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Biomedical subjects

M Karobath

Publications and source records attributed to M Karobath.

At least 55 records · Page 3Linked to original sources
PubMed1980

Sodium valproate in schizophrenia: some biochemical correlates.

Sodium valproate given in doses of 750-3000 mg daily to eight schizophrenic patients produced a qualitatively similar increase in symptoms in five. CSF showed no significant change in gamma-amino-butyric acid or methoxy hydroxyphenyl glycol, but homovanillic acid increased non-significantly in five patients.

Adult↗
PubMed1979

THIP and isoguvacine are partial agonists of GABA-stimulated benzodiazepine receptor binding.

The effects of THIP and isoguvacine on 3H-flunitrazepam binding to washed membranes prepared from the cerebral cortex of adult rats have been examined. THIP, which has only minimal stimulatory effects on benzodiazepine (BZ) receptor binding, has been found to inhibit the stimulation induced by small concentrations (2 microM) of exogenous GABA. While isoguvacine stimulates BZ receptor binding, although to a smaller extent than GABA, it also antagonizes the stimulation of BZ receptor binding induced by GABA. Thus THIP and isoguvacine exhibit the properties of a partial agonist of GABA-stimulated BZ receptor binding.

Animals↗
PubMed1979

[Biochemical effects of psychotropic drugs in central nervous system (author's transl)].

Studies on the biochemical effects of clinically used psychotropic drugs in brain have shown that they all exert their action by a direct or indirect interference with synaptic transmission. Thus, animal studies in vivo and in vitro have shown that the clinical efficacy of antipsychotic drugs correlates with their inhibitory action on dopamine receptors. In vivo these compounds enhance dopamine turnover in the brain and in vitro they inhibit the dopamine sensitive adenylate cyclase and the binding of dopamine to its receptor at neuronal membranes. Tricyclic antidepressants are drugs which have effects on many transmitter systems. No specific biochemical action has been found which is closely correlated with their clinical potency. However, it appears that a stimulation of the function of the noradrenergic system might have some clinical relevance. Benzodiazepines exert their pharmacological activity in the CNS by interacting with a brain specific receptor. This receptor appears to be part of a larger complex including a GABA receptor and the chloride conductance mechanism associated with the GABA receptor. By binding to their receptor, benzodiazepines appear to enhance the sensitivity of the GABA receptor, thus indirectly potentiating GABA-ergic neurotransmission in the brain.

Adenylyl Cyclase Inhibitors↗
PubMed1979

Properties of [3H]taurine release from crude synaptosomal fractions of rat cerebral cortex.

The release of previously accumulated [3H]taurine and [14C]GABA from crude synaptosomal (P2) fractions isolated from rat cerebral cortex was studied using a superfusion system. The spontaneous efflux of [3H]taurine and [14C]GABA was stimulated by elevated concentrations of K+ (15--133 mM) in a concentration-dependent manner. This K+-stimulated relase of [14C]Gaba but not of [3H]taurine was enhanced in the presence of Ca2+. However, addition of 3 mM Ca2+ to the superfusion medium in the presence of the ionophore A 23187 resulted in a stimulation of the release of both [3H]taurine and [14C]GABA. These results are discussed in connection with the cellular localization of taurine in the central nervous system.

Animals↗
PubMed1979

Stimulation of benzodiazepine receptor binding by gamma-aminobutyric acid.

The effect of the neurotransmitter gamma-aminobutyric acid (GABA) on high-affinity binding of benzodiazepines to brain membranes has been investigated. GABA stimulated [3H]diazepam binding by more than 100% when extensively washed membranes from brain tissue were used. This GABA-stimulated benzodiazepine binding occurred in all brain regions examined. The stimulation was specific for GABA agonist. It was inhibited by the GABA receptor blocker bicuculline methiodide. A large number of compounds structurally closely related to GABA but without direct effect on the GABA receptor failed to enhance [3H]diazepam binding. The stimulation of benzodiazepine binding was caused by an increase in affinity; the number of binding sites remained unchanged. Half-maximal activation of [3H]diazepam binding occurred in the presence of 300 nM muscimol or 900 nM GABA. beta-Guanidinopropionic acid and imidazoleacetic acid were much weaker activators. It is suggested that the described stimulation of benzodiazepine high-affinity binding is mediated by a receptor for GABA. This site of GABA action exhibits different properties when compared to GABA receptors, as characterized by high-affinity binding of GABA agonists.

Animals↗
PubMed1978

Evidence for an endogenous factor interfering with 3H-diazepam binding to rat brain membranes.

An in vitro "receptor" binding assay has been used to search for an endogenous compound which possibly interacts with benzodiazepine receptors in brain. Such an endogenous 3H-diazepam binding inhibitory factor (DIF) has been found. This compound is unevenly distributed in brain and in various peripheral organs. The partially purified compound appears to have a low molecular weight (below 500) and is not inactivated by proteolytic enzymes.

Animals↗
PubMed1977

Specific and sensitive method for the determination of gamma-aminobutyric acid using gas chromatography with electron-capture or mass fragmentographic detection.

A gas chromatographic method for the determination of gamma-aminobutyric acid (GABA) in brain tissue is described. After microwave fixation, the brains were dissected and homogenized in 0.1 N formic acid; delta-amino-n-valeric acid (AVA), a homologue of GABA, was then added as an internal standard. After centrifugation, aliquots of the supernatant were treated with cation-exchange paper to adsorb the amino acids. The eluates of this paper were dried and the residues subjected to reaction with trifluoroacetic anhydride and hexafluoroisopropanol. After removal of the derivatization reagents by evaporation, the residues were dissolved in ethyl acetate and an aliquot was analysed by gas chromatography with electron-capture or mass fragmentographic detection. Quantitation can be carried out by either peak-height or peak-area measurements. The specificity of this method has been demonstrated with brain tissue by simultaneous mass fragmentographic analysis. The sensitivity is comparable to that of mass fragmentographic methods and is in the femtomole range. The method is simple and readily automated.

Aminobutyrates↗
PubMed1977

Reversal by physostigmine of clozapine-induced delirium.

Clozapine, a new antipsychotic drug without extrapyramidal side effects and with strong sedating potency, can produce acute symptoms of central anticholinergic toxicity. The authors report that physostigmine, a reversible anticholinesterase agent, which can pass the blood-brain barrier, was effective in reversing the clozapine-induced brain syndrome in two patients. Physostigmine also reduced one patient's tachycardia.

Adult↗
PubMed1976

Quantitative determination of unconjugated pterins in urine by gas chromatography/mass fragmentography.

A gas chromatographic/mass fragmentographic method is described which permits the determination of unconjugated pterins in urine. After the addition of 6,7-dimethylpterin as an internal standard, the acidified urine samples are purified by liquid chromatography on Dowex-50 and Dowex-1 columns. The pterins are then converted to their corresponding trimethylsilyl derivatives and the base peaks of biopterin (m/e 409), neopterin (m/e 409) and 6,7-dimethylpterin (m/e 320) are determined. The method is sensitive and specific and permits the processing of large numbers of samples. By means of this method, the urinary excretion of biopterin and neopterin from 9 healthy subjects has been determined.

Chromatography, Gas↗