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Biomedical subjects

C S Hollander

Publications and source records attributed to C S Hollander.

At least 37 records · Page 2Linked to original sources
PubMed1983

Distribution, biosynthesis, and physiological role of corticotropin-releasing factor in the human: an overview.

Our findings to date indicate that: A peptide resembling oCRF is present in human and mammalian hypothalamus. oCRF is present in human lumbar cerebrospinal fluid. oCRF concentrations do not differ in CSF from normal individuals and from patients with Cushing's syndrome. oCRF appears to be synthesized via a large oligopeptide precursor. An oCRF-like molecule (oCRF-LI) is present in hypothalamic brain tissue. We have also observed more tentative evidence of low levels of oCRF-LI outside of the brain. oCRF is likely to be a central mediator of stress in its multiple forms. We believe that oCRF is clearly of major physiological importance, but that many critical unanswered questions remain. Probably, the most fascinating of these, which we are only beginning to comprehend, concerns the functions of CRF in extrahypothalamic brain as well as the CRF which appears to be present outside the brain.

Animals↗
PubMed1982

Acetylcholine, melatonin, and potassium depolarization stimulate release of luteinizing hormone-releasing hormone from rat hypothalamus in vitro.

We have examined the release of radioimmunoassayable luteinizing hormone-releasing hormone (LH-RH) from fragments of rat medial basal hypothalamus. These fragments were cultured overnight in medium containing serum and then preincubated in groups of three for 10 min in medium resembling cerebrospinal fluid in its electrolyte constituents and containing bacitracin. This was followed by 30-min incubation periods during which some of the hypothalami were exposed to test substances. Potassium depolarization, effected by the addition of 56 mM potassium chloride to the incubation medium, caused a marked stimulation in LH-RH release, but only in the presence of calcium. Acetylcholine at 10 nM and the parasympathomimetic anticholinesterase agent neostigmine at 1 microM markedly stimulated LH-RH release. Hexamethonium, a nicotinic antagonist, at 1 microM abolished the acetylcholine-induced increment in LH-RH release. Melatonin, a pineal indolamine, caused significant stimulation of LH-RH release at a concentration as low as 10 nM. Bacitracin (21 microM) was employed in all these experiments. It had no effect on LH-RH release but did prevent the degradation of LH-RH in this system. We conclude that acetylcholine and melatonin are capable of inducing LH-RH release from the rat medial basal hypothalamus. These actions may account for some of the progonadotropic properties previously ascribed to these agents.

Acetylcholine↗
PubMed1981

Brain beta-endorphin-like immunoreactivity in adult rats given beta-endorphin neonatally.

beta-endorphin-like immunoreactivity was measured by radioimmunoassay in the brains of adult rats treated neonatally with beta-endorphin, naloxone, or vehicle. After treatment with beta-endorphin, the decreases observed in beta-endorphin-like immunoreactivity in the hypothalamus, pineal, midbrain, pons-medulla, hippocampus, striatum, frontal cortex, occipital cortex, and posterior cortex were highly significant but the 23% decrease in the thalamus was not significantly different from that of control rats. Neonatal administration of naloxone only resulted in a significant decrease in beta-endorphin-like immunoreactivity in the hypothalamus. In contrast, no differences were discernible in content of either beta-endorphin-like immunoreactivity or ACTH-like immunoreactivity in the pituitary of rats treated with beta-endorphin, naloxone, or vehicle in the neonatal period. These same rats had shown an increased threshold to painful thermal stimulation by the tail-flick test after administration of either beta-endorphin or naloxone at birth. The results suggest that neonatally injected beta-endorphin may alter the levels of beta-endorphin-like immunoreactivity in rat brain as well as the response to pain.

Animals↗
PubMed1981

Opiate peptides modulate somatostatin release from dispersed hypothalamic cells.

An in vitro dispersed hypothalamic cell system was developed and utilized to investigate the effect of exposure to cold stress prior to sacrifice on release of somatostatin-like immunoreactivity (SRIF-LI). Exposure of the rats to cold stress prior to sacrifice significantly increased basal (or control) release of SRIF-LI from dispersed hypothalamic cells. The endogenous opiate peptides (beta-endorphin, Met-enkephalin and Leu-enkephalin)significantly inhibited the basal release of SRIF-LI from dispersed hypothalamic cells obtained from rats exposed to the cold prior to sacrifice. Naloxone, a specific opiate antagonist, had no effect on basal release but blocked inhibition by the endogenous opiate peptides. In marked contrast, the endogenous opiate peptides had no effect on basal release of SRIF-LI from dispersed hypothalamic cells of rats exposed to room temperature prior to sacrifice.

Animals↗
PubMed1981

Somatostatin release from rat hypothalamus in vitro: effects of melatonin and serotonin.

The release of immunoreactive somatostatin (SRIF) from explants of rat medial basal hypothalamus, which were maintained in culture for 24 h, was quantitated by a sensitive RIA. Validity of the specific SRIF assay has been previously established by chromatographic criteria using gel and high pressure systems and by the demonstration of immunological parallelism. After 24 h of culture in medium containing heat-inactivated fetal calf serum, hypothalamic fragments were incubated in serum-free medium, and the release of immunoreactive SRIF was quantitated. Melatonin at concentrations of 10(--8) and 10(--7) M stimulated SRIF release, and no significant increases were observed at concentrations of 10(--9) M or less or at concentrations of 10(--6) M or greater. Serotonin oxalate at concentrations of 10(--8)--10(--5) M significantly inhibited SRIF release. The serotonin antagonist cyproheptadine at a concentration of 10(--5)M had no effect on basal SRIF release but abolished the inhibitory effect of 10(--7) M serotonin. Finally, when hypothalami were incubated with melatonin and serotonin, each at 10(--7) M, SRIF release was unchanged compared to control values. The results suggest that the brain indoleamines, melatonin and serotonin, may modulate GH secretion by effects on SRIF release at a hypothalamic level.

Animals↗
PubMed1980

Sex and alcohol: the effects of alcohol on the hypothalamic-pituitary-gonadal axis.

Effects of alcohol on the hypothalamic-pituitary-gonadal axis are complex. Those at the gonadal level are best defined in studies such as those presented in this issue. However, there is an accumulating body of data supporting central effects of alcohol. The precise locus or loci is not certain. Further investigations probably including in vitro methodologies are likely to enhance our knowledge in this area. Our understanding of the effects of alcohol in the human female is especially limited.

Ethanol↗
PubMed1980

Acetylcholine inhibits the release of somatostatin from rat hypothalamus in vitro.

Acetylcholine, at concentrations of 10(-10)--10(-7) M, inhibited the release of immunoreactive somatostatin (SRIF) from rat hypothalamic segments which had been maintained in short term culture for 24 h. Neostigmine (10(-6) M), an anticholinesterase, also inhibited the release of SRIF, whereas atropine (10(-6) M), a muscarinic anticholinergic, had no effect on basal SRIF release but blocked the inhibition caused by acetylcholine (10(-8) M). However, hexamethonium (10(-6) M), a nicotinic antagonist, did not abolish the inhibition induced by acetylcholine. Potassium depolarization (56 mM KCl) caused stimulation of SRIF release, which was dependent on the presence of calcium in the incubation medium. SRIF was measured by a RIA sensitive to 1 pg/tube. Authenticity of immunoreactive SRIF released was suggested by immunological parallelism and chromatographic criteria using gel and high pressure liquid systems. These results suggest that muscarinic cholinergic mechanisms may have a regulatory role modulating the secretion of SRIF and, consequently, GH through actions at a hypothalamic level.

Acetylcholine↗
PubMed1979

Circulating melatonin in man: episodic secretion throughout the light-dark cycle.

A sensitive and specific RIA for melatonin has been validated for human plasma. Five young adult men had plasma samples obtained every 20 min during two 24-h periods. One was a normal active period and the other a basal period with complete bed rest. Melatonin was found to be secreted episodically throughout the 24 h in each condition, with secretory episodes clearly present during the waking day in the presence of bright light.

Adult↗
PubMed1978

A controlled crossover study of triiodothyronine in autistic children.

A placebo-controlled crossover study of behavioral effects of triiodothyronine (T3) was conducted in 30 young clinically euthyroid autistic children. Multiple independent raters and multiple rating scales were used. Except for a few symptoms that were reduced on T3, the drug did not differ from placebo. Time itself accounted for most of the improvement in the whole sample. As a group, the lower IQ children responded to T3. The individual children who were responders could not be defined by any parameter.

Autistic Disorder↗
PubMed1978

Somatostatin inhibits release of thyrotropin releasing factor from organ cultures of rat hypothalamus.

Somatostatin in concentrations of 10(-6) to 10(-8) M inhibited basal release of thyrotropin releasing factor in organ culture of rat hypothalamus. Norepinephrine in doses of 10(-4)--10(-6) M induced release of thyrotropin releasing factor which increased progressively with time and was temperature and dose dependent. This enhanced thyrotropin-releasing-factor release was inhibited by somatostatin at 10(-6)--10(-8) M.

Animals↗
PubMed1978

Effects of iodides on the hypothalamic-pituitary-thyroid axis in neurological endemic cretinism: evidence for compensated thyroidal failure in adult life.

Thyroid function studies, performed after iodide administration to five patients with neurological endemic cretinism, were indicative of hypothyroidism. All five subjects had either a low serum thyroxine (T4) or a high basal thyrotrophin (TSH) level and a clearly exaggerated TSH response to thyrotrophin releasing hormone (TRH). These findings are in sharp contrast with those we have previously described in goitrous patients without cretinism from the same geographical area. One interpretation of our observations is that there is an underlying mild defect in thyroid hormone synthesis in endemic cretinism predisposing to iodine induced hypothyroidism.

Adult↗
PubMed1976

Biosynthesis of prostaglandins in rabbit kidney medulla. Properties of prostaglandin synthase.

A simple radioactive-substrate assay for prostaglandin synthase (EC 1.14.99.1), which uses t.l.c. to measure simultaneously different prostaglandins synthesized from one precursor substrate, was developed. Rabbit kidney-medulla prostaglandin synthase catalyses the formation of prostaglandin E2, prostaglandin F2alpha and prostaglandin D2 from arachidonic acid. Fractionation of crude homogenates indicated that the microsomal fraction possessed the highest specific activity of prostaglandin synthase, whereas the soluble fraction exhibited little enzyme activity but rather contained a heat-labile inhibitory macromolecular factor(s), which might be attributed to the serum albumin present in this fraction. The microsomal fraction possessed low intrinsic enzyme activity, but the actvity could be fully stimulated by the presence of both GSH (reduced glutathione) and a phenolic cofactor. Only cysteine could partially replace GSH, whereas other thiols were inactive and some were even inhibitory. A variety of phenolic compounds, including catecholamines, dopamine (3,4-dihydroxyphenethylamine), 5-hydroxytryptamine and quinol, were active in stimulating prostaglandin synthase. In all cases, the stimulation was reflected in the synthesis of all three prostaglandins with ratios not significantly altered by different phenolic cofactors. The synthesis of each of the different prostaglandins appeared to have similar pH optima. The enzyme system was not inhibited by thiol-group inhibitors or a variety of metal chelators except for cyanide and 8-hydroxyquinoline. Characterization of the kidney-medulla prostaglandin synthase system indicated that it exhibited properties similar to those of the enzyme system present in seminal vesicles.

Animals↗
PubMed1976

Kinetic evidence of a distinct regulatory site on 15-hydroxyprostaglandin dehydrogenase.

15-Hydroxyprostaglandin dehydrogenase was inhibited by xylocaine, furosemide, and ethacrynic acid, but was activated by imipramine and other related drugs. Inhibition by xylocaine was uncompetitive with respect to both NAD+ and PGE1. Activation by imipramine was also uncompetitive with respect to both substrates. Kinetic studies on mixed inhibitor and activator showed a competitive pattern of inhibition of xylocaine vs imipramine activation. These studies suggest that either inhibitors or activators interact with the enzyme at a site distinct from substrate and coenzyme binding sites, and that inhibitors and activators probably interact with the enzyme at the same regulatory site.

Alcohol Oxidoreductases↗
PubMed1975

Effect of methylergonovine on puerperal prolactin secretion.

Serum prolactin concentration was measured by radioimmunoassay in 29 women, in the first 1 1/2 hours postpartum. Fourteen women received 0.2 mg methylergonovine maleate (Methergine) intramuscularly after the delivery of the placenta. Fifteen women who served as controls received only saline. The rise in serum prolactin concentration seen in the control women (266.4 ng/ml +/- 40.8 SE) was significantly greater than that seen in methylergonovine-treated patients (141.0 ng/ml +/- 29.0. SE).

Female↗