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Biomedical subjects

J Rossier

Publications and source records attributed to J Rossier.

At least 181 records · Page 10Linked to original sources
PubMed1982

Methyl-beta-carboline-induced convulsions are antagonized by Ro 15-1788 and by propyl-beta-carboline.

Injected i.v. into baboons, Ro 15-1788 (a benzodiazepine antagonist) and propyl-beta-carboline-3-carboxylate did not modify either the behavior or the electroencephalogram at doses up to 2 mg/kg. Methyl-beta-carboline-3-carboxylate is a potent convulsant at doses of 20 micrograms/kg in photosensitive baboons and 100 micrograms/kg in non-photosensitive baboons. These convulsive doses of methyl-beta-carboline-3-carboxylate are effectively antagonized by 0.5 mg/kg of Ro 15-1788 and also by 2 mg/kg of propyl-beta-carboline-3-carboxylate.

Animals↗
PubMed1982

Brain opiates.

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Adrenocorticotropic Hormone↗
PubMed1981

Proconvulsant effects in baboons of beta-carboline, a putative endogenous ligand for benzodiazepine receptors.

beta-Carboline-3-carboxylic acid ethyl ester (beta-CCE) was tested on two models of epilepsy in the baboon: kainic acid-induced limbic status epilepticus and photosensitive epilepsy. Beta-CCE, at very low doses ranging from 8 to 100 microgram/kg (i.v.), induced a reactivation of the limbic focus and photomyoclonic and generalized seizures in photosensitive and non-photosensitive baboons. The proconvulsant effect of beta-CCE may be associated with its binding to a particular subclass of benzodiazepine receptors.

Amygdala↗
PubMed1981

Co-release of enkephalin and catecholamines from cultured adrenal chromaffin cells.

The opioid peptides Leu-enkephalin and Met-enkephalin are stored intraneuronally in the brain where they are thought to act as neurotransmitters and/or neuromodulators. Evidence for their release from nerve terminals has come from biochemical and pharmacological studies in vitro with brain tissue slices and synaptosomes. Enkephalins also exist in the peripheral nervous system in nerve cell bodies and axon terminals in the gastrointestinal tract, sympathetic ganglia and adrenal gland. In the adrenal gland, high levels of enkephalins are present both in axon terminals of the splanchnic nerve and in the adrenal medullary chromaffin cells where they are stored together with the catecholamines in the chromaffin granules. Stimulation of the adrenal gland in vivo or the perfused gland in vitro causes release of catecholamines and enkephalins into the adrenal vein. However, it is not clear whether the origin of the released enkephalins is the adrenal medullary chromaffin cells or the enkephalin-containing splanchnic nerve terminals that innervate the medulla. We now show that enkephalin and catecholamines are released together from primary cultures of bovine adrenal medullary chromaffin cells by nicotine in a Ca2+-dependent manner.

Adrenal Medulla↗
PubMed1981

Marked increases in large enkephalin-containing polypeptides in the rat adrenal gland following denervation.

When rat adrenal glands are denervated, large increases in the amounts of enkephalin and enkephalin-containing polypeptides appear. In the normal gland, only trace amounts occur. One of the larger polypeptides (approximately 22,000 daltons) increases rapidly and by 48 hr following denervation, attains 20 times its original level. At this time, the levels of free enkephalins are essentially unchanged. By 96 hr, the 22,000-dalton polypeptide begins to decrease as free enkephalins and intermediate-sized enkephalin-containing polypeptides increase. This series of events is consistent with a precursor (22,000-dalton polypeptide)/product (enkephalin) relationship.

Adrenal Glands↗
PubMed1980

Met-enkephalin-Arg6-Phe7, present in high amounts in brain of rat, cattle and man, is an opioid agonist.

The enkephalins Met-enkephalin and Leu-enkephalin were first isolated from porcine brain by Hughes and co-workers. We have recently isolated from bovine adrenals another enkephalin with the structure Tyr-Gly-Gly-Phe-Met-Arg-Phe, or Met-enkephalin-Arg6-Phe7 (ref. 2). We report here that this new heptapeptide is found in human, rat and bovine striatum in concentrations comparable with or greater than that of Leu-enkephalin. This molecule should not be considered as a mere precursor of Met-enkephalin. A pharmacological study indicates that this naturally occurring enkephalin has similar properties to the two enkephalins characterized earlier.

Amino Acid Sequence↗
PubMed1980

An about 50,000-dalton protein in adrenal medulla: a common precursor of [Met]- and [Leu]enkephalin.

A protein that may be an enkephalin precursor has been identified in extracts of bovine adrenal medulla. This protein (about 50,000 daltons) appears to contain seven copies of [Met]enkephalin and one copy of [Leu]enkephalin. Digestion with trypsin and carboxypeptidase B yields [Met]enkephalin and [Leu]enkephalin in a ratio of almost 7 to 1. The enkephalins were identified by chromatography and by their binding to opiate receptors. Some characteristics of several other adrenal peptides that may serve as intermediates in the biosynthesis of the enkephalins are presented.

Adrenal Medulla↗
PubMed1980

Tetrahydropapaveroline inhibits dopamine uptake in rat brain synaptosomes.

THP, which can be formed by the condensation of dopamine with dopaldehyde, has been proposed to be involved in mediating some of the effects of ethanol on the central nervous system. We have observed that THP induces small granular vesicles (SGVs), visible with the electron microscope, in central dopamine fibers (Koda et al., 1978). In order to investigate the mechanism of SGV induction by THP, we examined dopamine and THP uptake into synaptosomes. [3H]THP (1.25 Ci/mmole), prepared by catalytic exchange labeling, exhibited no active uptake into synaptosomes (kinetics consistent with simple diffusion). THP did exhibit competitive inhibition (Ki = 4.2 x 10(-5) M) of [3H] dopamine uptake (Km = 2.6 x 10(-7) M; Vmax = 8.5 nmoles/min/g pellet) in these preparations. It is unlikely that endogenous THP would accumulate to concentrations sufficiently high to inhibit dopamine uptake under physiological conditions.

Animals↗
PubMed1980

Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation.

Basal levels of immunoreactive (ir) beta-endorphin, corticotropin (ACTH), and prolactin (PRL) in plasma of male rats decrease after dexamethasone pretreatment (400 microgram/kg at 24 hr and 200 microgram/kg at 2 hr before). Inescapable electric footshocks increase ir-beta-endorphin, ACTH, and PRL plasma levels and this effect is blocked by dexamethasone pretreatment. Morphine (20 mg/kg) also increases ir-beta-endorphin, ACTH, and PRL levels. Dexamethasone pretreatment blocks the morphine-induced release of ir-beta-endorphin but does not prevent the morphine-induced release of PRL. Naloxone, the opiate antagonist, decreases basal plasma levels of PRL and partially blocks the stress-induced increase of PRL, but it has no effect on the basal or stress-induced release of ir-beta-endorphin. These results are consistent with the proposal that beta-endorphin may interact with an opiate receptor involved in the regulation of PRL secretion.

Adrenocorticotropic Hormone↗
PubMed1980

Studies with [35S]methionine indicate that the 22,000-dalton [Met]enkephalin-containing protein in chromaffin cells is a precursor of [Met]enkephalin.

It has been shown that [35S]methionine is incorporated into the [Met]enkephalin sequences of a 22,000-dalton enkephalin-containing protein in the adrenal medulla. Pulse-chase experiments indicate that label is incorporated into the large polypeptide before it appears in free [Met]enkephalin and a smaller [Met]enkephalin-containing peptide. These findings provide direct evidence of a precursor-product relationship of these structurally related polypeptides.

Adrenal Medulla↗