摘要:

The influence of melatonin (MEL)-free pineal extract on luteinizing hormone (LH) and follicle stimulating hormone (FSH) was studied comparatively with that of MEL. Administration of pineal extract to rats, 3 days running, was found to induce a statistically significant decrease of serum LH and FSH. This effect was also demonstrated by the biological tests used, namely, a decrease in weight of both rat ventral prostate (anti-LH activity) and mouse uterus (anti-FSH activity). MEL administered for 3 days, in doses of 1 μg/day in the ventral prostate weight test or of 10 μg in the uterine weight test, failed to induce comparable effects. The identity of the pineal substances responsible for the anti-gonadotropic activity of the pineal gland is discusse

ISSN:0028-3835    

DOI:10.1159/000122788

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

Lesions of the median raphe (MR) nucleus were placed in cycling female rats and their ability to lactate was evaluated following subsequent pregnancies. Pups from MR-lesioned (MRL) animals grew more slowly and had greatly impaired survival rates compared to pups from sham-lesioned animals. Chronic treatment of MRL mothers with oxytocin (Oxy; 1 IU, s.c, once or twice/day) did not increase the growth rates of their litters. Acute responses to exogenous Oxy (1 IU, i.p.) in MRL mothers, measured by the weight gain of litters during ½-h suckling intervals before and after injection, were marginally significant. Milk yield during the total hour suckling period (stomach contents of pups) was clearly less in the MRL animals (p < 0.01). Treatment with either prolactin (Prl; 250 μg, twice/day), Prl + GTC (4 mg/kg growth hormone, 30 μg/kg thyroxine, 0.5 mg/rat cortisol, once/day), or 5-HTP (75 mg 5-hydroxytryptoρhan/kg, twice/day) did not improve the growth rates of litters from MRL animals. However, when milk yield (stomach contents after 1 h) following a 14-h non-suckling interval was measured, lactogenic hormones (Prl or Prl + GTC) restored milk yield in MRL animals to control levels. This response was clearly not dependent upon exogenous Oxy. These results suggest that deficits in the release of lactogenic hormones are involved in the impairments in lactation following lesions of the MR nucl

ISSN:0028-3835    

DOI:10.1159/000122789

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

It has been previously demonstrated that glutamate (GLU), a neuroexcitatory amino acid which destroys neurons in the arcuate nucleus of the hypothalamus (AH) when administered in high subcutaneous (s.c.) doses to rodents, induces an acute elevation of serum luteinizing hormone (LH) when administered in non-toxic doses, i.e., doses lower than those required to damage AH neurons. It is postulated that a neuroexcitatory mechanism (excitation of AH neurons) underlies the acute rise in serum LH induced by GLU. To explore this hypothesis, we administered several potent excitatory analogs of GLU – kainic acid (KA), N-methyl-aspartic acid (NMA) and homocysteic acid (HCA) -in low doses to 25-day-old male rats and found that each analog mimics GLU in producing acute elevations of serum LH. The lowest doses effective (LED) in inducing significant elevations in LH were: 0.03 μM/g KA, 0.1 μM/g NMA and 0.3 μ HCA) for inducing LH elevations was the same as has been shown for either the neuroexcitatory or neurotoxic activities of these compounds. With the possible exception of KA, each compound induced LH elevations at 1/3–1/4 the lowest effective toxic doses (LETD). It is tentatively concluded that these potent neuroexcitatory analogs of GLU readily penetrate AH from blood and stimulate firing of AH neurons which triggers discharge of luteinizing hormone-releasing hormone (LH-RH) into portal blood to give rise to pituitary output of LH. This interpretation, if corroborated, suggests that these compounds may be useful tools for studying mechanisms of neuro-endocrine regu

ISSN:0028-3835    

DOI:10.1159/000122790

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

Hemicastration of male rats produced rapid changes in plasma testosterone (T) levels both in summer and in winter. However, in winter, after unilateral castration, the duration of T maximum decrease was found to be longer, but the compensatory increase of blood T following its drop was more dramatic as compared to the summer season. The intraperitoneal (i.p.) 5-hydroxytryptophan (5-HTP) administration blocked the compensatory increase in plasma T that followed its drop induced by hemicastration. At the same time, under similar experimental conditions, a preliminary injection of p-chlorophenyl-alanine (PCPA) was accompanied by a more marked rise of plasma T than in control unilaterally castrated rats. After the injection of serotonin (5-HT) into the lateral ventricle of the brain there was no effect on the blood T content in rats with intact gonads. However, 5-HT injection to hemicastrated animals under similar conditions completely prevented the compensatory increase of T level in blood after its fall caused by the operation. On the other hand, double intraventricular injection of methysergide was followed by a more marked rise of blood T content as compared with the control hemicastrated rats. The conclusion is drawn that brain serotoninergic neurons are involved in feedback mechanisms related to the control of hypothalamic-pituitary-testicular complex.

ISSN:0028-3835    

DOI:10.1159/000122791

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

The pituitary-adrenal and gonadal responses following stress were evaluated in the squirrel monkey. Plasma levels of cortisol (CS), ACTH and testosterone (T) were determined during a 4-h period following the combined stress of capture and ether anesthesia. The results indicated that the squirrel monkey manifests higher basal levels of steroids than typically found in other mammals. The endocrine response following stress was biphasic, involving an initial elevation and subsequent decline in hormone levels. Males manifested significantly higher plasma levels of CS and T and lower plasma levels of ACTH than did females.

ISSN:0028-3835    

DOI:10.1159/000122792

出版商:S. Karger AG    

年代:1978

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000122793

出版商:S. Karger AG    

年代:1978

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000122794

出版商:S. Karger AG    

年代:1978

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000122787

出版商:S. Karger AG    

年代:1978

数据来源: Karger