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The Journal of Neuroscience, October 26, 2005, 25(43):9883-9892; doi:10.1523/JNEUROSCI.1531-05.2005
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Cellular/Molecular
Role of Hippocampal Cav1.2 Ca2+ Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory
Sven Moosmang,1 Nicole Haider,1 Norbert Klugbauer,1 Helmuth Adelsberger,1 Nicolas Langwieser,1 Jochen Müller,1 Michael Stiess,1 Else Marais,1 Verena Schulla,1 Lubica Lacinova,1 Sandra Goebbels,2 Klaus-Armin Nave,2 Daniel R. Storm,3 Franz Hofmann,1 andThomas Kleppisch1 1Institut für Pharmakologie und Toxikologie, Technische Universität München, 80802 München, Germany, 2Max-Planck-Institut für Experimentelle Medizin, 37075 Göttingen, Germany, and 3Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280
Current knowledge about the molecular mechanisms of NMDA receptor (NMDAR)-independent long-term potentiation (LTP) in the hippocampus and its function for memory formation in the behaving animal is limited. NMDAR-independent LTP in the CA1 region is thought to require activity of postsynaptic L-type voltage-dependent Ca2+ channels (Cav1.x), but the underlying channel isoform remains unknown. We evaluated the function of the Cav1.2 L-type Ca2+ channel for spatial learning, synaptic plasticity, and triggering of learning-associated biochemical processes using a mouse line with an inactivation of the CACNA1C (Cav1.2) gene in the hippocampus and neocortex (Cav1.2HCKO). This model shows (1) a selective loss of protein synthesis-dependent NMDAR-independent Schaffer collateral/CA1 late-phase LTP (L-LTP), (2) a severe impairment of hippocampus-dependent spatial memory, and (3) decreased activation of the mitogen-activated protein kinase (MAPK) pathway and reduced cAMP response element (CRE)-dependent transcription in CA1 pyramidal neurons. Our results provide strong evidence for a role of L-type Ca2+ channel-dependent, NMDAR-independent hippocampal L-LTP in the formation of spatial memory in the behaving animal and for a function of the MAPK/CREB (CRE-binding protein) signaling cascade in linking Cav1.2 channel-mediated Ca2+ influx to either process.
Key words: calcium channels; learning; memory; NMDA receptor independent; Cav1.2; synaptic plasticity
Received April 19, 2005; revised September 5, 2005; accepted September 6, 2005.
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