Together, our results implicate Rac1 hyperactivity in synaptic plasticity and cognitive deficits observed in <i>Cc2d1a</i> cKO mice and reveal a novel role for CC2D1A in regulating hippocampal synaptic function.<b>SIGNIFICANCE STATEMENT</b> CC2D1A is abundantly expressed in the brain, but there is little known about its physiological function.
The results of the study suggest that Rac1 GTPase has a critical role in mediating ischemia/reperfusion injury-induced NADPH oxidase activation, ROS generation and oxidative stress in the hippocampal CA1 region of the rat, and thus contributes significantly to neuronal degeneration and cognitive dysfunction following cerebral ischemia.