The influence of diazepam (1 and 5 mg/kg, i. p.) and buspirone (5 and 10 mg/kg) on the Fourier's spectral EEG power of sensomotor cortex and a conflict behavior in freely moving rats were studied. Diazepam (1 mg/kg) and buspirone (5 mg/kg) produced slowing of EEG theta-activity. Large doses of diazepam and buspirone produced different and multiple EEG effects. To 15-1788 (10 mg/kg) completely antagonized all the effects of diazepam (5 mg/kg). The authors discuss possible mutual relations between the influence on EEG and anxiolytic effect of these tranquilizers.

Animals↗

PubMed1987

[Change in the behavioral and electrophysiological indices in rats with cerebrovascular disorders].

Behavioural and electrophysiological indexes have been investigated during bilateral ligation of common carotid arteries in rats. It has been established that 24 hours after cerebrovascular disorders blood flow in parietal cortex decreased by 61 +/- 7.8%. At the same time disorders of the vital functions have been observed, namely, death of animals, progressive weight loss, reduced resistance to anoxia. Disorders in instinctive behaviour were noted, such as inversion in preference of dark section to the light one, and diminished elaboration of conditioned reflex in a shuttle-box, as evidenced by the low correct responses to intersignal reactions ratio. In case of cerebrovascular disorders test response was depressed, it reflecting disorders in the cortical system of recurrent inhibition and indicating the decrease in the functional activity of GABAergic processes.

Animals↗

PubMed1986

[Piracetam correction of deficient GABA-ergic inhibition due to early postnatal exposure to cycloheximide].

Cycloheximide, administered to 7-day-old rats, caused the delay of CNS activity changes in grown-up rats. The animals showed impaired memory function, expressed in the decrease of habituation in the "open field" test, and the alteration of passive avoidance reflex. The increased number of intersignal reactions due to hypermotility was found during elaboration of avoidance reflex. The analysis of evoked potential recovery revealed the deficiency of GABA-ergic inhibition in the neocortex. Piracetam was shown to prevent completely behavioural disturbances and deficiency of GABA-ergic processes in grown-up animals.

Animals↗

PubMed1985

[Antagonism of RO 15-1788 with benzodiazepines in the effect on motivated aggression and the action of analgesics].

The influence of Ro 15-1788 and bicuculline on the action of GABA-positive drugs (muscimol), GABA cethyl ester, piracetam and depakine and benzodiazepine tranquilizers (diazepam, phenazepam) on motivated aggression has been studied. It has been shown that Ro 15-1788 which has a weak antiaggressive effect selectively antagonizes the anti-aggressive effect of tranquilizers but not that of GABA-positive drugs. Bicuculline antagonizes antiaggressive activity of the drugs of both types. The action of these antagonists on the effect of the drugs under study as regards the analgetic activity of morphine was also studied. It has been shown that Ro 15-1788 antagonizes the potentiation of morphine analgesia caused by diazepam. At the same time Ro 15-1788 does not influence morphine analgesia potentiated by muscimol. Bicuculline removes the potentiation of morphine analgesia caused both by diazepam and muscimol it is concluded that bicuculline-sensitive GABA receptors modulate the antiaggressive effect of benzodiazepines and their influence on the analgetic action of opiates.

Aggression↗

PubMed1985

[Effect of the antioxidant dibunol and its combination with phenazepam on the behavior of rats in a conflict situation].

The influence of dibunol, phenazepam used alone and combined on rat conflict behavior and rat blood and brain malonic dialdehyde content was studied. It was shown that dibunol exerts an unmarked anticonflict action that can be removed by bicuculline. Combined administration of dibunol and phenazepam potentiates appreciably the anticonflict effect. This permits reducing the doses of the drugs. The anxiolytic effect of dibunol alone and combined with phenazepam is attended by a decrease in the content of malonic dialdehyde in rat blood and brain, evidence of the reduction of the lipid peroxidation intensity.

Animals↗

PubMed1983

[Effect of triftazin and haloperidol on the activity of phenazepam].

The effects of trifluoperazine and haloperidol on protective activity of phenazepam were studied during seizures in mice treated with pentylenetetrazole (an index used for the appraisal of tranquilizing activity) as was their action on the phenazepam-induced depression of the test potential in the recovery cycles of somatosensory primary response. Trifluoperazine administered in doses of 0.1-0.5 mg/kg potentiated anticonvulsant action of phenazepam but did not change its effects on the recovery cycles of primary response. Haloperidol also potentiated anticonvulsant action of phenazepam. However, the doses administered were 4-5-fold lower than the tranquilizing doses of haloperidol. The drug also increased the depression of the test potential in the somatosensory recovery cycle, caused by phenazepam. This suggests an increment of GABA-positive effect of the tranquilizer. It appears that higher activity of haloperidol in elevating anticonvulsant and, probably, anxiolytic effects of phenazepam is determined by interaction of these drugs on the level of cortical GABA-ergic receptors.

Animals↗

PubMed1982

[Neuropharmacological properties of piracetam derivatives].

Piracetam and its 8 derivatives were studied in experiments on mice and rats with the use of standard neurotropic tests and nootropic activity tools. The electrophysiological index of GABA-ergic inhibition (the recovery cycle of cortical evoked potentials) was also investigated. It was shown that piracetam derivatives as well as piracetam itself have a pronounced antihypoxic activity and prevent the amnestic effect of electroshock in experimental passive avoidance. Most of them were inactive according to the standard neurotropic test. Piracetam derivatives with a hydrazide grouping in the side chain combine nootropic activity and a specific stimulant effect, while the derivatives possessing a phenyl ring combine nootropic and depressant activity.

Amnesia, Retrograde↗

PubMed1982

[GABA-ergic cortical component in the action of piracetam and cetyl GABA].

The effect of piracetam on the electrophysiological and biochemical characteristics of the GABA system was studied and compared to that of cethyl ether of GABA (CEGABA). It was shown that piracetam (250-500 mg/kg) enhances the test response depression in the primary response recovery cycle and produces synchronization of the ECoG of the sensomotor cortex similarly to the previously described GABA-positive substances. The synchronizing effects of piracetam are retained upon isolation of the cortex and can be removed by bicucullin (rather than by strychnine) applied to the cortex. Piracetam decreases the GABA content in the brain cortex and inhibits the activity of glutamate decarboxylase. Analogous effect is exerted by CEGABA. A conclusion is drawn that GABA-ergic processes get potentiated under the effect of both the drugs. The selectivity of piracetam effects as to the cortical GABA-ergic inhibitory systems is likely to be the reason for the absence in the drug of anticonvulsant effect inherent in GABA mimetics with more generalized effects (CEGABA, muscimol).

Animals↗

PubMed1981

[Study of the activating effect of small doses of haloperidol].

The effect of low doses of haloperidol was studied by means of screening and electrophysiological tests. In doses of 0.05--0.15 mg/Kg haloperidol exerts an activating effect which manifests in the elevation of motility, in the potentiation of the convulsant effect of bicuculline, EEG desynchronization and decrement of test response depression in the recovery cycle of the somatosensory primary response. The data obtained suggest that the activating effect of haloperidol is due to the weakening of inhibitory processes in the brain.

Animals↗

PubMed1980

[Participation of GABA-ergic structures in producing the effects of haloperidol].

A study was made of the effect of haloperidol on convulsions induced in mice by bicuculline and thiosemicarbazide and on the recovery cycles of the primary response in the rat sensorimotor cortex. In doses of 0.3--0.5 mg/kg producing a tranquilizing effect, haloperidol exerts a protective action in convulsions induced by bicuculline blocking of the GABA receptors and enhances the depression of the testing response during recovery cycle of the rat sensorimotor cortex primary response. It means that over this dosage range haloperidol potentiates GABA-induced effects. An increase in the neuroleptic dose up to 1--2 mg/kg entails disappearance of the efficacy shown by both the tests. The authors' own and reported data suggest an important role played by the postsynaptic GABA-positive effect in realization of the tranquilizing action of haloperidol and other neurotropic agents.

Animals↗

PubMed1978

[Participation of cholinergic mechanisms in realizing the effects of bicuculline].

Screening and electrophysiological methods were applied to the verification of the hypothesis on a possibility of participation of cholinergic structures in the realization of bicucullin effects. M- and N-cholinolytics (benactizine, atropine, aprophen, and pediphen) failed to arrest the convulsions induced in mice by bicucullin adminstration. At the same time substances inducing accumulation of gamma-aminobutyric acid (GABA) in the brain, i.e. aminooxycetic acid and depakin produced a manifest protective action in convulsions caused by bicucullin administration. In electrophysiological experiments there was also revealed an incapacity of M-cholinolytic benaltizine to arrest the bicucullin effects. Bicucullin proved to diminish depression of the test response in the restoration cycle of the primary response of the rat sensory motor cortex at the intervals of 40--125ms between the stimuli, whereas benactizine decreased the late facilitation of the test response at the intervals of 150--300ms between the stimuli. There was also noted no interaction between benactizine and bicucullin by this test. On the basis of these data a conclusion was drawn that bicucullin effects were caused by the block of postsynaptic GABA receptors, and were not connected with the cholinergic structures activity.

Animals↗