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Amygdala protein kinase C epsilon regulates corticotropin-releasing factor and anxiety-like behavior

  1. H. M. B. Lesscher1,2,
  2. T. McMahon1,
  3. A. W. Lasek1,
  4. W.-H. Chou1,
  5. J. Connolly1,
  6. V. Kharazia1,
  7. R. O. Messing1,*

Article first published online: 27 AUG 2007

DOI: 10.1111/j.1601-183X.2007.00356.x

Issue

Genes, Brain and Behavior

Genes, Brain and Behavior

Volume 7, Issue 3, pages 323–333, April 2008

Additional Information

How to Cite

Lesscher, H. M. B., McMahon, T., Lasek, A. W., Chou, W.-H., Connolly, J., Kharazia, V. and Messing, R. O. (2008), Amygdala protein kinase C epsilon regulates corticotropin-releasing factor and anxiety-like behavior. Genes, Brain and Behavior, 7: 323–333. doi: 10.1111/j.1601-183X.2007.00356.x

Author Information

  1. 1

    Department of Neurology, Ernest Gallo Clinic and Research Center, University of California at San Francisco, Emeryville, CA, USA

  2. 2

    Present address: Department of Pharmacology and Anatomy, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, 3584 CG Utrecht, the Netherlands

* *R. O. Messing, Ernest Gallo Clinic and Research Center, 5858 Horton Street, Suite 200, Emeryville, CA 94608, USA. E-mail: romes@gallo.ucsf.edu

Publication History

  1. Issue published online: 27 AUG 2007
  2. Article first published online: 27 AUG 2007
  3. Received 4 June 2007, revised 16 August 2007, accepted for publication 22 August 2007

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Keywords:

  • Addiction;
  • anxiety;
  • corticotropin-releasing factor;
  • ethanol;
  • protein kinase C;
  • RNA interference

Corticotropin-releasing factor (CRF), its receptors, and signaling pathways that regulate CRF expression and responses are areas of intense investigation for new drugs to treat affective disorders. Here, we report that protein kinase C epsilon (PKCɛ) null mutant mice, which show reduced anxiety-like behavior, have reduced levels of CRF messenger RNA and peptide in the amygdala. In primary amygdala neurons, a selective PKCɛ activator, ψɛRACK, increased levels of pro-CRF, whereas reducing PKCɛ levels through RNA interference blocked phorbol ester-stimulated increases in CRF. Local knockdown of amygdala PKCɛ by RNA interference reduced anxiety-like behavior in wild-type mice. Furthermore, local infusion of CRF into the amygdala of PKCɛ−/− mice increased their anxiety-like behavior. These results are consistent with a novel mechanism of PKCɛ control over anxiety-like behavior through regulation of CRF in the amygdala.

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