摘要:

Brain activity during the spontaneous ovulatory surge of luteinizing hormone (LH) has been studied by measuring local cerebral glucose utilization (LCGU) by the [14C]-2-deoxyglucose method. The LCGU was determined in 37 brain areas and the pituitary gland in conscious, freely moving female rats in the morning and the late afternoon of proestrus. No increases in LCGU were detected, but, unexpectedly, there was a significant decrease in the LCGU measured in the afternoon compared with the morning of proestrus in the medial preoptic and anterior hypothalamic areas, the arcuate nucleus, median eminence and amygdala. Significant reductions in LCGU also occurred in the midbrain central grey and reticular formation. These results suggest that the LH and/or the prolactin surge is associated with a significant reduction in the activity of brain areas known to be essential components of the central control of gonadotropin and prolactin secretion. In the case of the arcuate nucleus and median eminence, for example, the results could be explained by a decreased activity of the opioid and dopaminergic neurons which are known to inhibit the release of luteinizing hormone releasing hormone (LHRH). Disinhibition of LHRH neurons would result in the increased release of LHRH into the hypophysial portal vessels. Reduction in the activity of the arcuate dopamine neurons could also play a major role in the prolactin surge. The decreased LCGU of the midbrain central grey may be related to the onset of lordosis behaviour which appears to be time-locked to the LH surge.

ISSN:0028-3835    

DOI:10.1159/000124968

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Somatostatin-28 (SS-28) acted within the central nervous system (CNS) to produce a dose-dependent elevation of mean arterial pressure (MAP), a reduction of heart rate (HR), and an elevation of the plasma concentration of vasopressin. SS-28 given intravenously did not affect MAP or HR. Furthermore, these changes of cardiovascular functions were not prevented by systemic passive immunization against SS-28, thus supporting a CNS site of action. Microinjections of SS-28, in amounts ineffective when given into the lateral cerebroventricle or other brain parenchymal areas, into the paraventricular nucleus of the hypothalamus produced significant elevations of MAP. Neither ganglionic blockade with chlorisondamine nor treatment with the α-adrenergic receptor antagonist, phentolamine, prevented SS-28-induced changes of cardiovascular function; however, treatment of animals with the vasopressin antagonist [1-deaminopenicillamine, 2-(0-methyl)Tyr]-vasopressin completely prevented SS-28-induced elevation of MAP and slowing of HR. These results suggest that SS-28 acts within the CNS to increase MAP and decrease HR by stimulating pituitary vasopressin secretion

ISSN:0028-3835    

DOI:10.1159/000124975

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Long-term effects of gonadotropin-releasing hormone (GnRH) and/or estrogen on pituitary mRNA levels for the β-subunit of luteinizing hormone (LH-β) were determined in anterior pituitary glands from ovariectomized (OVX) ewes. The relative roles of these two factors were assessed by studying hypothalamopituitary disconnected (HPD) ewes with appropriate hormonal treatments. Levels of LH-β mRNA were increased by ovariectomy and substantially reduced by HPD. Treatment of OVX-HPD ewes with pulses of GnRH (250 ng each 2 h) for 1 week restored LH-β mRNA levels to OVX levels, whereas treatment with estrogen alone did not alter the low levels found in OVX-HPD ewes. Combined GnRH and estrogen treatment for one week produced LH-β mRNA levels that were similar to those found in OVX-HPD ewes given GnRH alone; plasma LH pulse amplitudes were also similar in these two groups. From these data we conclude that the long-term negative feedback effect of estrogen to reduce LH secretion is due to a primary inhibition of GnRH secretion and is not a pituitary effect of estrogen. Long-term regulation of LH-β mRNA is thus primarily regulated by

ISSN:0028-3835    

DOI:10.1159/000124969

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Vasoactive-intestinal-peptide (VΙP)-containing nerve fibers impinge upon both follicle cells and blood vessels in the thyroid gland. We have previously shown that VIP induces a specific, dose-related increase in thyroid blood flow in the rat. However, our VIP treatments had no effect on circulating thyroid hormone levels. Since a number of reports have indicated that VIP can enhance thyroid hormone secretion, we have expanded our studies to characterize more completely the conditions under which VIP might stimulate thyroid hormone secretion in the rat. In unanesthetized, unstressed rats with chronic catheters, 33 µg VIP/100 g body weight failed to alter triiodothyronine (TO or thyroxine (T4) levels and did not affect the thyroid secretory response to a submaximal dose of bovine TSH. In euthyroid and hyperthyroid rats, the release of 125I was increased after exogenous TSH, but was not altered by VIP. The only condition in which we observed a rise in circulating T3 levels in response to VIP was during a continuous 2 h infusion of a high dose (0.25 µg/min, i.v.) of this peptide. However, plasma TSH levels tended to be elevated in these rats, suggesting an indirect effect via TSH. This suggestion is strengthened by our observation that VIP failed to alter T3 or T4 release after topical application (0.1 µg/µl for 3 h) in vivo or after in vitro treatment (10–6M for 4 h), even though these preparations were fully responsive to bovine TSH. Despite the lack of a thyroid hormone secretory response, VIP did stimulate cyclic AMP release in vitro, indicating that at least some component of the thyroid is responsive to this peptide. Thus, while it appears that VIP can elicit thyroid hormone secretion, such effects are observed only under treatment conditions which greatly exceed those shown to modulate thyroid blood flow. This leads us to believe that thyroidal VIP has little or no importance in the normal physiological regulation of thyroid hormone sec

ISSN:0028-3835    

DOI:10.1159/000124970

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

A method has been devised for collecting hypophysial portal blood from the anaesthetised guinea pig in order to measure the release in vivo of the neurohypophysial peptides, oxytocin (OT), vasopressin (AVP), neurophysin (NP), and the glycopeptide (GP) found at the carboxyl terminus of the AVP precursor. These peptides were measured in samples of portal and peripheral venous plasma by specific radioimmunoassays. The concentration of OT and AVP was 50- to 100-fold higher in hypophysial portal blood than in peripheral blood, with more OT than AVP usually present. There were correspondingly large amounts of NP and GP also present in portal blood. In particular, GP levels paralleled AVP levels over a wide range of concentrations and in virtually equimolar proportions. These results provide the first in vivo evidence which shows that, as for the magnocellular neurohypophysial system, GP is synthesised, processed and released in equal amounts with AVP from their common precursor in the subpopulation of parvocellular AVP neurons which project from the paraventricular nucleus to the median eminence.

ISSN:0028-3835    

DOI:10.1159/000124971

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124972

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124973

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124974

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124957

出版商:S. Karger AG    

年代:1988

数据来源: Karger