Abstract
Rac1 is a small GTPase of the Rho family. A previous study showed that the activation of Rac1 had an opposing effect on induction and maintenance of long-term potentiation (LTP) in the hippocampus. However, the molecular mechanism underlying this opposing effect remains to be addressed. In the present work, we find that the activation of Rac1 during the induction of LTP leads to an activation of PKCι/λ by phosphatidylinositol-3-kinase (PI3K), whereas the activation of Rac1 during the maintenance of LTP leads to the inhibition of PKMζ by LIM_kinase (LIMK) in the hippocampus. This result suggests that during different stages of LTP, the activation of Rac1 can modulate different signaling pathways, which leads to an opposing effect on the induction and maintenance of LTP in the hippocampus.
Highlights
Small GTPases are important signaling molecules in neurons
Martinez and Tejada-Simon (2011) reported that the induction of longterm potentiation (LTP) in the hippocampus was coupled with the activation of Rac1 and the inhibition of Rac1 suppressed the induction of LTP in a dose-dependent manner (Martinez and Tejada-Simon, 2011)
Martinez and Tejada-Simon (2011) reported that the induction of LTP in the hippocampus was coupled with the activation of Rac1 in area CA1 and the inhibition of Rac1 suppressed the induction of LTP in a dose-dependent manner (Martinez and Tejada-Simon, 2011)
Summary
One of the best characterized subfamilies of the small GTPases is the Rho family, which includes Rac, Cdc, and Rho (Hall, 2005). Rac has been reported to be involved in morphological plasticity in the hippocampus. Rac participates in functional plasticity in the hippocampus. During the maintenance phase of LTP in the hippocampus, it appeared that the activation of Rac had an opposing effect on LTP. Liu et al reported that the application of an adeno-associated virus that carried transgene to activate Rac during the maintenance phase of LTP resulted in an accelerated LTP decay in the hippocampus (Liu et al, 2016). The molecular mechanism underlying the opposing effect of the activation of Rac on the induction and maintenance of LTP in the hippocampus remains to be addressed
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