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R Y Ilyutchenok

Publications and source records attributed to R Y Ilyutchenok.

11 recordsLinked to original sources

Memory retrieval enhancement by kappa opioid agonist and mu, delta antagonists.

The present study sought to identify specific opioid receptor subtypes involved in the modulation of reactivation of amnesic or forgotten memory traces by use of a one-trial inhibitory avoidance training procedures in mice. The effects of naloxone, ICI 174,864 (mu and delta opioid receptor antagonists, respectively) and dynorphin (kappa agonist) were investigated. The results indicated that preretention test administration of naloxone (2 mg/kg) or ICI 174,864 (3 mg/kg) attenuated the amnesia and forgetting as indicated by prolongation of step-through latency. On the other hand, the activation of kappa opioid receptors by dynorphin (1 mg/kg) also showed reactivating effects both after amnesia and forgetting. On the basis of the parallelism of the effects for mu and delta opioid receptor antagonists and kappa agonist, and on the finding that all three opioids demonstrated a different degree of reactivation of amnesic and forgotten memory traces, it was concluded that mu, delta, and kappa opioid receptors contribute to the modulation of amnesia and forgetting by independent mechanisms.

Analysis of Variance↗

Neurochemical mechanisms of memory control.

Modulation of memory trace retrieval in emotiogenic brain structures, cortex and brainstem reticular formation by postsynaptic noradrenergic and dopaminergic drugs was found. At the initial stage of latent inhibition-a most significant mechanism of information selection-memory trace retrieval is retarded in all structures and in the cortex and the zona incerta later on. A haloperidol model of latent inhibition was obtained. Most important role of dopaminergic system in latent inhibition was shown. Inhibition of the GABA-benzodiazepine-ionophore complex by the blockade of GABA-receptors induced by bicuculline, the chloride channels by picrotoxin, the benzodiazepine receptors by flumazenil (R015-1788) and R015-3505 facilitates the memory trace retrieval damaged by amnesic agent. The dopaminergic activation enhances the dominant state and developes conditions for switching on the interferential GABA-ergic inhibition.

Amnesia↗

The emotiogenic brain structures in conditioning mechanisms: conditioned evoked potentials and motor responses.

The emotiogenic rnorphofunctional control system consists of the amygdaloid complex (AM), the zona incerta, the peri- and paraventricular nuclei of the hypothalamus and the midbrain central gray matter (CG). The neuronal relationships between the structures of this system were established. Lesions of these structures prevented one-trial learning, whereas electrical stimulation of the AM or the CG permitted retrieval of a trace which was lower than threshold. AM stimulation accelerated learning by 5-10 times. The possible mechanisms of the emotiogenic control system of memory' are discussed. The contribution of the identified structures of the emotiogenic control system of memory was quantitatively estimated, by employing a matrix of the interaction of these structures during the performance of conditioned neurographic responses of the radial nerve. The approach established the role of the emotiogenic control system in the spatial-temporal organization of brain structures needed for the retrieval of conditioned motor responses. Weakly trained cats, in which the AM-CG had been stimulated, did not differ from well trained ones in the patterns and correlation matrices of the conditioned evoked potentials. AM-CG activation may accelerate learning by reproducing such spatial-temporal relationships that are characteristic of well trained animals.

Amygdala↗