2022 Undergraduate Research Symposium

Sana Latif (neuroscience)

Faculty mentor: Joongkyu Park

Abstract

Learning and memory are critical functions that allow organisms to adapt to and respond to their environment. Long-term potentiation (LTP) is an important model for memory and involves the persistent strengthening of synapses. Ca2+/calmodulin-dependent protein kinase II alpha (CaMKIIα) is a kinase that has been identified as essential for the establishment of LTP.

Due to its critical role in synaptic plasticity and memory formation, the enhancement of CaMKIIα function has been studied as a mechanism to improve memory formation. The novel intrabody VHH Anti-GluN1 (VHHAN1) developed by our lab has been shown to localize to and bind to endogenous N-methyl-D-aspartate receptors (NMDARs) in mouse models. The influx of Ca2+ was expected to activate the downstream target CaMKIIα which has been implicated in LTP. Previously, we showed that VHHAN1 could bind endogenous NMDARs in mouse brains and that we could bring CaMKIIα to the NMDAR location, where LTP initiates. This molecular approach was termed CLEVIR (CaMKIIα Local Enrichment by VHH for Improvement of memory).

This local enrichment of CaMKIIα by the intrabody in the hippocampus improved contextual memory. Nevertheless, many questions remain. Since long-term memory is linked to the cerebral cortices, it is possible that applying the CLEVIR approach to broader regions of the brain can improve contextual memory better. We hypothesized that global expression of the CLEVIR (VHHAN1-CaMKIIα) approach in CaMKIIα expressing neurons of the hippocampal CA3, dentate gyrus, and cortices could improve memory processes more effectively as compared to CaMKIIα alone.

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