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Tiunova, A.

Publications and source records attributed to Tiunova, A..

2 recordsLinked to original sources

Co-allocation of distinct contextual memories within a wide time window temporal dynamics and neuronal co-reactivation during retrieval

Recent studies have shown that a shared neuronal ensemble in the hippocampus links distinct contextual memories encoded within a certain time window (specifically, 5 hours, 2 and 7 days). Here we explored the temporal dynamics of two contextual (neutral and aversive) memories linking and analysed neuronal ensembles in the hippocampus, amygdala and different cortical regions reactivated during retrieval. Firstly, we have found that memories integrated across different time-points including several hours, days and weeks but not if learning phases was separated by short-term and very long-term time intervals. Secondly, we have demonstrated a higher neuronal co-reactivation in the hippocampus and amygdala during retrieval in case of memories integration that supports the hypothesis that shared neuronal ensembles link distinct memories. Finally, we have elicited that proportions of reactivated neuronal ensembles in these brain regions are greater in case of contextual memories integration.

neuroscience↗

Experience-specific anterograde amnesia: memory reacquisition deficit phenomenon and its characterization in the vertebrate learning model

A common assumption from experiments that interfere with memory consolidation is that the resultant amnesia returns the brain of an animal to a tabula rasa state with respect to disturbed experience. However, recent studies in terrestrial snail classical conditioning revealed an odd phenomenon: animals were unable to relearn conditioned avoidance of specific food after this memory had been impaired by protein-synthesis inhibitors or N-methyl-D-aspartate (NMDA) receptor antagonists. Here we examined whether such specific memory reacquisition deficit can also be observed in vertebrate learning. We trained day-old chicks in a one-trial passive avoidance task by presenting them a bead of a specific color covered with a repellent substance, methyl anthranilate. Training was preceded by administration of the protein synthesis inhibitor anisomycin or the NMDA receptor antagonist MK-801. Both drugs produced permanent amnesia, and no spontaneous recovery of memory was observed. A second training was given to the amnestic animals either using a bead of the same color (retraining) or a new color (novel training). The interval between the first and second training was 2 or 24 h, and the retention test was given from 30 min to 48 h after the second training. Retraining of the amnestic chicks with the bead that was presented during the initial training failed to produce new avoidance memory for this stimulus at all the between-training and training-to-test intervals. This memory reacquisition deficit was specific and was not transferred to a new conditioned stimulus, which was readily learned. We suggest that such pharmacologically induced experience-specific anterograde amnesia might reflect general properties of normal memory allocation, and we discuss its possible neural bases.

neuroscience↗