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Biomedical subjects

M Salis

Publications and source records attributed to M Salis.

10 recordsLinked to original sources
PubMed1984

Stress and beta-carbolines decrease the density of low affinity GABA binding sites; an effect reversed by diazepam.

Cerebral cortex membranes from rats habituated to manipulations preceding decapitation (habituated rats) had 40% higher GABA binding than membranes from naive animals. Diazepam (5 X 10(-6) M), added to membranes from naive rats, increased GABA binding to the level of habituated rats, but failed to induce any further increase in membranes from the latter animals. Vice versa, beta-carbolines (FG 7142, beta-CCE, DMCM) added to membranes from habituated rats lowered GABA binding to the level of naive animals, but caused no further decrease in the membranes from this last group. Diazepam removed the effect of beta-carbolines in membranes from habituated rats. It is suggested that handling represents a stressful stimulus for naive animals and that stress lowers GABA binding by releasing an endogenous ligand for benzodiazepine receptors possessing similar properties to beta-carbolines. Finally, the results indicate that the emotional status of animals from which brain tissue is obtained should be considered when connections between GABA and benzodiazepine receptors are studied.

Animals↗
PubMed1984

Evidence for an involvement of GABA receptors in the mediation of the proconvulsant action of ethyl-beta-carboline-3-carboxylate.

The kinetic characteristics of binding of [3H]-GABA and the pattern of isoniazid-induced convulsions were studied in rats treated with repeated intraventricular injections of ethyl-beta-carboline-3-carboxylate (beta-CCE) (10 micrograms/rat, twice daily for 8 days). Thirty-six hours after the last injection, the total number of binding sites for [3H]-GABA was decreased (25%) in the cerebral cortex and hippocampus. On the other hand, there was no significant difference in the dissociation constant (KD) between beta-CCE and solvent-treated rats. The decrease in binding sites for [3H]-GABA was paralleled by a strong potentiation of the convulsant pattern elicited by isoniazid. The results suggest that the proconvulsant effect elicited by beta-CCE is mediated by the decrease in the total number of binding sites for GABA, secondary to the interaction between beta-CCE and the benzodiazepine receptor coupled to the GABA receptor.

Animals↗
PubMed1983

Increase of cyclic GMP in cerebellum by methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM).

The intraperitoneal administration of DMCM (0.5-3 mg/kg) produced a dose-related increase in the content of cyclic GMP in the rat cerebellar cortex. The effect of DMCM on cyclic GMP was abolished by pretreatment with benzodiazepine receptor ligands, diazepam and Ro15-1788 and by the GABA agonist muscimol. The results suggest that DMCM increases cerebellar cyclic GMP content through a direct action on benzodiazepine receptors located in the cerebellar cortex. The interaction between DMCM and the GABAergic system associated with benzodiazepine receptors is discussed. Cerebellar cyclic GMP content can be used as a biochemical index to differentiate agonists and antagonists for benzodiazepine receptors.

Animals↗
PubMed1983

Effect of a vitamin A-free diet on [3H]diazepam and [3H]GABA binding in the rat retina.

Benzodiazepine and GABA binding sites in the rat retina are influenced by a vitamin A-free diet. In rats fed a vitamin A-free diet, the total number of [3H]GABA and [3H]diazepam binding sites was markedly higher than in rats given a balanced diet. No differences were found in the apparent affinities of [3H]GABA and [3H]diazepam for their specific binding sites. The results suggest that GABA and benzodiazepine binding sites have a role in the function of the retina.

Animals↗
PubMed1983

Brain benzodiazepine receptors increase after chronic ethyl-beta-carboline-3-carboxylate.

Rats were treated with repeated intraventricular injections of ethyl-beta-carboline-3-carboxylate (beta-CCE) (10 micrograms/rat, twice daily for 8 days), 36 h after the last injection, the total number of 3H-diazepam binding sites was increased in the cerebral cortex, cerebellum and hippocampus by 63, 51 and 38%, respectively. On the other hand, there were no significant differences in the dissociation constants (KD) between beta-CCE and solvent treated rats. In contrast, chronic beta-CCE administration failed to change the number of the apparent affinity of 3H-beta-CCE binding sites in all the brain areas examined. The results suggest that beta-CCE is an antagonist at the 3H-diazepam binding sites.

Animals↗
PubMed1983

Biochemical changes in the rat cerebellar cortex elicited by chronic treatment with methyl mercury.

Long-term (20 days) treatment with methyl mercury (MeHg) increases the total number of benzodiazepine binding sites and decreases essentially the content of cyclic GMP in the cerebellar cortex. In contrast, this treatment fails to modify the content of GABA and cyclic AMP, GAD activity and GABA binding sites in the same brain area. The changes in cyclic GMP and benzodiazepine binding sites in the cerebellar cortex are discussed in relation to the motor disturbances associated with MeHg intoxication.

Animals↗
PubMed1982

Age-related changes of benzodiazepine and GABA binding sites in the rat retina.

The changes in the number and sensitivity of benzodiazepine and GABA binding sites in the rat retina during postnatal development, adulthood and ageing and their functional relationship at different ages have been studied. Data indicate an increase in the total number of both GABA and benzodiazepine binding sites with age. In contrast, the activation of retinal benzodiazepine receptor binding by GABA is significantly reduced in aged rats with respect to young adult and newborn rats. Moreover, the activation of retinal benzodiazepine receptor binding induced by dark exposure of the animals is present in young adult rats but is lost in aged rats. These results suggest that in the retina of aged rats there is an increase of GABA and benzodiazepine receptors which have lost their functional connection.

Aging↗