版商:S. Karger AG    

年代:1987

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124832

出版商:S. Karger AG    

年代:1987

数据来源: Karger