Abstract
It is well established that neurons are plastic and can change the strength of their connections with other neurons depending on their recent history. While many molecular entities involved in plastic processes were already described, the role of a store-operated calcium channel ORAI1 in neuronal plasticity is not known as yet. Using dominant negative form of ORAI1, we were able to show that ORAI1 is needed for formation of new dendritic spines following chemical induction of long term potentiation (cLTP), and that this is due to the release of Ca+2 from ryanodine receptor-associated endoplasmic reticulum stores. We propose that when ORAI1 is deficient, there is less Ca+2 in the stores, less releasable Ca+2 and consequently less LTP and spine formation.
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