MODULATION OF BEHAVIORAL TAGGING–MEDIATED MEMORY CONSOLIDATION AND SYNAPTIC PLASTICITY BY AMYLOID BETA<S>​</S>

Behavioral Tagging (BT) offers a conceptual framework for investigating the consolidation of transient learning experiences into long-term memory when paired with short novelty exposure. This method relies on the tagging of active synapses during learning and the ensuing availability of plasticity-related proteins (PRPs) induced by the new experience. This research utilized a contextual fear conditioning paradigm in adult male Wistar rats to examine BT-induced memory consolidation. Animals exposed to novelty shortly after minimal training exhibited significantly heightened freezing behavior throughout a 24-hour recall period, with no differences noted during acquisition indicating enhanced long-term memory consolidation.
A molecular investigation revealed increased expression of synaptic plasticity markers, including BDNF, PSD-95, and CaMKII, in the hippocampus and prefrontal cortex of rats subjected to novel stimuli. CAPRIN-1, an RNA-binding protein involved in synaptic translation, demonstrated elevated expression correlated with memory capacity, hence supporting its potential role in PRP regulation.
To explore how BT mechanisms are modulated under pathological conditions, we are extending this approach to a rat model of Alzheimer’s disease via intrahippocampal injection of Aβ^₁–₄₂ . In this phase, we will evaluate whether novelty can still enhance or fails to rescue novelty driven memory consolidation markers such as PSD-95 and Homer1, a synaptic scaffolding protein implicated in glutamatergic signaling in the presence of amyloid burden.
Learning and consolidation may change hippocampal-prefrontal synchronization, hence in vivo electrical recordings are proposed.
These findings position BT as a sensitive tool for studying synaptic plasticity, with relevance for understanding early cognitive decline in Alzheimer’s disease.