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HIPPOCAMPAL CIRCUIT UNDERLYING THE ENCODING OF NOVEL APPETITIVE FOOD
Hazim Eldirdiri Abdelrahmanand 6 co-authors
Centre de Neuroscience Sorbonne Université
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS06-09PM-256
Presentation
Date TBA
Board: PS06-09PM-256
Event Information
Poster Board
PS06-09PM-256
Poster
View posterAbstract
Novel experiences must be prioritized over familiar ones to optimize learning and memory. Hippocampal CA2 pyramidal cells are typically resistant to long-term potentiation (LTP) at the CA3-CA2 synapse. We show that exposure to a novel appetitive stimulus, sweetened condensed milk (SCM), transiently enables robust LTP following a theta-burst stimulation via NMDA receptor activation. Pharmacological activation of D1/D5 receptors with SKF38393 mimicked this facilitation, whereas prior SCM exposure occluded SKF-induced potentiation, indicating convergence on a dopaminergic mechanism. Dopamine dependence was confirmed when SCH23390 was used to block D1/D5 receptors, preventing the novelty-induced LTP. Additionally, social novelty also allowed TBS induced LTP in hippocampal area CA2, and prior social exposure occluded SKF-induced potentiation. Furthermore, it was shown that CA2 transmission onto CA1 is a key contributor in the well-established dopamine-mediated increase in CA1 output. This was demonstrated by chemogenetic suppression of CA2 pyramidal neurons using Gi-DREADDs and resulted in a loss of LTP in CA1. Taken together, these results demonstrate a novel role for hippocampal area CA2 in dopaminergic modulation of the hippocampal circuit during novel appetitive experience.
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