INTRODUCTION: The brain is a highly dynamic structure capable of adapting to environmental changes and encoding experiences as memories. Learning involves activity-dependent modifications of synaptic connectivity, including the formation of new synapses through long-term potentiation (LTP) and the elimination of existing ones via long-term depression (LTD). Both processes can transiently produce glutamatergic synapses that are functionally silent, characterized by the presence of NMDA receptors and the absence of AMPA receptors. Our previous work demonstrated the formation of silent synapses in the central nucleus of the amygdala (CeA) during appetitive learning in mice. However, the underlying mechanisms—specifically whether these synapses result from LTP or LTD—remain unclear.

AIM(S): This study aimed to evaluate the role of LTP in appetitive learning

METHOD(S): by selectively knocking out the NR2B subunit of the NMDA receptor in the CeA, thereby impairing LTP. Behavioral assay and electrophysiological patch-clamp recordings were performed on NR2B knockout mice.

RESULTS: Behavioral assays in the IntelliCage system revealed a decreased sucrose preference in NR2B knockout mice compared with wild-type controls, indicating altered appetitive behavior. Complementary electrophysiological recordings demonstrated significant changes in NMDA receptor–mediated current kinetics, consistent with modified synaptic function in the CeA.

CONCLUSIONS: Our results indicate a significant alteration in neuronal functional activity.

FINANCIAL SUPPORT: Narodowe Centrum Nauki 2022/47/B/NZ4/02787