Dopamine and cAMP-regulated phosphoprotein 32 kDa controls both striatal long-term depression and long-term potentiation, opposing forms of synaptic plasticity

J Neurosci. 2000 Nov 15;20(22):8443-51. doi: 10.1523/JNEUROSCI.20-22-08443.2000.

Abstract

A complex chain of intracellular signaling events, critically important in motor control, is activated by the stimulation of D1-like dopamine (DA) receptors in striatal neurons. At corticostriatal synapses on medium spiny neurons, we provide evidence that the D1-like receptor-dependent activation of DA and cyclic adenosine 3',5' monophosphate-regulated phosphoprotein 32 kDa is a crucial step for the induction of both long-term depression (LTD) and long-term potentiation (LTP), two opposing forms of synaptic plasticity. In addition, formation of LTD and LTP requires the activation of protein kinase G and protein kinase A, respectively, in striatal projection neurons. These kinases appear to be stimulated by the activation of D1-like receptors in distinct neuronal populations.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials / drug effects
  • Animals
  • Corpus Striatum / drug effects
  • Corpus Striatum / metabolism*
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Cyclic GMP / metabolism
  • Cyclic GMP-Dependent Protein Kinases / metabolism
  • Dopamine and cAMP-Regulated Phosphoprotein 32
  • Electric Stimulation
  • Enzyme Inhibitors / pharmacology
  • In Vitro Techniques
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / physiology*
  • Male
  • Mice
  • Mice, Knockout
  • Nerve Tissue Proteins*
  • Neural Inhibition / drug effects
  • Neural Inhibition / physiology*
  • Neuronal Plasticity / drug effects
  • Neuronal Plasticity / physiology*
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / metabolism
  • Nitric Oxide / metabolism
  • Phosphoprotein Phosphatases / antagonists & inhibitors
  • Phosphoproteins / genetics
  • Phosphoproteins / metabolism*
  • Phosphoproteins / pharmacology
  • Phosphorylation / drug effects
  • Protein Kinase C / metabolism
  • Receptors, Dopamine D1 / metabolism
  • Receptors, Glutamate / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology

Substances

  • Dopamine and cAMP-Regulated Phosphoprotein 32
  • Enzyme Inhibitors
  • Nerve Tissue Proteins
  • Phosphoproteins
  • Receptors, Dopamine D1
  • Receptors, Glutamate
  • Nitric Oxide
  • Cyclic AMP-Dependent Protein Kinases
  • Cyclic GMP-Dependent Protein Kinases
  • Protein Kinase C
  • Phosphoprotein Phosphatases
  • Cyclic GMP