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

Overview

abstract

  • 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.

publication date

  • February 2, 2001

Research

keywords

  • Corpus Striatum
  • Cyclic AMP Response Element-Binding Protein
  • Membrane Potentials
  • Neurons
  • Potassium Chloride
  • Receptors, N-Methyl-D-Aspartate

Identity

PubMed Central ID

  • PMC4203340

Scopus Document Identifier

  • 0035793442

Digital Object Identifier (DOI)

  • 10.1016/s0006-8993(00)03163-2

PubMed ID

  • 11164788

Additional Document Info

volume

  • 890

issue

  • 2