Not only do neurons lacking Pten have drastic morphological aberrations, but they also have significant changes in firing properties and synaptic plasticity. Pten+/− mice have decreased LTP and completely abolished NMDA-dependent LTD in hippocampal CA1 synapses (Wang et al., 2006). Moreover, Pten conditional knockouts (GFAP-Cre) also have decreased LTP in CA1 synapses (Fraser et al., 2008), whereas dentate granule cell synapses have impaired mGluR-dependent LTD (Takeuchi et al., 2013). Importantly, postnatal deletion of Pten with CamKIIα-Cre reproduced the deficits in LTP and LTD at CA1 synapses but had no effect on neuronal or dendritic morphology, thus indicating these phenotypes are not necessarily associated (Sperow et al., 2012).
