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Biomedical subjects

J B Martin

Publications and source records attributed to J B Martin.

At least 253 records · Page 14Linked to original sources
PubMed1982

Depletion of somatostatin-like immunoreactivity in the rat central nervous system by cysteamine.

Selective neurotoxins have been of value in providing a means for specifically interfering with the actions of endogenous neurotransmitter candidates. Others have shown cysteamine (CSH) to deplete the gastrointestinal tract and hypothalamus of rats of immunoreactive somatostatin, suggesting a toxic action of that compound directed against somatostatin-containing cells. The present study further defines the actions of cysteamine on somatostatin in the central nervous system. (CNS). Cysteamine hydrochloride administered subcutaneously results in a depletion of somatostatin-like immunoreactivity (SLI) in the retina, brain, and cervical spinal cord of rats. The effect is demonstrable at doses of 30 mg/kg of body weight and above, occurs within 2 to 4 hr of a single injection of the drug, and is largely reversible within 1 week. The mean depletion of SLI observed within the CNS varies from 38% in cerebral cortex to 65% in cervical spinal cord 24 hr following administration of CSH, 300 mg/kg of body weight, s.c. By gel permeation chromatography, all molecular weight forms of SLI are affected, with the largest reductions in those forms that co-chromatograph with synthetic somatostatin-14 and somatostatin-28. These results indicate that CSH has a generalized, rapid, and largely reversible effect in depleting SLI from the rat CNS.

Animals↗
PubMed1982

Temporal patterns of somatostatin immunoreactivity in the cerebrospinal fluid of the rhesus monkey: effect of environmental lighting.

A rabbit antiserum to somatostatin was used to develop radioimmunoassay methods for measuring somatostatin in monkey cerebrospinal fluid (CSF). By gel permeation chromatography, at least five molecular weight forms of immunoreactive somatostatin (IRS) were identified in monkey CSF; two of these species co-migrated with either synthetic somatostatin-14 or somatostatin-28. The 24-hr profile of CSF somatostatin immunoreactivity was obtained from five monkeys during diurnal lighting, constant light, and constant darkness. During diurnal lighting, all five monkeys had a clear ultradian component in CSF IRS of 4 to 5 hr duration; this pattern was not affected significantly by constant light or dark. In addition, there of the five monkeys exposed to diurnal lighting showed a diurnal rhythm in CSF IRS, with higher hormone levels during darkness. In some animals, this diurnal rhythm also could be demonstrated during constant light or dark.

Animals↗
PubMed1981

The regional distribution of somatostatin, substance P and neurotensin in human brain.

The regional distribution of somatostatin-, substance P- and neurotensin-like immunoreactivity was determined in 41 areas of 10 human brains. Each peptide is distributed widely in the human central nervous system and for each the pattern of distribution is unique. No significant relationship was found between peptide levels and patient age, interval between death and autopsy, and tissue storage time prior to assay. The regional distribution of these peptides is similar to that seen in several animal species and the pattern of this distribution is consistent with the idea that peptides function as neurotransmitters within the central nervous system. The problems of using human post-mortem material for peptide assay are discussed.

Adult↗
PubMed1981

Monosodium glutamate: acute and chronic effects on rhythmic growth hormone and prolactin secretion, and somatostatin in the undisturbed male rat.

The present in investigation was designed to determine the chronic effects of neonatal monosodium glutamate (MSG) administration (4 g/kg s.c.) and the acute effects of MSG (1 g/kg i.p.) on episodic growth hormone (GH) and prolactin (PRL) secretion and brain somatostatin (SRIF) in unanesthetized, chronically cannulated male rats. Adult rats showed the typical physical characteristics that result from neonatal MSG administration. Analysis of episodic GH secretion showed a significant reduction in : (1) the amplitude of GH secretory peaks. and (2) the mean 5.5-h plasma level of GH. Bursts of plasma PRL were inhibited by MSG, but the mean 5.5-h plasma levels were not affected. SRIF concentrations in the medial basal hypothalamus were reduced by 60% after neonatal MSG. Acute administration of MSG to adult rats caused an immediate, long-lasting suppression of rhythmic GH secretion and a rapid, transient release of PRL. These results suggest: (1) neonatally administered MSG causes a marked disturbance in episodic GH and PRL secretion in adult rats; (2) MSG induces a decrease in hypothalamic SRIF and possibly GH-releasing factor; and (3) the acute effects of MSG on GH and PRL may be due to the inhibition and/or excitation of a complex neuronal network involving monoaminergic and peptidergic systems.

Animals↗
PubMed1981

Calcitonin: regional distribution of the hormone and its binding sites in the human brain and pituitary.

Immunoreactive calcitonin (CT), indistinguishable from human CT-(1-32) and its sulfoxide, has been identified in extracts of the hypothalamus, the pituitary, and the thyroid obtained from human subjects at autopsy. DCT concentrations were highest in a region encompassing the posterior hypothalamus, the median eminence, and the pituitary; intermediate in the substantia nigra, the anterior hypothalamus, the globus pallidus, and the inferior colliculus; and low in the caudate nucleus, the hippocampus, the amygdala, and the cerebral and cerebellar cortices. Specific CT binding measured with 125I-labeled salmon CT was highest in homogenates of the posterior hypothalamus and the median eminence, shown to contain the highest concentrations of endogenous CT in the brain; CT binding was less than 12% of hypothalamic binding in all of the other regions of the brain examined and was negligible in the pituitary. Half-maximal binding was achieved with 0.1 nM nonradioactive salmon CT-(1-32), and the binding was directed to structural or conformational sites, or both, in the COOH-terminal half of salmon CT. The rank order of the inhibition of the binding by CT from different species and analogues of the human hormone was the same as in receptors on a human lymphoid cell line (Moran, J., Hunziker, W. & Fischer, J. A. (1978) Proc. Natl. Acad. Sci. USA 75, 3984-3988). The functional role of CT and of its binding sites in the brain remains to be elucidated.

Binding Sites↗
PubMed1981

Evidence for a growth hormone releasing factor mediating alpha-adrenergic influence on growth hormone secretion in the rat.

The effects of adrenergic receptor agonists on GH secretion were studied in adult, male rats pretreated with reserpine and somatostatin antiserum. Frequent blood samples were obtained from intra-aortic cannulae. Plasma GH was determined by radioimmunoassay. Reserpine (10 mg/kg i.p.) caused a complete suppression of the normal, pulsatile secretion of GH in all animals. Administration of somatostatin antiserum resulted in rapid elevations of plasma GH in reserpine-pretreated rats with peak levels at 30 min. GH levels then fell but remained slightly elevated for the duration of the sampling period (8 h). Apomorphine (0.5 mg/kg i.p.) had no effect on plasma GH levels, whereas clonidine (0.5 mg/kg i.p.) induced release of GH in both antiserum treated and control rats. The results indicate that the alpha-adrenergic influence on the secretion of GH is mediated not by inhibition of somatostatin release but rather by effects on the release of a GHRF.

Animals↗
PubMed1981

Evidence for alpha-adrenergic regulation of episodic growth hormone and prolactin secretion in the undisturbed male rat.

The present experiments were designed to study the effect of the centrally active alpha-adrenergic receptor agonist, clonidine, on episodic GH and PRL secretion in male rats after selective blockade of norepinephrine (NE) and epinephrine (EP) synthesis with the dopamine-beta-hydroxylase inhibitor, FLA-63. Freely behaving, chronically cannulated rats were maintained on a constant light-dark cycle in isolation test chambers. Beginning at 1000 h, blood samples were removed every 20 min for 5-h periods without disturbing the animal. FLA-63 was administered (10 or 20 mg/kg ip) at 0845 h. Clonidine (15 or 150 microgram/kg iv) was given at times that coincided with the spontaneous occurrence of episodic GH peaks or troughs observed in control animals. Results of the present study are summarized as follows: 1) selective blockade of NE and EP synthesis with FLA-63 (20 mg/kg) caused complete suppression of episodic GH but had no significant effect on PRL release; 2) clonidine (150 microgram/kg) restored the pulsatile pattern of GH secretion in FLA-63-treated rats, and 3) clonidine (15 and 150 microgram/kg) stimulated PRL release in a dose-dependent manner. These findings suggest a major stimulatory role of alpha-adrenergic receptors in episodic GH and PRL secretion.

Animals↗
PubMed1981

The effects of lateral hypothalamic-medial forebrain stimulation and somatostatin antiserum on pulsatile growth hormone secretion in freely behaving rats: evidence for a dual regulatory mechanism.

The purpose of this investigation was to examine the role of somatostatin (SRIF) and electrical stimulation of the lateral hypothalamic-medial forebrain bundle (LH-MFB) on dynamics of pulsatile GH secretion in freely behaving, chronically cannulated male rats with implanted brain electrodes. The effects of administration of anti-SRIF serum (AS-SRIF) on pulsatile GH and on TSH and PRL secretion was also studied. The results are: 1) circulating AS-SRIF increases trough levels of GH in freely behaving rats but has no significant effect on the amplitude of GH secretory bursts or mean GH levels; 2) LH-MFB excitation can stimulate GH release if delivered when circulating GH levels are low; 3) LH-MFB stimulation inhibits secretion of GH if given at the time of a spontaneous GH burst; 4) stimulation-induced GH inhibition is prevented by pretreatment with AS-SRIF, suggesting that this response is mediated by endogenous SRIF; and 5) AS-SRIF increases TSH secretion but has no effect on PRL. These results provide evidence to support the hypothesis that pituitary GH secretion is regulated by a combination of excitatory and inhibitory influences, the inhibitory component of which is mediated by SRIF.

Animals↗
PubMed1981

Pulsatile somatostatin release from the median eminence of the unanesthetized rat and its relationship to plasma growth hormone levels.

The technique of push-pull perfusion was combined with a sensitive somatostatin RIA to determine in vivo immunoreactive somatostatin (IRS) release from the median eminence (ME) of the freely behaving rat. IRS release was compared to plasma GH levels. Concentrations of IRS in ME perfusates indicated pulsatile release, with an interpeak interval of about an hour. In rats with normal plasma GH pulses and normal plasma PRL levels, IRS secretion ranged from 10-100 pg/15 min. In rats with suppressed GH secretion and high plasma PRL levels, IRS secretion was greater, ranging between 50-500 pg/15 min. A rise in the level of IRS in the ME perfusate often coincided with an increase in GH levels in plasma, suggesting that somatostatin may act by a short-loop negative feedback mechanism to regulate GH release. Gel chromatography of IRS from the perfusate suggested that somatostatin is released in more than one molecular weight form.

Animals↗
PubMed1981

Plasma melatonin increases during exercise in women.

Melatonin was measured in plasma of seven women volunteers before and after serial acute submaximal exercise tests performed during the course of a two-month, progressive endurance training program. Plasma melatonin increased during all exercise sessions and declined towards baseline values when re-measured thirty minutes after completion of each exercise. This finding indicates that vigorous physical activity elicits transient increases in plasma melatonin in both sedentary and trained women.

Adolescent↗
PubMed1981

Water-drinking as ictal behavior in complex partial seizures.

The urge to demand, pour, and drink water at the time of an attack was encountered in 20 patients who had seizures with complex partial symptomatology. Two patients were studied with bitemporal stereotaxically implanted depth electrodes. Drinking was associated with electrographic and clinical seizures starting in the amygdala, hippocampus, and parahippocampal gyrus. Sometimes, this was the only clinical manifestation of an attack, and its significance would not have been recognized without depth recording. Ictal drinking was never encountered in patients without electroencephalographic evidence of temporal epileptic abnormality, and therefore seems to have localizing significance.

Adolescent↗