Potassium chloride depolarization mediates CREB phosphorylation in striatal neurons in an NMDA receptor-dependent manner.
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.
Macías
W
W
Molecular and Developmental Neuroscience Laboratory, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Carlson
R
R
Rajadhyaksha
A
A
Barczak
A
A
Konradi
C
C
D000818:Animals; D002120:Calcium Channel Agonists / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000378:metabolism; D054729:Calcium-Calmodulin-Dependent Protein Kinase Type 1; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000187:drug effects / Q000378:metabolism; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D017362:Cyclic AMP Response Element-Binding Protein / Q000187:drug effects / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000187:drug effects / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005333:Fetus; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009687:Nuclear Proteins / Q000187:drug effects / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D011189:Potassium Chloride / Q000494:pharmacology*; D011758:Pyrroles / Q000494:pharmacology; D051381:Rats; D018079:Receptors, GABA / Q000187:drug effects / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000378:metabolism*; D026362:Serum Response Factor
D002120:Calcium Channel Agonists; D020746:Calcium Channels, L-Type; D017362:Cyclic AMP Response Element-Binding Protein; D004268:DNA-Binding Proteins; D018691:Excitatory Amino Acid Antagonists; D009687:Nuclear Proteins; D011758:Pyrroles; D018079:Receptors, GABA; D016194:Receptors, N-Methyl-D-Aspartate; D026362:Serum Response Factor; C071658:FPL 64176; D011189:Potassium Chloride; D054729:Calcium-Calmodulin-Dependent Protein Kinase Type 1; D017871:Calcium-Calmodulin-Dependent Protein Kinases; C517599:Camk1 protein, rat; C517682:Pnck protein, rat