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Impaired synaptic plasticity and cAMP response element-binding protein activation in Ca2+/calmodulin-dependent protein kinase type IV/Gr-deficient mice.

http://www.ncbi.nlm.nih.gov/pubmed/10964952

The Ca(2+)/calmodulin-dependent protein kinase type IV/Gr (CaMKIV/Gr) is a key effector of neuronal Ca(2+) 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 Ca(2+)/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 Ca(2+)-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.

Pubmed ID: 10964952 RIS Download

Mesh terms: Animals | Brain | Calcium Signaling | Calcium-Calmodulin-Dependent Protein Kinase Type 4 | Calcium-Calmodulin-Dependent Protein Kinases | Cerebral Cortex | Cyclic AMP Response Element-Binding Protein | Electric Stimulation | Hippocampus | Long-Term Potentiation | Male | Maze Learning | Memory | Mice | Mice, Knockout | Motor Activity | Neuronal Plasticity | Neurons | Posture | Purkinje Cells | Pyramidal Cells | Reverse Transcriptase Polymerase Chain Reaction | Swimming | Synapses

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