Search PubMed⌕ Search

Biomedical subjects

J Rivier

Publications and source records attributed to J Rivier.

At least 361 records · Page 20Linked to original sources
PubMed1980

Bombesin: receptor distribution in brain and effects on nociception and locomotor activity.

The radioreceptor assay was used to examine the distribution of bombesin receptors in the rat brain. The highest concentrations of receptors appeared to be associated with limbic forebrain and midbrain structures such as the hippocampus, amygdala, hypothalamus and the periaqueductal gray matter. The caudate-putamen of the extrapyramidal motor system and the forebrain also exhibited high bombesin binding. Intraventricular injections of bombesin (0.1, 1.0 and 10 microgram) produced a dose-dependent increase in locomotor activity in rats. Injections of bombesin into the periaqueductal gray matter produced an antinociceptive reaction in the hot-plate as well as the tail-flick test. This apparent analgesia was not antagonized by naloxone.

Animals↗
PubMed1980

The biologic activity of a potent analogue of gonadotropin-releasing hormone in normal and hypogonadotropic men.

We studied the biologic activity of a long-acting analogue of luteinizing hormone-releasing hormone, D-Trp6-Pro9-NEt-LHRH (LHRHa), in five normal men and four hypogonadotropic men previously unresponsive to natural LHRH. All subjects responded to LHRAa, but there were quantitative and qualitative differences between the normal and hypogonadotropic men. Normal men showed a linear dose-response relation, endogenous gonadal steroid secretion, and an adult pattern of gonadotropin secretion characterized by a high ratio of luteinizing hormone (LH) to follicle-stimulating hormone (FSH). Hypogonadotropic men had improving pituitary responses to each dose of LHRHa (priming response), no demonstrable gonadal steroid secretion, and a prepubertal pattern of gonadotropin release characterized by reversal of the normal ratio of LH to FSH. When compared with native LHRH, LHRHa had an augmented ability to discharge gonadotropins acutely and to sustain their release in normal and hypogonadotropic men.

Adolescent↗
PubMed1980

Brain regulation of gastric secretion: influence of neuropeptides.

Several neuropeptides injected intracisternally were assessed for their effects on gastric secretion in rats. Bombesin (1 microgram) completely suppressed gastric acid secretion, produced the volume of gastric secretion, and partially blocked insulin- or 2-deoxy-D-glucose-induced stimulation of gastric acid output. The inhibitory effect of this peptide is dose-dependent, long-acting, reversible, and specific. Bombesin response appears to be central nervous system-mediated; its expression is not dependent on the vagus nerve or the adrenal glands, and does not rely on a decrease in gastrin secretion. Among seven other peptides tested, only beta-endorphin and a potent gonadotropin releasing-factor (gonadoliberin) agonist significantly reduced gastric acid secretion, with an activity ca. 100 times less than that of bombesin. The presence of bombesin-like material in rat brain and the high potency of bombesin to inhibit gastric secretion suggest that this peptide may be of physiologic significance as a chemical messenger involved in brain modulation of gastric secretion.

Adrenalectomy↗
PubMed1979

Somatostatin analogs inhibit somatostatin release.

To determine if, like insulin, somatostatin inhibits its own secretion from the pancreas, nonimmunoreactive analogs of somatostatin were perfused in an isolated dog pancreaticoduodenal preparation using a nonrecirculating system. [D-Trp8-D-Cys14]somatostatin, at a concentration of 200 ng/ml, blocked the response of somatostatin-like immunoreactivity (SLI) to cholecystokinin and arginine. When perfusion of the analog was discontinued, SLI release increased. At a concentration of 0.1 ng/ml, des Asn5-[D-Trp8]somatostatin lowered SLI levels significantly without significantly reducing glucagon levels. At a concentration of 1 ng/ml, des Asn5-[D-Trp8]somatostatin significantly inhibited SLI as well as insulin and glucagon release. Perfusion of glucagon at a concentration of 10 ng/ml failed to overcome the blockade of SLI and insulin release caused by 50 ng/ml des Asn5-[D-Trp8]somatostatin. The results are compatible with a direct inhibitory effect of somatostatin analogs upon SLI release and raise the possibility of a self-inhibiting action of the native hormone.

Animals↗
PubMed1979

Somatostatin: central nervous system actions on glucoregulation.

Somatostatin (SRIF) has been tested for its actions on the central nervous system to affect glucoregulation. In doses ineffective when given systemically , SRIF and SRIF analogs given intracisternally (ic) reduce hyperglycemia and hyperglucagonemia after ic bombesin administration. The SRIF analog, des-AA1, 2, 4, 5, 12, 13-[D-Trp8]SRIF, decreases plasma insulin and elevates plasma glucose and glucagon when given systemically. However, when given ic, this peptide prevents the rise in glucose and glucagon after ic bombesin administration and is 10 times more potent than SRIF in reducing bombesin-induced hyperglycemia. Other analogs of SRIF and various unrelated peptides were found to be ineffective in reducing bombesin-induced hyperglycemia. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF prevented the hyperglycemia induced by surgical stress or by ic administration of beta-endorphin or carbacol. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF given ic did not prevent hyperglycemia induced by systemic administration of epinephrine, arginine, or glucagon. These studies suggest that SRIF and its analogs may act within the brain to affect glucoregulation.

Animals↗
PubMed1979

Chronic effects of [D-Trp6,Pro9-NEt]luteinizing hormone-releasing factor on reproductive processes in the male rat.

Chronic administration of a potent LRF agonist, [D-Trp6,Pro9-NEt]LFR (A), to intact adult male rats induced a dose-related decrease in testicular and accessory organ weights, diminished production of testosterone (T), and disrupted tubular morphology, indicative of suppression of spermatogenesis. Transient elevations of plasma progesterone levels and a marked reduction of PRL secretion were also observed in A-treated rats. The effects of A on testicular weights, T levels, and seminiferous tubule morphology were already apparent 3 days after the first injection. Administration of A was equally effective when administered daily or at 1- to 4-day intervals in lowering steroid levels and testicular weights. After a 1-week daily exposure to A, seminal vesicles and prostate weights as well as T levels returned to control values within 1--2 weeks. Testicular weights, however, were still depressed 4 weeks after cessation of treatment, and germinal epithelium was disrupted in 30--40% of the tubules. Measurement of T and LH plasma levels after each daily injection of A indicated a blunting of succeeding A-induced elevations of LH and T, which lasted up to 72 h after a single administration of A. The observation that cultured pituitary cells repeatedly exposed to A showed a similar blunting of LRF-induced LH elevation suggests that the decrease in pituitary responsiveness was not exclusively due to steroid feedback. Administration of T propionate to A-treated intact rats was unable to restore normal testicular weights and seminiferous tubule morphology, whereas in hypophysectomized rats, T propionate maintained qualitatively normal spermatogenesis even in the presence of A. These results coupled with the observation that high levels of hCG and PMS gonadotropin had effects similar to those of A on the tubular morphology of intact rats suggest the importance of pituitary secretion in mediating the deleterious effects of A on reproductive functions in the male rat.

Animals↗
PubMed1978

Bomebesin: specific binding to rat brain membranes.

The binding of a radiolabeled bomebesin analogue to rat brain membranes was studied. [125I-Tyr4]Bombesin bound with high affinity (KD = 3 nM) to a single class of non-interacting sites. Binding was specific, saturable (3.8 pmol of sites/g of wet tissue), and reversible. Regional and subcellular distribution studies showed that the density of sites was 7-fold greater in the hippocampus than the medulla/pons and greater in synaptosomal fractions than in mitochondrial or nuclear fractions. The abilities of numerous bombesin analogues to induce hypothermia and to inhibit [125I-Tyr4]bombesin-binding activity correlate well. Numerous amino acid residues near the CONH2-terminal are required for high-affinity binding and biological potency.

Animals↗
PubMed1978

The effect of bombesin and related peptides on prolactin and growth hormone secretion in the rat.

Bombesin and other related peptides isolated from the skin of anuran species and found in mammalian brain stimulate PRL and GH release in steroid-primed male rats. On a molar basis, bombesin and alytesin are the most active peptides in this assay system. Their PRL- and GH-releasing activity is not affected by the type of anesthetics used, but their minimal effective dose is lower after intravenous administration as compared with intracisternal administration. The in vivo stimulatory effect of bombesin on PRL secretion is not modified by the histamine antagonist diphenhydramine or the opiate antagonist naloxone. By contrast, naloxone reverses the GH-releasing activity of bombesin, suggesting an opiate-dependent mechanism of action of this peptide on GH secretion. The absence of an in vitro effect of bombesin and related peptides on PRL and GH secretion and a minimal effective dose of approximately 30 ng in bombesin and alytesin administered in steroid-primed rats, make them the most active peptides reported so far to act on the brain to modify PRL and GH secretion.

Animals↗
PubMed1978

Chronic effects of [D-Trp6-Pro9-NEt]luteinizing hormone-releasing factor on reproductive processes in the female rat.

LRF and one of its highly potent analogs, [D-Trp6-Pro9-NEt]LRF (A), were tested for their effects on pregnancy. Daily doses of A prevented implantation and/or caused resorption of implanted blastocysts in mated female rats. This effect was dose related and was most evident when given in regimens including days 5-7 or days 9-10 or pregnancy. LRF also has antigonadal effects, but at much higher doses than A. The use of corn oil vs. 0.1% gelatin-saline improved the effectiveness of low doses of A. Termination of pregnancy in A- or LRF-treated rats is most probably due to the markedly diminished progesterone secretion, which could result from the secretion of biologically inactive gonadotropins, reduced pituitary responsiveness to endogenous LRF, or down-regulation of gonadal receptors for LH.

Animals↗