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Amphetamine sensitization elevates CaMKIIbeta mRNA.

Rachel Greenstein1, Gabriela Novak, Philip Seeman

  • 1Department of Pharmacology, University of Toronto, Toronto, Ontario, Canada M5S 1A8.

Synapse (New York, N.Y.)
|July 3, 2007
PubMed
Summary

Amphetamine sensitization, a model for psychosis, increased calcium/calmodulin-dependent protein kinase II (CaMKII) beta subunit mRNA. This suggests dysregulated CaMKII may contribute to psychosis.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Calcium/calmodulin-dependent protein kinase II (CaMKII) elevation is linked to amphetamine-induced dopamine release and psychosis.
  • Amphetamine sensitization is a key animal model for studying psychosis and schizophrenia.

Purpose of the Study:

  • To investigate if amphetamine sensitization increases CaMKII alpha and beta subunits.
  • To explore the role of CaMKII in psychosis through an animal model.

Main Methods:

  • Real-Time Quantitative PCR was used to measure CaMKII alpha and beta subunit mRNA expression.
  • Experiments were conducted on rat striata from amphetamine-sensitized and saline-treated control groups.
  • Beta-glucuronidase was used as a housekeeping gene for standardization.

Main Results:

  • A statistically significant increase in CaMKII beta subunit mRNA was observed in sensitized rats.
  • An increase in CaMKII alpha subunit mRNA was noted but did not reach statistical significance.
  • Both CaMKIIbeta and CaMKIIalpha subunits are crucial for neuronal function and synapse formation.

Conclusions:

  • Elevated CaMKII beta and alpha subunit mRNA levels in an amphetamine-sensitized rat model suggest potential dysregulation in human psychosis.
  • Findings highlight CaMKII's potential role in the pathophysiology of psychosis.