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Effects of aripiprazole on MK-801-induced prepulse inhibition deficits and mitogen-activated protein kinase signal

Daisuke Ishii1, Daisuke Matsuzawa, Nobuhisa Kanahara

  • 1Department of Integrative Neurophysiology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chiba 260-8670, Japan.

Neuroscience Letters
|January 20, 2010
PubMed

Insights

Aripiprazole reversed MK-801-induced deficits in prepulse inhibition (PPI) in mice, suggesting it may regulate mitogen-activated protein kinase (MAPK) phosphorylation, similar to clozapine.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Psychiatry

Background:

  • Schizophrenia's negative symptoms and cognitive deficits are linked to NMDA hypofunction.
  • MK-801-induced animal models offer insights into typical vs. atypical antipsychotic effects.
  • Mitogen-activated protein kinase (MAPK) signaling pathways may mediate antipsychotic actions.

Purpose of the Study:

  • To investigate aripiprazole's effects on MK-801-induced prepulse inhibition (PPI) disruption in mice.
  • To examine aripiprazole's impact on MAPK phosphorylation in the context of MK-801 administration.

Main Methods:

  • Utilized MK-801-induced animal model in 51 ddY male mice.
  • Administered aripiprazole prior to MK-801 to measure PPI.
  • Assessed MAPK phosphorylation (pMEK/MEK, pERK/ERK) via western blotting in cytosol and nuclear fractions.

Main Results:

  • Aripiprazole (4.0 mg/kg) significantly reversed MK-801 (0.15 mg/kg)-induced PPI deficits.
  • Aripiprazole (40 mg/kg) tended to suppress MK-801 (1.0 mg/kg)-induced pMEK/MEK activation.
  • Aripiprazole treatment significantly decreased pERK/ERK levels.

Conclusions:

  • Aripiprazole demonstrates efficacy in reversing MK-801-induced PPI deficits in mice.
  • The findings suggest aripiprazole's antipsychotic action may involve the regulation of MAPK phosphorylation.
  • Aripiprazole's mechanism appears similar to clozapine in modulating MAPK pathways.

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