Severe and excessive anxiety is associated with irregular levels of neurotransmitters in the brain but the precise biochemical mechanisms involved have been incompletely understood. In October 1 Journal of Clinical Investigation Clyde Hodge and colleagues at the Ernest Gallo Clinic and Research Center at the University of California, San Francisco, USA, show that absence of protein kinase Cε in mice reduces anxiety-like behavior and stress responses by enhancing gamma aminobutyric acid (GABAA) receptor function in the brain (Journal of Clinical Investigation, 110:1003-1010, October 1, 2002).

Hodge et al. used PKCε-null mice and observed that they showed reduced anxiety-like behavior and reduced levels of the stress hormones corticosterone and adrenocorticotrophic hormone (ACTH). This was associated with increased sensitivity to neurosteroid modulators of GABAA receptors. In addition, they demonstrated that treatment of PKCε-null mice with the GABAA receptor antagonist bicuculline restored corticosterone levels and anxiety-like behavior...

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