RT Journal Article SR Electronic T1 Impaired Synaptic Plasticity and cAMP Response Element-Binding Protein Activation in Ca2+/Calmodulin-Dependent Protein Kinase Type IV/Gr-Deficient Mice JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 6459 OP 6472 DO 10.1523/JNEUROSCI.20-17-06459.2000 VO 20 IS 17 A1 Nga Ho A1 Jason A. Liauw A1 Frank Blaeser A1 Feng Wei A1 Silva Hanissian A1 Lisa M. Muglia A1 David F. Wozniak A1 Anthony Nardi A1 Kara L. Arvin A1 David M. Holtzman A1 David J. Linden A1 Min Zhuo A1 Louis J. Muglia A1 Talal A. Chatila YR 2000 UL http://www.jneurosci.org/content/20/17/6459.abstract AB The Ca2+/calmodulin-dependent protein kinase type IV/Gr (CaMKIV/Gr) is a key effector of neuronal Ca2+ signaling; its function was analyzed by targeted gene disruption in mice. CaMKIV/Gr-deficient mice exhibited impaired neuronal cAMP-responsive element binding protein (CREB) phosphorylation and Ca2+/CREB-dependent gene expression. They were also deficient in two forms of synaptic plasticity: long-term potentiation (LTP) in hippocampal CA1 neurons and a late phase of long-term depression in cerebellar Purkinje neurons. However, despite impaired LTP and CREB activation, CaMKIV/Gr-deficient mice exhibited no obvious deficits in spatial learning and memory. These results support an important role for CaMKIV/Gr in Ca2+-regulated neuronal gene transcription and synaptic plasticity and suggest that the contribution of other signaling pathways may spare spatial memory of CaMKIV/Gr-deficient mice.