Overexpression of PKMz Alters Morphology and Function of Dendritic Spines in Cultured

Protein kinase M zeta (PKMz), an atypical isoform of protein kinase C (PKC), has been implicated in long-term maintenance of neuronal plasticity and memory. However, the cellular machinery involved in these functions has yet to be elucidated. Here, we investigated the effects of PKMz overexpression on the morphology and function of cortical neurons in primary cultures. Transfection with a plasmid construct expressing the PKMz gene modified the distribution of spine morphologies and reduced spine length, while leaving total spine density and dendritic branching unchanged. A significant increase in magnitude but not frequency of miniature excitatory post synaptic currents was detected in the PKMz overexpressing cells. These results suggest that PKMz is involved in regulation of dendritic spine structure and function, which may underlie its role in long-term synaptic and behavioral plasticity.