ABSTRACT
Anticonflict and antiamnestic effects of original D,L-carnitine chloride have been studied. By using a model of electroshock amnesia, carnitine chloride showed a pronounced antiamnestic effects, by positively affecting the behaviour of animals exposed to a conflict situation. The neuropharmacological effects of carnitine chloride have been found to be implicated in the metabolism of proteins and lipids.
Subject(s)
Amnesia/prevention & control , Anti-Anxiety Agents/pharmacology , Carnitine/pharmacology , Conflict, Psychological , Animals , Avoidance Learning/drug effects , Conditioning, Classical/drug effects , Diazepam/pharmacology , Dose-Response Relationship, Drug , Male , RatsABSTRACT
During experiments conducted on albino rats the deficiency of passive avoidance retention was shown to correlate not only with the reduction in REM sleep and SWS, but also with disappearance of phasic component of theta-rhythm. Drugs with nootropic mode of action (cleregyl, centrophenoxin, antioxidant 3-xypyridine) recovered the deficiency of passive avoidance retention and increased phasic component of theta-Rhythm, while phenazepam enhanced tonic component of theta-rhythm, and failed to act upon learning deficits. It seems likely from these results that the electrophysiological correlates of antiamnestic effect is the maintenance of proper two-component theta-rhythm and the increase in its phasic component, whereas the destructuring of sleep, including REM sleep reduction is not considered to be key determinant in the action upon memory and learning procedure.
Subject(s)
Amnesia/drug therapy , Electroencephalography/drug effects , Psychotropic Drugs/therapeutic use , Sleep Deprivation/physiology , Sleep, REM/physiology , Amnesia/physiopathology , Animals , Avoidance Learning/drug effects , Avoidance Learning/physiology , Conditioning, Classical/drug effects , Conditioning, Classical/physiology , Drug Evaluation, Preclinical , Electrodes, Implanted , Male , Rats , Sleep, REM/drug effectsABSTRACT
The influence of nootropic drugs of different chemical structure and mechanism of action (piracetam 200-800 mg/kg, meclofenoxate 50-100 mg/kg, nicergoline 1-4 mg/kg) on amnestic disturbances induced with electroconvulsive shock (ECS), scopolamine (2.5 mg/kg) and phenazepam (2.0 mg/kg) was studied in mice using passive avoidance test. All the investigated drugs possess distinct protective properties concerning different models of amnesia. In ECS-induced amnesia meclofenoxate was most effective, in scopolamine-induced amnesia--meclofenoxate and nicergoline, in phenazepam-induced amnesia all drugs were equally potent in profundity. It is supposed that neurophysiological mechanism of action of nootropic drugs is connected with directed activation of weakened memory trace of different etiology and its transmission into form receivable for transcription.
Subject(s)
Benzodiazepines , Memory Disorders/drug therapy , Psychotropic Drugs/therapeutic use , Amnesia/drug therapy , Amnesia/etiology , Animals , Anti-Anxiety Agents , Avoidance Learning/drug effects , Benzodiazepinones , Conditioning, Classical/drug effects , Drug Evaluation, Preclinical , Electroshock , Male , Meclofenoxate/therapeutic use , Memory Disorders/etiology , Mice , Nicergoline/therapeutic use , Piracetam/therapeutic use , Reaction Time/drug effects , Scopolamine , Structure-Activity RelationshipABSTRACT
The spectrum of the pharmacological activity of piracetam administered for a long time was studied in experiments on mice and rats. It was established that administration of piracetam (300-400 mg/kg i. p.) for 10-42 days brought about potentiation of its antiamnestic effect, retardation of the processes of extinction, an increase in the emotional responsiveness, and preservation of the tranquilizing effect with no side effects (sedative or myorelaxant). The characteristic feature of piracetam effect on the extinction is its ability to decelerate this process only after its prolonged administration. It is assumed that under prolonged administration of piracetam there takes place the formation of a new functional system ensuring the memory trace stabilization.