1,721,117 research outputs found
Partial protection by CDP-choline against kainic acid-induced lesion in the rat caudate nucleus.
No full textThe acute intraperitoneal administration of CDP-choline to rats caused an increase in striatal dopamine (DA) synthesis, measured by DOPA accumulation after decarboxylase inhibition. Moreover, the chronic treatment with CDP-choline induced a decrease in the total number of 3H-spiroperidol binding sites, while partially antagonizing the disappearance of DA-sensitive adenylate cyclase activity elicited by intrastriatal kainic acid. These results suggest that CDP-choline may have a trophic and/or stimulant action on the function of nigrostriatal dopaminergic neurons
Selective blockade of benzodiazepine receptors by Ro 15-1788 prevents foot shock-induced decrease of low affinity gamma-aminobutyric acid receptors.
No full textThe cerebral cortex of unstressed rats has a higher density of low affinity gamma-aminobutyric acid (GABA) receptors than that of stressed animals. Stress (handling or foot shock) produces a sudden decrease in the total number of low-affinity GABA receptors in the cerebral cortex of unstressed rats but leaves unchanged the density of GABA receptors in the cortex of stressed animals. The in vivo administration of Ro 15-1788 (30 mg/kg per os), a specific benzodiazepine receptor antagonist, completely prevents the effect of footshock on the low-affinity GABA receptors. The results suggest that (a) benzodiazepine recognition sites are involved in the action of stress on GABA receptors, and (b) stress may release an endogenous ligand for the benzodiazepine recognition site
Brain benzodiazepine receptors increase after chronic ethyl-beta-carboline-3-carboxylate.
No full textRats 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
Effect of stress on the function of chloride channels associated with the GABA receptor complex.
No full textGABAergic synaptic transmission: Molecular, Pharmacological, and Clinical Aspects
No full textThis volume reviews research on the pharmacology and physiopathology of GABA(A) receptors in the mammalian central nervous system. More than 200 international investigators discuss the most recent findings on the molecular structure of the GABA(A) receptor complex and its role in the pharmacology of steroids, ethanol, general anaesthetics, benzodiazepines, and nonbenzodiazepine GABAergic drugs. The coverage ranges from molecular biology, to molecuar and clinical pharmacology, to new approaches to pharmacotherapy of convulsive, sleep, and anxiety disorders
Foot shock stress decreases chloride efflux from rat brain synaptoneurosomes.
No full textFoot shock stress delivered continuously for 20 min decreased the 36Cl- efflux from cerebral cortex synaptoneurosomes of handling-habituated (unstressed) rats but failed to have the same effect on the synaptoneurosomes of naive (stressed) rats. The presence of pentobarbital (500 microM), GABA (100 microM) or muscimol (50 microM in the dilution buffer reversed the stress-induced decrease of 36Cl- efflux from synaptoneurosomes of unstressed rats. Moreover, these drugs also stimulated 36Cl- efflux from cortical synaptoneurosomes of naive stressed rats. The results indicate that stress decreases the function of Cl- channels coupled to the GABA/barbiturate receptor complex
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