Biomedical subjects

S M Gabriel

Publications and source records attributed to S M Gabriel.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Tissue-specific sex differences in galanin-like immunoreactivity and galanin mRNA during development in the rat.

Galanin-like immunoreactivity (Gal-LI), as determined by radioimmunoassay, was detectable in the brain and gastrointestinal tract by day 15 of gestation. Concentrations of Gal-LI increased after birth in the hypothalamus but decreased in the stomach and duodenum. A sex difference in Gal-LI concentrations appeared during puberty in the median eminence, neurointermediate lobe, and the anterior pituitary (AP), where females had higher Gal-LI concentrations compared to males. This difference was most pronounced in the AP; adult females had up to 4-fold greater Gal-LI concentrations and 5-fold more abundant rGal-specific mRNA compared to males.

Aging↗

PubMedDate not supplied

Modulation of hypothalamic galanin gene expression by estrogen in peripubertal rats.

Hypothalamic galanin gene expression was investigated during reproductive maturation in peripubertal rats. Rat galanin-like immunoreactivity (rGAL-LI) increased in the median eminence and anterior pituitary during the extended first estrous and diestrous phases relative to anestrous phase female or male rats. In the neurointermediate lobe, rGAL-LI was elevated in first diestrous phase compared to anestrous phase females or males. In a second study, hypothalamic tissue was divided into quadrants for analysis of rat galanin (rGAL) mRNA by Northern blot hybridization. Two days after the injection of pregnant mare's serum gonadotropin (PMSG), rGAL mRNA increased approximately twofold in the paraventricular area and preoptic area quadrants. No effects of PMSG on galanin gene expression were found in medial basal or supraoptic hypothalamic quadrants. Because PMSG acts through the stimulation of ovarian estrogen secretion, these studies conclude that galanin gene expression in dorsal hypothalamic nuclei is under the stimulatory influence of estrogen and suggest that galanin may be a mediator of central ovarian steroid feedback.

Animals↗

PubMedDate not supplied

The galanin antagonist, M-15, inhibits growth hormone release in rats.

The neuropeptide, galanin, has been implicated in the regulation of rat growth hormone (rGH) release. In the present study, adult male rats were implanted dually with cannulae to the lateral cerebral ventricle and the right atrium. After surgical recovery, rats were infused with M-15, a specific galanin antagonist, into the lateral ventricle. During the course of this brain infusion, rats were subjected to serial blood sampling with red cell and artificial plasma replacement under stress-free conditions. Plasma was saved for rGH assay. Treatment with M-15 reduced rGH pulse amplitude and pulse frequency when compared to vehicle-infused controls. These data suggest that brain galanin participates in the ongoing stimulation of pulsatile rGH release in the adult male rat.

Animals↗

PubMedDate not supplied

Neuroendocrine and monoaminergic responses to acute administration of alprazolam in normal subjects.

The effect of a single dose (3 mg) of alprazolam on plasma cortisol, growth hormone (GH), prolactin, norepinephrine (NE) and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) was studied in 10 healthy males. Alprazolam and placebo were administered orally in a crossover design and blood was sampled for 24 h. In comparison to placebo, alprazolam significantly reduced plasma cortisol levels and raised plasma GH levels. Prolactin levels were elevated by 100% from 2 to 8 h after alprazolam administration. The robust increase in prolactin levels is less consistent with previously reported data on traditional benzodiazepines. Plasma NE levels following alprazolam were lower than following placebo administration only at one time point, and MHPG concentrations were not affected. The lack of change in NE and MHPG levels suggests that the acute effect of alprazolam in normal subjects is not mediated via the central noradrenergic system.

Adult↗