Upregulation of L-type Ca(v)1 channels in the development of psychological dependence

Synapse. 2010 Jun;64(6):440-4. doi: 10.1002/syn.20745.

Abstract

Although L-type voltage-dependent Ca2+ channels regulate activity-dependent processes including synaptic plasticity and synapse formation, there are few data on the changes of Ca(v)1 channel expression in psychological dependence. This study investigated the role of L-type Ca(v)1 channel expression in the brain of mouse that was psychologically dependent on methamphetamine (2 mg/kg, subcutaneous injection [s.c.]), cocaine (10 mg/kg, s.c.), and morphine (5 mg/kg, s.c.) with the conditioned place preference paradigm. Intracerebroventricular administration of nifedipine (3, 10, and 30 nmol/mouse) dose-dependently reduced the development of methamphetamine-, cocaine-, and morphine-induced rewarding effect. Under such conditions, protein levels of both Ca(v)1.2 and Ca(v)1.3 in the frontal cortex and the limbic forebrain were significantly increased on methamphetamine-, cocaine-, and morphine-induced psychologically dependent mice. These findings suggest that the upregulation of Ca(v)1.2 and Ca(v)1.3 participated in the development of psychological dependence.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / drug effects*
  • Brain / metabolism*
  • Brain / physiopathology
  • Brain Chemistry / drug effects
  • Brain Chemistry / physiology
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels, L-Type / drug effects*
  • Calcium Channels, L-Type / metabolism
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology
  • Cocaine / pharmacology
  • Disease Models, Animal
  • Frontal Lobe / drug effects
  • Frontal Lobe / metabolism
  • Frontal Lobe / physiopathology
  • Limbic System / drug effects
  • Limbic System / metabolism
  • Limbic System / physiopathology
  • Male
  • Methamphetamine / pharmacology
  • Mice
  • Morphine / pharmacology
  • Nifedipine / pharmacology
  • Substance-Related Disorders / drug therapy
  • Substance-Related Disorders / metabolism*
  • Substance-Related Disorders / physiopathology
  • Up-Regulation / drug effects
  • Up-Regulation / physiology

Substances

  • CACNA1C protein, mouse
  • Cacna1d protein, mouse
  • Calcium Channel Blockers
  • Calcium Channels, L-Type
  • Methamphetamine
  • Morphine
  • Cocaine
  • Nifedipine