title: Long-Term Potentiation: From CaMKII to AMPA Receptor Trafficking.
abstract: For more than 20 years, we have known that Ca(2+)/calmodulin-dependent protein kinase (CaMKII) activation is both necessary and sufficient for the induction of long-term potentiation (LTP). During this time, tremendous effort has been spent in attempting to understand how CaMKII activation gives rise to this phenomenon. Despite such efforts, there is much to be learned about the molecular mechanisms involved in LTP induction downstream of CaMKII activation. In this review, we highlight recent developments that have shaped our current thinking about the molecular mechanisms underlying LTP and discuss important questions that remain in the field.
authors: Department of Cellular and Molecular Pharmacology and.
authors: Bruce E
authors: BE
authors: Herring
authors: Department of Cellular and Molecular Pharmacology and.|Department of Physiology, University of California, San Francisco, California 94143; email: Bruce.Herring@ucsf.edu , Roger.Nicoll@ucsf.edu.
authors: Roger A
authors: RA
authors: Nicoll
mesh_terms: D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D006801:Humans; D017774:Long-Term Potentiation / Q000502:physiology*; D021381:Protein Transport / Q000502:physiology*; D018091:Receptors, AMPA / Q000378:metabolism*
chemical_list: D018091:Receptors, AMPA; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2
keywords: LTP; memory; plasticity; spine; synapse