Memory reconsolidation and amnesia induction: Separate processes dependent on specific protein and RNA synthesis.

The reconsolidation hypothesis posits that memory retrieval initiates a phase of memory destabilization, followed by restabilization through protein synthesis-dependent processes. The disruption of reconsolidation by amnestic agents can lead to memory loss. Yet, this hypothesis leaves unanswered questions regarding the mechanisms driving amnesia induction and reversal of molecular and structural changes underlying memory retention.

Proteins or RNA synthesis inhibitors suppressed induction of amnesia developing under impairment of memory reconsolidation by serotonin receptors antagonist.

Studies have shown that retrieval of long-term memory can cause memory reconsolidation, and impaired reconsolidation leads to amnesia development. However, the mechanisms of amnesia induction due to impaired memory reconsolidation remains poorly described. Using experiments involving grape snails trained to conditioned food aversion, we studied the role of translation and transcription processes and the role of serotonin receptors in the mechanisms of amnesia induction.

AUDITORY EVOKED POTENTIALS EVIDENCE FOR DIFFERENCES IN INFORMATION PROCESSING BETWEEN HIGH AND LOW HYPNOTIZABLE SUBJECTS.

N100 and P300 auditory evoked potentials in 2-stimulus oddball paradigm were analyzed in high (HH, n = 18) and low (LH, n = 15) hypnotizable participants under waking condition. LH subjects committed more errors than HH subjects. HH subjects demonstrated shorter N100 latencies at frontal electrodes and significant N100 differences between target and nontarget stimuli (higher N100 amplitude and increased latency at parietal sites to targets vs.

Different components of conditioned food aversion memory.

Memory reconsolidation processes and protein kinase Mzeta (PKMzeta) activity in memory maintenance and reorganization are poorly understood. Therefore, we examined memory reconsolidation and PKMzeta activity during the maintenance and reorganization of a conditioned food aversion memory among snails. These processes were specifically evaluated after administration of a serotonin receptor antagonist (methiothepin), NMDA glutamate receptor antagonist (MK-801), protein synthesis inhibitor (cycloheximide; CYH), or PKMzeta inhibitor (zeta inhibitory peptide; ZIP) either 2 or 10 days after aversion training.

Transcription inhibitors prevent amnesia induced by NMDA antagonist-mediated impairment of memory reconsolidation.

Recent studies report that long-term memory retrieval can induce memory reconsolidation, and impairment of this reconsolidation might lead to amnesia. Previously, we found that reconsolidation of a conditioned food aversion memory could be disrupted by translation inhibitors for up to 3 h following a reconsolidation event, thus inducing amnesia. We examined the role of transcription processes in the induction of amnesia in the land snail, Helix lucorum.