Circannual variations of GABA content in cytosolic and crude synaptosomal fractions in some brain areas of the european hamster

In the European hamster,Cricetus cricetus, a common hibernator, over a year, the γ-aminobutyric acid (GABA) content has been followed, in the cytosolic and crude synaptosomal fractions of the olfactocy bulbs, hypothalamus and cerebellum. In these 3 areas, the GABA content shows circannual variations of endogenous origin: in this period, in both fractions two peaks can be observed, at the beginning of spring and in autumn. These circannual variations do not follow the circannual variation of food intake or body weight.     

Event-related potentials before and after training: chronometry and lateralization of visual N1 and N2

Event-related potentials (ERPs) were recorded from normal right-handed males in visual-matching tasks before and after training to a high level of automaticity. The amplitude and latency of the left and right hemispheric N1 and N2 components were analyzed. While changes of N1 "after training" relative to "before training" were statistically non-significant, the N2 component appeared to be a sensitive indicator of the variability in chronometry and lateralization of cerebral processes modified by training. The N2 results suggest that with practice the physiological processes underlying performance in a visual-cognitive task become more efficient, selective and localized.     

Effect of sodium n-dipropylacetate on audiogenic seizures and brain -aminobutyric acid level

A brain γ-aminobutyric acid (GABA) level increase has been observed after n-dipropylacetate (nDPA) treatment. A relation between brain GABA level increase and protection against seizures has been pointed out; in fact, as long as the GABA rate is higher than 1.7 μmoles/g, mice are protected against audiogenic fits.Enzymatic studies have shown that nDPA inhibits competitively GABA-transaminase (GABA-T) in regard to GABA. Dreiding models show that there is a close structural relationship between GABA and nDPA, explaining the competitive inhibition.     

Inhibition of mouse killing behavior by serotonin-mimetic drugs: effects of partial alterations of serotonin neurotransmission

Rats which do not kill mice and which acquire mouse killing behavior after partial lesion of the serotonin neurotransmission, either by p-chlorophenylalanine treatment or by electrolytical lesions of dorsal and median raphe nucleus, were treated by IP injection of serotonin-mimetics. The following drugs were used: 5-methoxy-N-N-dimethyl-tryptamine and 8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide, serotonin-agonists, fluoxetine and citalopram, inhibitors of serotonin uptake. All these serotonin-mimetics inhibit mouse killing behavior without apparent secondary effects. When these compounds were tested on killer rats, a stronger antimuricidal effect was observed in rats having altered serotonin neurotransmission. These results support a role for the serotoninergic supersensitivity in a model of aggressive behavior.     

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