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beta carboline/seizures

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Two mouse lines were selectively bred according to their sensitivity (BS line) or resistance (BR line) to seizures induced by a single i.p. injection of methyl beta-carboline-3-carboxylate (beta-CCM), an inverse agonist of the GABA(A) receptor benzodiazepine site. Our aim was to characterize both
Agonists acting at subtypes of glutamate receptors, N-methyl-D-aspartate, kainate and quisqualate, induce convulsions in rodents. Clonic seizures induced in mice by intracerebral administration of N-methyl-D-aspartate, kainate or quisqualate were used to study the anti- and proconvulsant potential

Characterization of convulsions induced by methyl beta-carboline-3-carboxylate in mice.

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The convulsive properties of methyl beta-carboline-3-carboxylate (beta-CCM) were evaluated in mice. When injected subcutaneously at a dose of 10 mg/kg beta-CCM induced convulsions in 75% of the mice with a median latency of 2.12 +/- 0.25 min. The CD50 was determined to be about 5 mg/kg.
The benzodiazepine antagonists Ro 15-1788 and CGS 8216 blocked the clonic and tonic convulsions elicited by 3-carbomethoxy-beta-carboline (beta-CCM). The PD50 values for Ro 15-1788, CGS 8216, and diazepam were: 2.0, 0.6, and 2.0 mg/kg, respectively. Neither Ro 15-1788 nor CGS 8216 potentiated the

Effects of 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (6-MeO-THbetaC) on audiogenic seizures in DBA/2J mice.

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It was found previously that 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (6-MeO-THbetaC) increased brain concentration of the neurotransmitter serotonin (5-HT) and decreased the concentration of its metabolite 5-hydroxyindole acetic acid (5-HIAA) at the same time the compound attenuated audiogenic
Fifteen beta-carboline derivatives, including those found in the South American hallucinogenic plant Banisteriopsis caapi, were injected IP and IVC into mice. Subsequent behavioral changes were observed and the levels of the compounds in brain tissue were determined. It was found that following IP

Comparisons between patterns of convulsions induced by two beta-carbolines in 10 inbred strains of mice.

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The beta-carbolines, methyl-beta-carboline-3-carboxylate (beta-CCM) and 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) are known to have pharmacological properties opposite to those of agonistic benzodiazepines. Convulsions induced by these drugs lead to differential patterns, such as

From the behavioral pharmacology of beta-carbolines to seizures, anxiety, and memory.

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A number of beta-carbolines are inverse agonists of the GABA-A receptor complex, acting on the benzodiazepine site. They show convulsive properties when administered at high doses, anxiogenic properties at moderate doses, and learning-enhancing effects at low doses. These data suggest a possible
Among the ligands of the benzodiazepine site, one can mention the benzodiazepines as agonists and some beta-carbolines (e.g. methyl-beta-carboline-3-carboxylate, abbreviated hereafter beta-CCM) as inverse agonists. Most benzodiazepines and beta-carbolines act on processes involved in memory,

beta-Carboline-induced seizures in mice: genetic analysis.

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The inbred mouse strains BALB/cBy (C) and C57BL/6By (B6) differed significantly in their susceptibility to seizures induced by the benzodiazepine inverse agonist methyl beta-carboline-3-carboxylate (beta-CCM). Following a 5 mg/kg injection of beta-CCM, 74% of C (n = 35) and 13% of B6 (n = 40) mice

Evidence for a multigenic system controlling methyl-beta-carboline-3-carboxylate (beta-CCM)-induced seizures.

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beta-CCM is a beta-carboline known to have properties opposite to those of benzodiazepines. Our approach was to analyze, in mice, the genetic mechanisms involved in beta-CCM-induced myoclonic seizures using recombinant congenic strains and F1 hybrids issued from these strains. Our aim was to define

Chromosomes 4 and 13 in beta-carboline-induced seizures in mice: benzodiazepine binding.

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Methyl beta-carboline-3-carboxylate (beta-CCM) is a ligand for the benzodiazepine (BZD) binding site of the GABA-A receptors with convulsive properties. We provided evidence for the involvement of a fragment of mouse chromosomes 4 and 13 in beta-CCM-induced seizures in a previous paper. Here, we

A mouse mutant strain highly resistant to methyl beta-carboline-3-carboxylate-induced seizures.

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The convulsant properties of methyl beta-carboline-3-carboxylate (beta-CCM) were evaluated in the TaT-fm/GncTa+/+Tfm strain carrying the tabby coat color (Ta) and/or the testicular feminization (Tfm) gene. When injected intraperitoneally within a 5-60 mg/kg dose range, beta-CCM-induced convulsions

Bidirectional effects of beta-carbolines in rats with spontaneous petit mal-like seizures.

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Seven benzodiazepine-receptor ligands of the beta-carbolines' group were administered IP in Wistar rats from (1) a strain displaying spontaneous petit mal-like seizures (PMLS) characterized by spike and wave discharges (SWD) and, (2) a strain where no seizure is ever observed (NS). Five different
The brain regions that may be functionally involved in the control of anxiety and the development of seizures were examined using quantitative 1-14C-deoxyglucose autoradiography. For this purpose, beta-carbolines FG 7142 and DMCM were employed. They exert their effects via the benzodiazepine
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