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Unlocking the Mechanism Behind Structural Plasticity of Dendritic Spines
Researchers from the Institute of Genetics and Developmental Biology of the Chinese Academy of Science uncovered the role of endophilin A1 in acute structural plasticity of dendritic spines during the acute phase of long-term potentiation.

Synapses are specialised cellular structures that facilitate communication between neurons. Synaptic plasticity is the ability of synapses to strengthen or weaken over time in response to neural activity. Exerting its effects on our emotions, thoughts, and behaviours, synaptic plasticity is considered the cellular basis of how we learn.

While mechanisms underlying long-term potentiation (LTP) have been extensively studied, how acute spine enlargement is achieved immediately after LTP stimulation remains to be known.

In this study, the researchers used super-resolution microscopy to visualise changes in the plasma membrane and F-actin content in dendritic spines of hippocampal neurons undergoing LTP.

They found that upon LTP induction, Ca2+/calmodulin protein in dendritic spines enhances endophilin A1 binding to the plasma membrane and p140Cap, a cytoskeletal regulator. This binding of endophilin A1 to the plasma membrane and the recruitment of p140Cap promotes local actin polymerisation, leading to spine head enlargement.

Further studies revealed that these molecular functions of endophilin A1 are needed for LTP and long-term memory. These findings uncovered a mechanism to explain acute spine enlargement in response to neuronal activity and demonstrated that this ability to change and expand plays an important role in LTP and long-lasting memory.

Source: Yang et al. (2021). Endophilin A1 drives acute structural plasticity of dendritic spines in response to Ca2+/calmodulin. Journal of Cell Biology, 220(6), e202007172.

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