Biomedical subjects
Publications and source records attributed to A Płaznik.
Gray's conception hypothesizes that anxiolytics act indirectly to impair the behavioural inhibition system through GABA-ergic modulation of the ascending NA and 5-HT pathways to the hippocampus. The obtained results support this theory.
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The influence of chronic treatment with desipramine upon GABAergic mechanisms within the nucleus accumbens septi (NAS) affecting rat motor behavior was studied in the automatic open fields. It was shown that intra-accumbens injections of picrotoxin on one hand and muscimol and baclofen on the other, produced dose-dependent increase or decrease in rat motility, respectively. Locomotor stimulation usually observed after picrotoxin did not occur in rats given local injections of a solution containing both picrotoxin and GABA A receptor agonist muscimol. Muscimol (130 ng as a pure compound) blocked also hypermotility produced by intra-accumbens administration of dopamine releasing drug d-amphetamine (10 micrograms). This part of the experiment was summarized as indicating that both GABA A and GABA B receptor-related mechanisms, which are under negative control of dopaminergic neurons in the NAS, play an important role in regulating behavior in the rat. In the second part of the experiment it was observed that chronic treatment of rats with desipramine (DMI) (10 mg/kg, PO, twice daily for 21 days, rats were tested 24 hr after the last dose of the drug) significantly attenuated or blocked the inhibitory effect on locomotion of both baclofen and muscimol. The stimulatory influence of picrotoxin seemed also to be diminished, but it still attained the level of accepted statistical significance. On the basis of these and other data it is concluded that observed changes in the effects of GABAergic agonists in DMI-treated rats are probably due to an enhancement of local dopaminergic mechanisms, thus leading to the potentiation of a negative interaction between dopaminergic and GABAergic mechanisms within the NAS.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of microinjections of noradrenaline (NA) and serotonin (5HT) into the basomedial part of the amygdaloid body (BM AB) on various forms of behavior were studied in rats. NA as well as 5HT administered to the BM AB had dose-related and general inhibitory influence on the rats' behavior in the open field test. The reactivity of rats to pain (tail compression) was attenuated by 5HT injections. The effect of NA in this test was less clear, though some inhibitory tendency was also present. Pretrial injections of NA (40 micrograms) and 5HT (40 micrograms) significantly impaired the retention of a passive avoidance reaction. NA injections also produced some disinhibitory effects on shock-suppressed drinking in the conflict test. The effects of intra-amygdalar administration of NA and 5HT on open field behavior were potentiated by pretreatment of rats with nialamide, a monoaminooxidase inhibitor. The results are discussed in terms of an involvement of the amydalar NA and 5HT in the regulation of animal behavior.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effects of repeated administration of nicotine on contextual fear conditioning, locomotor activity, and pain threshold, were examined in rats. It was found that a single injection of nicotine prior to the training session (three 0.7-mA footshocks, each 0.5 s long), decreased the freezing reaction during the retest 24 h later. The locomotor activity was moderately enhanced, and the pain threshold remained unchanged. The baseline freezing measured immediately after administration of a single dose of nicotine was not significantly different from the saline-treated group. The anxiolytic-like effect of nicotine was as potent as that of midazolam, a benzodiazepine derivative. After five day-by-day injections, the anxiolytic-like effect of nicotine (0.6 mg/kg, sc) was no longer present, independently whether the last drug injection was given 24 h or 5 min (i.e., the sixth, additional, nicotine injection), prior to the training session. Thus, it appeared that the expression of tolerance to the nicotine-induced anxiolytic-like action did not require a direct stimulation of nicotinic receptors. Simultaneously, in this group of animals, nicotine caused a potent stimulation of locomotor activity in the open field test. The applied dosage and regimen of nicotine administration did not change rat pain threshold (flinch-jump test). Collectively, the present data showed for the first time, that short-term, intermittent, administration of nicotine was sufficient to induce tolerance to the anxiolytic-like effect of this drug, in the model of fear conditioning to context. Importantly, a clear dissociation between the locomotor and anxiolytic-like effects of nicotine was present. This effect appeared independent also of changes in rat pain threshold. The possible mechanisms of this phenomenon are discussed.
Microinjections of clonidine into the locus coeruleus (LC) area synchronized rat cortical EEG. This effect of clonidine was attenuated by local pretreatment of rats with idazoxan, an alpha-2 adrenoceptor antagonist. The data indicate functional role of alpha-2 adrenoceptors within LC area in regulation of ceruleocortical activity, and point at the LC as one of brain targets for the sedative action of clonidine.
Effect of treatment with p-bromo-methamphetamine (V-111), the serotonin depleting drug, on two way avoidance conditioning (CAR) was studied in raphe lesioned male Wistar rats. Both sham lesioned and raphe lesioned animals treated with V-111 showed increased avoidance acquisition and increased number of inter-trial responses. Lesions of the raphe nuclei increased by itself the number of avoidance responses, the treatment with V-111 however produced further facilitation of avoidance acquisition. These results are discussed in terms of the role oserotonergic system in the processes of learning and retention of CAR, and direct action of V-111 on serotonergic system of the brain is suggested.