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Potassium chloride depolarization mediates CREB phosphorylation in striatal neurons in an NMDA receptor-dependent manner.

Macías W, Carlson R, Rajadhyaksha A, Barczak A, Konradi C
Brain Res. 2001 890 (2): 222-32

PMID: 11164788 · PMCID: PMC4203340 · DOI:10.1016/s0006-8993(00)03163-2

Potassium chloride (KCl)-depolarization has been used to study the properties of L-type Ca2+ channel-mediated signal transduction in hippocampal neurons. Calcium influx through L-type Ca2+ channels stimulates a second messenger pathway that transactivates genes under the regulatory control of the Ca2+-and cyclic AMP-responsive element (CRE). Here, we show that in striatal neurons, but not in hippocampal neurons, CRE binding protein (CREB) phosphorylation and CRE-mediated gene expression after KCl-depolarization depends on functional NMDA receptors. This difference in NMDA receptor dependence is not due to different properties of L-type Ca2+ channels in either neuronal type, but rather to different neuron-intrinsic properties. Despite this variation, the second messenger pathway activated by KCl requires Ca2+/calmodulin (CaM) kinase for CREB phosphorylation in both neuronal types. We conclude that depolarization by KCl works differently in striatal and hippocampal neurons.

MeSH Terms (23)

Animals Calcium-Calmodulin-Dependent Protein Kinases Calcium-Calmodulin-Dependent Protein Kinase Type 1 Calcium Channel Agonists Calcium Channels, L-Type Cells, Cultured Corpus Striatum Cyclic AMP Response Element-Binding Protein DNA-Binding Proteins Excitatory Amino Acid Antagonists Fetus Gene Expression Regulation Hippocampus Membrane Potentials Neurons Nuclear Proteins Phosphorylation Potassium Chloride Pyrroles Rats Receptors, GABA Receptors, N-Methyl-D-Aspartate Serum Response Factor

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