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Exposure to predator odor and resulting anxiety enhances the expression of the α 2 δ subunit of voltage‐sensitive calcium channels in the amygdala
Author(s) -
Nasca Carla,
Orlando Rosamaria,
Marchiafava Moreno,
Boldrini Paolo,
Battaglia Giuseppe,
Scaccianoce Sergio,
Matrisciano Francesco,
Pittaluga Anna,
Nicoletti Ferdinando
Publication year - 2013
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2012.07895.x
Subject(s) - pregabalin , amygdala , gabapentin , anxiogenic , anxiolytic , neuropathic pain , neuroscience , psychology , anxiety , hippocampus , elevated plus maze , protein subunit , medicine , chemistry , endocrinology , pharmacology , psychiatry , pathology , biochemistry , alternative medicine , gene
The α 2 δ subunit of voltage‐sensitive calcium channels ( VSCC s) is the molecular target of pregabalin and gabapentin, two drugs marked for the treatment of focal epilepsy, neuropathic pain, and anxiety disorders. Expression of the α 2 δ subunit is up‐regulated in the dorsal horns of the spinal cord in models of neuropathic pain, suggesting that plastic changes in the α 2 δ subunit are associated with pathological states. Here, we examined the expression of the α 2 δ‐1 subunit in the amygdala, hippocampus, and frontal cortex in the trimethyltiazoline ( TMT ) mouse model of innate anxiety. TMT is a volatile molecule present in the feces of the rodent predator, red fox. Mice that show a high defensive behavior during TMT exposure developed anxiety‐like behavior in the following 72 h, as shown by the light–dark test. Anxiety was associated with an increased expression of the α 2 δ‐1 subunit of VSCC s in the amygdaloid complex at all times following TMT exposure (4, 24, and 72 h). No changes in the α 2 δ‐1 protein levels were seen in the hippocampus and frontal cortex of mice exposed to TMT . Pregabalin (30 mg/kg, i.p.) reduced anxiety‐like behavior in TMT ‐exposed mice, but not in control mice. These data offer the first demonstration that the α 2 δ‐1 subunit of VSCC s undergoes plastic changes in a model of innate anxiety, and supports the use of pregabalin as a disease‐dependent drug in the treatment of anxiety disorders.