title: Overexpression of PKMζ alters morphology and function of dendritic spines in cultured cortical neurons.
abstract: Protein kinase M zeta (PKMζ), 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 PKMζ overexpression on the morphology and function of cortical neurons in primary cultures. Transfection with a plasmid construct expressing the PKMζ 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 PKMζ overexpressing cells. These results suggest that PKMζ is involved in regulation of dendritic spine structure and function, which may underlie its role in long-term synaptic and behavioral plasticity.
authors: Department of Neurobiology, The Weizmann Institute of Science, Rehovot 76100, Israel.
authors: Shiri
authors: S
authors: Ron
authors: Yadin
authors: Y
authors: Dudai
authors: Menahem
authors: M
authors: Segal
mesh_terms: D000818:Animals; D048429:Cell Size; D002470:Cell Survival; D002540:Cerebral Cortex / Q000201:enzymology* / Q000648:ultrastructure*; D049229:Dendritic Spines / Q000648:ultrastructure*; D055724:Electrophysiological Phenomena; D019706:Excitatory Postsynaptic Potentials / Q000235:genetics / Q000502:physiology; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology; D007150:Immunohistochemistry; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000201:enzymology* / Q000648:ultrastructure*; D010957:Plasmids / Q000235:genetics; D011493:Protein Kinase C / Q000096:biosynthesis* / Q000502:physiology; D051381:Rats; D013569:Synapses / Q000502:physiology; D014162:Transfection
chemical_list: D011493:Protein Kinase C; C504730:protein kinase M zeta, rat