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Biomedical subjects

J B Martin

Publications and source records attributed to J B Martin.

At least 235 records · Page 13Linked to original sources
PubMed1983

Cysteamine depletes prolactin in young and old hyperprolactinemic rats.

Studies were undertaken to evaluate the effects of cysteamine on serum and anterior pituitary concentrations of prolactin in hyperprolactinemic female rats. Serum prolactin was elevated in young (4 to 5 months old) rats by implantation of 17 beta-estradiol while 26- to 28-month-old rats were in constant estrus and exhibited an age-related hyperprolactinemia. At 4 h after treatment with cysteamine (90 mg/kg body wt) serum and anterior pituitary prolactin concentrations were reduced in young animals by 98 and 85%, respectively. In old constant-estrous rats, cysteamine reduced serum prolactin by 92% and anterior pituitary prolactin by 82%. In young pseudopregnant rats, cysteamine induced a prompt resumption of estrous cycles. These studies indicate that cysteamine is an effective depletor of serum and pituitary prolactin in hyperprolactinemic rats.

Aging↗
PubMed1983

Somatostatin analogs: correlation between receptor binding affinity and biological potency in GH pituitary cells.

Somatostatin (SRIF) is a hypothalamic tetradecapeptide which acts on several different types of pituitary cells to inhibit hormone release both in vivo and in vitro. We have previously shown that the GH4C1 clonal strain of rat pituitary tumor cells contains a single class of specific high-affinity SRIF receptors and that SRIF is a potent inhibitor of GH and PRL release by these cells. In this study, we have determined the relationship between the apparent binding affinity and biological potency of 19 SRIF analogs in GH4C1 cells. Receptor binding and biological activity were assayed under identical conditions. A good correlation (r = 0.96) was observed over a 10,000-fold range between the receptor binding affinities and biological potencies of SRIF analogs. Modifications at the C- and N-terminal regions of the SRIF molecule had minimal effects on binding to the receptor or potency to inhibit PRL release. However, substitution of residues 6 through 10 or reduction of the disulfide bond resulted in a 100-fold or greater decrease in both activities. The N-terminal extended SRIF analogs, SRIF-28, [D-Trp22]SRIF-28, and SRIF-25, were all somewhat less potent than SRIF. These results strongly support the involvement of the characterized SRIF receptor in initiating the biological actions of SRIF in GH4C1 cells and define the structural features of the SRIF molecule required for both receptor binding and activation.

Animals↗
PubMed1983

Cysteamine induces depletion of both immunological and biological prolactin activity in the anterior pituitary and blood of the rat.

Previous studies have shown that cysteamine [2-aminoethanethiol (CSH)], given in vivo or in vitro, rapidly but reversibly depletes immunoreactive PRL from the anterior pituitary (AP) through a mechanism which, in vitro, does not appear to involve the dopamine (DA) receptor. In the present investigation, these effects of CSH were explored further with emphasis on determining whether CSH; (1) depletes biological as well as immunological PRL activity from the AP and blood, (2) has effects on plasma PRL in chronically cannulated male rats, (3) alters the PRL response to drugs which stimulate the secretion of the hormone, and (4) acts in vivo via DA receptors to deplete PRL. CSH produced a dose-dependent depletion of both immunological and biological PRL activity from the AP and blood. In chronically cannulated animals, PRL levels in the plasma were undetectable 90 min after CSH administration and remained so for 4 h. However, by 24 h plasma PRL in treated animals had returned to control levels. The PRL response to both domperidone and morphine was virtually abolished in CSH-treated animals. Blockade of DA receptors by pretreatment with domperidone did not alter the ability of CSH to reduce AP PRL stores. These results indicate that CSH: 1) alters both biological and immunological PRL activity by a rapid but reversible effect, and 2) circumvents the DA receptor to deplete pituitary PRL content. Thus, CSH or similar compounds may serve as a prototype for a new class of drugs which can be used in the treatment of hyperprolactinemia.

Animals↗
PubMed1982

The effect of cysteamine on immunoreactive somatostatin in the rabbit retina.

Cysteamine hydrochloride was administered to rabbits at doses ranging from 0.3 to 10 mg by two intravitreal injections 24 h apart. Retinal immunoreactive somatostatin concentrations were reduced by about 50% at 24 h following the second injection. At doses of 0.3-3 mg, there was no demonstrable effect on retinal concentrations of immunoreactive substance P or of dopamine. Ten milligrams of cysteamine produced non-specific retinal damage. Cysteamine injected locally into the retina is a relatively specific drug for depletion of somatostatin.

Animals↗
PubMed1982

Caffeine stimulates beta-endorphin release in blood but not in cerebrospinal fluid.

Plasma beta-endorphin and prolactin profiles were obtained from groups of unstressed, adult male rats. The infusion of caffeine (20 mg/kg) via a chronic, indwelling intra-atrial cannula results in a prompt and sustained (2-2.5 h) rise In plasma beta-endorphin levels. The infusion of the opiate antagonist naloxone causes a modest (40%) decrease in plasma beta-endorphin and blunts the elevation in plasma beta-endorphin following caffeine administration. In contrast, plasma prolactin levels were unchanged following caffeine administration and were decreased by treatment with naloxone. Caffeine treatment did not effect CSF beta-endorphin levels or the release of beta-endorphin from hemipituitaries incubated in vitro.

Animals↗
PubMed1982

Endotoxin-stimulated opioid peptide secretion: two secretory pools and feedback control in vivo.

Small doses of endotoxin evoked a dramatic biphasic response of opioid peptide secretion into blood in sheep. The first phase began within minutes and coincided with a brief hypertensive response to endotoxin well before the appearance of fever or hypotension. The ratio of beta-endorphin to beta-lipotropin fell abruptly at the onset of the second phase of release, suggesting early depletion of a pool rich in beta-endorphin and subsequent emergence of a pool rich in unprocessed precursor. The concentration of cerebrospinal fluid opioids increased tenfold during the second phase. Naloxone administration augmented endotoxin-induced opioid secretion in both early and late phases, suggesting a short-loop feedback regulation of stress-induced endorphin secretion.

Animals↗
PubMed1982

Cysteamine: a potent and specific depletor of pituitary prolactin.

Cysteamine rapidly reduces the concentration of prolactin in pituitary tissue in vivo and in vitro. The effect is dose-dependent, reversible, and cannot be accounted for by prolactin release. Cysteamine does not appear to exert its effect through dopamine receptors and does not alter lactotrope morphology, as determined by electron microscopy.

Animals↗
PubMed1982

Somatostatin-like immunoreactive material in the rabbit retina.

Somatostatin-like immunoreactivity was detected by a specific radioimmunoassay in extracts of retinas of Dutch-belted rabbits at a mean concentration of 1.1 +/- 0.1 ng/retina, or 170 +/- 30 pg/mg protein. On both gel permeation chromatography and reversed phase high performance liquid chromatography, the majority of this material was indistinguishable from somatostatin-14; a smaller amount of immunoreactive material co-chromatographed with somatostatin-28. The somatostatin-like immunoreactivity was concentrated in a P2 (synaptosomal) fraction prepared by differential centrifugation. The concentration of somatostatin-like immunoreactivity was unaffected by the prior intravitreal injection of the selective neurotoxins 6-hydroxydopamine and 5, 7-dihydroxytryptamine. The rabbit retina, therefore, contains readily detectable amounts of material chemically similar to somatostatin-14 and somatostatin-28. This material is concentrated in neurosecretory elements of the retina, but is not contained in cells which accumulate dopamine or indoleamines. The rabbit retina is suitable for in vitro studies of the central nervous system function of the somatostatin family of peptides.

5,7-Dihydroxytryptamine↗
PubMed1982

Cysteamine reduces serum gonadotropin concentrations in adult male rats.

We have examined the effects of cysteamine on the hypothalamic-pituitary-gonadal axis of the adult male rat. A single subcutaneous injection of cysteamine (300 mg/kg) reduces significantly (p less than or equal to 0.05 serum concentrations of LH, FSH and T. Cysteamine blocked LH secretion induced by castration and administration of naloxone and LHRH. Neither acute nor chronic treatment (7 days) altered the hypothalamic LHRH content. These results suggest that cysteamine acts to reduce pituitary responsiveness to LHRH, resulting in lower mean serum gonadotropin and testosterone concentrations. It is possible, however, that cysteamine acts also at the hypothalamus to reduce LHRH secretion and/or at the testes to reduce testosterone release.

Animals↗
PubMed1982

D-lactic acidosis simulating a hypothalamic syndrome after bowel bypass.

A 36-year-old man had one year of periodic symptoms suggestive of episodic hypothalamic dysfunction: hypersomnia, thirst, ravenous hunger and gorging behavior, pallor, and irritability. However, neuroendocrine testing proved normal. A mild transient acidosis at the onset of his attacks and a history of bowel bypass five years earlier prompted metabolic screening. Markedly increased urinary D-lactic and phenolic acids were present, as were intermittent elevations of plasma D-lactic acid during two symptomatic episodes. Prompt and sustained clinical remission coincided with disappearance of abnormal organic acid excretion during oral antibiotic therapy. D-Lactic acidosis must be considered in the differential diagnosis of otherwise unexplained neurological syndromes, particularly in patients with altered bowel anatomy.

Acidosis↗
PubMed1982

A P Nuclear Magnetic Resonance Study of Intracellular pH of Plant Cells Cultivated in Liquid Medium.

(31)P nuclear magnetic resonance has been used to study the vacuolar and cytoplasmic pH of Acer pseudoplatanus, Catharanthus roseus, and Glycine max cells grown as cell suspensions. The adaptation of this technique to plant cells grown in liquid medium is described with emphasis on the removal of Mn(2+) and phosphate from the extracellular medium and on providing the O(2) supply of the cells in the nuclear magnetic resonance tube and the various problems of calibration. Aerobic and anaerobic cells show large differences in their glucose-6-phosphate, their cytoplasmic inorganic phosphate pools, and their cytoplasmic pH. Differences in the relative sizes of the cytoplasmic and vacuolar inorganic phosphate pools have been observed for the three cell strains studied.

Journal Article↗
PubMed1982

Altered release of growth hormone and thyrotropin induced by endotoxin in the rat.

Plasma growth hormone (GH) and thyrotropin (TSH) levels were measured in freely behaving rats for 6 h on three consecutive days. On the 1st and 3rd days there was no treatment, and on the 2nd day endotoxin (150 mg/kg) was administered intravenously. Endotoxin causes a biphasic temperature response: an initial hypothermia persisting for 1 h, followed by hyperthermia evident from 5 to 8 h after injection. Normal pulsatile GH release observed on the 1st day was abolished on the 2nd day by the endotoxin treatment. On the 3rd day, however, GH secretion was greater than on the initial control day. TSH release was also suppressed by endotoxin and showed a rebound release on the subsequent day. The suppression of GH secretion by endotoxin was reversed in all animals by antisomatostatin serum, and the suppression of TSH secretion by endotoxin was reversed in some animals. These results suggest that endotoxin is a potent stimulus for hypothalamic somatostatin release in the rat. Endotoxin profoundly alters adenohypophyseal hormone release.

Animals↗
PubMed1982

Evidence that reduced growth hormone secretion observed in monosodium glutamate-treated rats is the result of a deficiency in growth hormone-releasing factor.

The present experiments were designed to examine various aspects of GH secretion in adult male rats given monosodium glutamate (MSG; 4 mg/g BW, sc) during the neonatal period. MSG-treated animals sustained lesions localized to the hypothalamic arcuate nuclei (ARC) and had reduced nasal-anal lengths and body weights. Anterior pituitary (AP) weights were decreased, but AP concentrations of GH and PRL were not significantly altered. Analysis of pulsatile GH secretion showed depressed GH pulses and prolonged GH trough periods. Mean 5-h plasma GH levels were reduced, whereas PRL levels were not affected. Morphine sulfate (MS) at doses of 0.01, 0.1, 1.0, and 3.0 mg/kg induced a prompt rise in GH during the 45 min after drug administration in controls. MSG-treated animals showed a significant rise in GH only with 1.0 and 3.0 mg/kg MS. A significant elevation in PRL was found in both control and MSG-treated animals after 1.0 and 3.0 mg/kg MS. The pentobarbital-induced rise in GH was also blunted in MSG-treated animals. MSG-treated animals which were administered antisomatostatin serum showed elevated GH trough and mean GH levels, with no apparent effect on GH peak levels. In view of the mechanisms by which MS and pentobarbital act to increase GH secretion, the present data suggest that the GH regulatory deficit observed in MSG-treated rats is due to a relative loss of GH-releasing factor secondary to ARC damage.

Animals↗