Authors:

Amina Basharat

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About Paper:

Neuronal junctions have the ability to change their connective strength depending on the input signal received at the post-synaptic area. This concept, known as synaptic plasticity, is crucial for learning and memory formation. A major decline in synaptic plasticity is characteristic of patients with neurodegenerative diseases such as Alzheimer's (AD). To comprehend this decline, it is necessary to better grasp the protein interactions of this phenomenon. Ca2+ signaling is key in controlling long-term potentiation (LTP). Its influx into dendritic spines initiates signaling pathways that modify the shape of spines through actin remodeling. Within dendrites, actin filament structure and organization undergo dynamic modifications. Actin polymerization is mainly governed by Ca2+/Calmodulin Dependent Kinase II (CaMKII) activity. Calcium dysregulation renders the cells to lose structure and ability to form synaptic connections. Thus, there is a need to investigate the role of CaMKII and actin colocalization in the dendritic growth dynamics. Protein interactions were detected via the proximity ligation assay (PLA) to measure the proximity of actin and CaMKII colocalization after chemically induced LTP vs control. Immunostaining of rat cultured hippocampal neurons with antibodies visualized the proteins of interest to study these interactions in more detail. Fluorescence results in cellular imaging showed the proximity of labeled CaMKII and actin, as well as potential interaction sites in a given frame of time. These results give insights into how CaMKII and actin interactions occur in space and time, as well as how they influence dendritic dynamics to establish LTP.

Source:

Purdue University / 2023

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Co-authors:

Amina Basharat