Defining the molecular targets of cerebellar PKG by quantitative (phospho)proteomics in a knock-out mouse model

Abstract

Background The NO/cGMP/PKG pathway plays a crucial role in the induction of cerebellar long term depression (LTD), synaptic plasticity, and motor learning. Previous studies showed that Purkinje cell specific PKG I knock-out mice exhibit strongly reduced LTD and deficits in adaptation of the vestibular ocular reflex [1]. To better understand the molecular mechanisms of PKG I and its involvement in LTD and motor learning, we combined the use of a mouse model deficient for PKG I expression with an LC-MS/MS based in-depth proteomics and phosphoproteomics analysis directly in cerebellum tissue.