Biomedical subjects

B Krespan

Publications and source records attributed to B Krespan.

5 recordsLinked to original sources

PubMed1985

Statistical analysis of temperature-dependent neuronal activity.

A set of computer programs which collect and analyze data on the temperature dependence of neuronal activity is described. Data on the response to thermal stimulation of cultured neurons of the rat preoptic area were collected and displayed on-line and were stored on disk for off-line analysis. Statistical analysis of the data examined two alternate models of thermosensitivity: one that the relationship between neuronal activity and temperature was well fit by a linear relationship and the other, that it was well fit by semi-log regression. For each of the models, a neuron was considered to have temperature-dependent activity if two criteria were met: first, that the model was considered adequate by a lack-of-fit F-test and second, that the slope of the regression line differed from zero using a t-test. A statistical method was also used to test the hypothesis that the neuronal response to temperature displays a change point. This method did not identify any neurons whose thermal response relationship could be better fit by two intersecting regression lines than by one regression line.

Action Potentials↗

PubMed1984

Electrophysiological studies on benzodiazepine antagonists.

The actions of the benzodiazepine (BDZ) antagonists 3-hydroxymethyl-beta-carboline (3-HMC), Ro 14-7437 and Ro 15-1788 were tested on single cell activity of rat hypothalamic neurons in tissue cultures and on membrane properties of CA1 hippocampal pyramidal neurons in transverse slices. In addition, we examined the interactions of some of these agents with inhibitions elicited by gamma-aminobutyric acid (GABA) as well as the ability of Ro 14-7437 to reverse the GABA-enhancing action of the BDZ agonist flurazepam. BDZ antagonists did not alter patterns of spontaneous activity of hypothalamic neurons and did not affect resting membrane potential or membrane conductance in CA1 pyramidal cells. Ro 14-7437 either partially or totally reversed the potentiation by flurazepam of GABA-elicited depression of hypothalamic neuronal activity. Small and inconsistent actions on GABA-mediated inhibitions of hypothalamic neurons were noted. Electrically-elicited inhibitions of hypothalamic neurons were either not altered or slightly reduced. In the hippocampal slice, the frequency of spontaneous IPSPs, the amplitude of stratum-radiatum evoked IPSPs and the conductance increase caused by stratum-radiatum stimulation were either not altered or slightly reduced. These findings demonstrate that non-convulsant BDZ antagonists block the action of BDZ agonists in facilitating GABA and further that the presence of a BDZ agonist is not required for these GABA-mediated events to occur. However, these experiments do not exclude a modulatory role for an endogenous BDZ agonist on GABA-mediated events.

Animals↗

PubMed1984

Anticonvulsant actions of fominoben: possible involvement of benzodiazepine receptors.

The purpose of this study was to examine the benzodiazepine-like activity of fominoben-HCl, a compound with prominent antitussive and respiratory stimulant actions. Towards this end we examined the anticonvulsant actions of fominoben as well as its ability to displace benzodiazepine (BDZ) binding from brain membranes. Scatchard analysis of binding data demonstrated that fominoben displaced 3H-flunitrazepam binding from rat cortical membrane preparations. Furthermore when tested against 3H-ethyl-beta-carboline-3-carboxylate, the addition of GABA resulted in a mean (+/- SE) shift of the IC50 from 4.05 +/- 0.10 microM to 2.2 +/- 0.05 microM, a characteristic of benzodiazepine agonists. Seizures were induced in male, Swiss Webster mice with pentylenetetrazol (PTZ) or 3-mercaptoproprionic acid (3-MP). Fominoben (50 and 100 mg/kg) completely protected mice from seizures induced by 50 mg/kg PTZ and elevated the seizure latency against 75 mg/kg of PTZ. The anticonvulsant effects of fominoben were less pronounced against 3-MP-induced seizures. The benzodiazepine antagonist Ro 15-1788 antagonized the anticonvulsant action of fominoben against both convulsants. Taken together, these data suggest that the anticonvulsant action of fominoben may be mediated by agonistic actions at benzodiazepine binding sites.

3-Mercaptopropionic Acid↗

PubMed1982

Alteration in neuronal-glial metabolism of glutamate by the neurotoxin kainic acid.

The effect of the excitotoxin kainic acid on glutamate and glutamine metabolism was studied in cerebellar slices incubated with D-[2-14C]glucose, [U-14C]gamma-aminobutyric acid, [3H]acetate, [U-14C]glutamate, and [U-14C]glutamine as precursors. Kainic acid (1 mM) strongly inhibited the labeling of glutamine relative to that of glutamate from all precursors except [2-14C]glucose and [U-14C]glutamine. Kainic acid did not inhibit glutamine synthetase directly. The data indicate that in the cerebellum kainic acid inhibits the synthesis of glutamine from the small pool of glutamate that is thought to be associated with glial cells. Kainic acid also markedly stimulated the efflux of glutamate from cerebellar slices and this release was not sensitive to tetrodotoxin. Kainic acid stimulated efflux of both glucose- and acetate-labeled glutamate. In contrast, veratridine released glucose-labeled glutamate preferentially via a tetrodotoxin-sensitive mechanism. Kainic acid did not release [U-14C]glutamate from synaptosomal fractions. These results suggest that the bulk of the glutamate released from cerebellar slices by kainic acid comes from nonsynaptic pools.

Acetates↗

PubMed1980

Effect of kainate on ATP levels and glutamate metabolism in cerebellar slices.

The levels of ATP and amino acids were measured in rat cerebellar slices incubated in the presence of the neurotoxin, kainic acid (KA). 0.1--1 mM KA caused a significant decrease in tissue content of ATP, glutamate, aspartate and glutamine. The levels of glutamate and aspartate, but not glutamine, rose concomitantly in the incubation medium. The results are consistent with a multiaction mechanism for the neurotoxicity of KA.

Adenosine Triphosphate↗