PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 3753526

gamma-Acetylenic GABA antagonizes the decrease in synaptosomal GABA concentrations but not the seizures induced by 3-mercaptopropionic acid in rats.

W Löscher
View original source ↗Export metadata ↓

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

3-Mercaptopropionic AcidAlkynesAminocaproatesAnimalsFemaleRatsRats, Inbred StrainsSeizuresSulfhydryl CompoundsSynaptosomesTissue Distributiongamma-Aminobutyric AcidJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

W Löscher. 1986-09-15. gamma-Acetylenic GABA antagonizes the decrease in synaptosomal GABA concentrations but not the seizures induced by 3-mercaptopropionic acid in rats.. https://doi.org/10.1016/0006-2952(86)90408-9

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

Antiulcer and gastric secretory activity of N-phthaloyl gamma-aminobutyric acid.

N-Phthaloyl gamma-aminobutyric acid, a new gamma-aminobutyric acid derivative synthesized in this laboratory, has been found to possess anticonvulsant, antinociceptive and antistress activities. Effects of this derivative on gastric lesions induced by aspirin and ethanol were studied in rats. N-Phthaloyl gamma-aminobutyric acid significantly inhibited both aspirin and alcohol ulceration. The ED50 in each case being 76.34 and 43.65 mg/kg i.p. respectively. The volume of gastric acid secretion was diminished but gastric mucus secretion was significantly enhanced. The antiulcer effect was blocked by bicuculline and 3-mercaptopropionic acid. We conclude that (a) N-phthaloyl gamma-aminobutyric acid possesses antiulcer activity (b) the new derivative is probably a non-specific gamma-aminobutyric acid receptor agonist (c) the observed activity may be due to a mucoprotective action.

3-Mercaptopropionic Acid↗
PubMed1992

Inhibition of baroreflex bradycardia by ethanol involves both GABAA and GABAB receptors in the brainstem of the rat.

The effects of ethanol on baroreceptor reflex bradycardia and its interactions with cardiovascular effects mediated by GABA receptors in the dorsal vagal complex were studied in urethane-anaesthetised rats. Ethanol, 1 g kg-1 administered i.v. or 25-200 nmol microinjected bilaterally into the dorsal vagal complex, inhibited the reflex bradycardic response to bolus i.v. doses of phenylephrine both in spontaneously breathing and in paralysed, artificially ventilated animals, and this effect could be prevented by pretreatment with the GABA-depleting agent, 3-mercaptopropionate in both groups of rats. Ethanol, 1 g kg-1 i.v., did not influence the bradycardic response to electrical stimulation of the cervical vagus. Microinjection of muscimol into the dorsal vagal complex caused a dose-dependent pressor response and inhibited baroreflex bradycardia. The pressor response was potentiated and a tachycardic response to muscimol emerged following microinjection of ethanol into the dorsal vagal complex. Similar administration of baclofen caused dose-dependent increases in blood pressure and heart rate and inhibited baroreflex bradycardia. Injection of ethanol into the dorsal vagal complex potentiated the pressor response to a low dose of baclofen but did not affect the tachycardic response. Bicuculline, 10 pmol/side into the dorsal vagal complex, blocked the effects of muscimol but not those of baclofen and reduced the baroreflex inhibitory action of ethanol. 2-Hydroxysaclofen, microinjected at 400 pmol to 1 nmol/side, blocked the effects of baclofen but not those of muscimol. 2-Hydroxysaclofen or phaclofen, 2 mg kg-1 s.c., prevented the baroreflex inhibitory action of ethanol and also prevented ethanol potentiation of the pressor and, less effectively, the tachycardic effects of muscimol. It is concluded that ethanol inhibits baroreflex bradycardia through potentiation of the actions of endogenous GABA in the dorsal vagal complex. Both GABAA and GABAB receptors appear to be involved in this action of ethanol.

3-Mercaptopropionic Acid↗
PubMed1992

Time-dependent anticonvulsant activity of melatonin in hamsters.

The objective of the present study was to assess whether the anticonvulsant activity of melatonin displays diurnal variability in hamsters. Convulsions were induced by administering 3-mercaptopropionic acid (3-MP). There was a significant diurnal variation in 3-MP-induced convulsions, hamsters being more prone to exhibit seizures during the night than during the day. Melatonin (50 mg/kg i.p.) had a maximal anticonvulsive effect in the early evening (20:00 h). The administration at 20:00 h of the central-type benzodiazepine antagonist, Ro 15-1788, although unable by itself to modify seizure threshold, blunted the anticonvulsant response to melatonin. The results indicate that the time-dependent anticonvulsant activity of melatonin is sensitive to central-type benzodiazepine antagonism.

3-Mercaptopropionic Acid↗