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Biomedical subjects

V H Sethy

Publications and source records attributed to V H Sethy.

8 recordsLinked to original sources
PubMed1992

Modulation of release of acetylcholine from the striatum by a proposed excitatory amino acid antagonist U-54494A: comparison with known antagonists, diazepam and phenytoin.

The effect of (U-54494A) cis-3,4-dichloro-N-methyl-N-[2-(1-Pyrrolidinyl)- cyclohexyl] benzamide monohydrochloride, an excitatory amino acid antagonist, on N-methyl-D-aspartic acid (NMDA)- and K(+)-evoked release of [3H]acetylcholine [( 3H]ACh) from slices of striatum was investigated. For the purpose of comparison, MK 801, PCP, CGP 37849, CPP, phenytoin and diazepam were investigated under identical conditions. Both U-54494A and the excitatory amino acid antagonists blocked NMDA-evoked release of [3H]ACh but these compounds failed to inhibit K(+)-evoked release of this neurotransmitter. Phenytoin blocked both NMDA and K(+)-evoked release of [3H]ACh, whereas diazepam was ineffective under similar conditions. These observations indicate that excitatory amino acid antagonists, including U-54494A, may mediate their anticonvulsant effect by blocking the activity of NMDA receptors, diazepam by activating the benzodiazepine receptors and phenytoin by inhibiting the activity of various depolarizing agents.

2-Amino-5-phosphonovalerate↗
PubMed1978

Is GABA involved in analgesia?

The effect of morphine and naloxone on gamma-aminobutyric acid (GABA) concentration in discrete areas of the rat brain has been studied. Neither morphine nor naloxone had a significant effect on regional steady-state concentrations of GABA. The results have been discussed with respect to the role of GABA in pain and analgesia.

Aminobutyrates↗
PubMed1976

Effect of anesthetic doses of gamma-hydroxybutyrate on the acetylcholine content of rat brain.

Gamma-hydroxybutyrate administered in anesthetic doses produces a time dependent increase in the levels of rat barin acetylcholine. A maximal increase in whole brain and subcortical levels of acetylcholine is observed about 15 min after administration of the lactone form of the drug. A similar GHB-induced increase in acetylcholine is observed in the striatum and a 75% increase in the hippocampus 15 min after administration of the drug. A good temporal correlation was not obtained between the increase in acetylcholine and the depth of anesthesia produced by the drug. Gamma-hydroxybutyrate did not cause a significant change in the striatal or hippocampal levels of choline. Possible mechanisms involved in the production of this increase in acetylcholine are discussed.

4-Butyrolactone↗
PubMed1975

Therapy of intention myoclonus with L-5-hydroxytryptophan and a peripheral decarboxylase inhibitor, MK 486.

Three patients with postanoxic intention myoclonus, two patients with intention tremor, and one patient with cerebral palsy were administered L-5-hydroxytryptophan (L-5HTP), the precursor of serotonin, in combination with MK 486, a peripheral amino acid decarboxylase inhibitor. L-5HTP combined with MK 486 were potent long-term therapeutic agents for postanoxic intention myoclonus, but had no effect on intention tremor or cerebral palsy. These drugs were well-tolerated by the patients, and more effective than any other known therapy for intention myoclonus. Cerebrospinal fluid concentration of 5-hydroxyindoleacetic acid, the main catabolite of serotonin, appeared low in two patients with intention myoclonus and increased markedly during drug therapy. Postanoxic intention myoclonus may be causally related to a deficiency of brain serotonin.

5-Hydroxytryptophan↗
PubMedDate not supplied

Effect of hypnotic and anxiolytic agents on regional concentration of acetylcholine in rat brain.

Pentobarbital (30 and 60 mg/kg) and chloral hydrate (300 and 600 mg/kg) administered in anesthetic/hypnotic doses produced significant increases in acetylcholine concentration in the cerebral cortex, striatum, hippocampus and brainstem. Hypnotic/anxiolytic agents like diazepam, flurazepam (100 mg/kg each) and triazolam (30 mg/kg) significantly increased the acetylcholine concentration only in the cerebral cortex and striatum. Alprazolam and ketazolam had no significant effect on regional distribution of acetylcholine in the brain. The results have been discussed with respect to the role of central cholinergic system in anesthetic and hypnotic actions of these drugs.

Acetylcholine↗