1. ¹Division of Neuropsychiatry, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, USA
2. ²Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, USA
3. ³Department of Biology, University of Pennsylvania, Philadelphia, PA, USA
4. ⁴Department of Biology, Rider University, Lawrenceville, NJ, USA

Correspondence: Dr SJ Siegel, Department of Psychiatry, University of Pennsylvania, Clinical Research Building, Rm 145a, 415 Curie Boulevard, Philadelphia, PA 19104, USA. Tel: +1 215 573 0278, Fax: +1 215 573 2041, E-mail: siegels@mail.med.upenn.edu

Received 20 April 2005; Revised 16 June 2005; Accepted 7 July 2005; Published online 24 August 2005.

Abstract

Previous studies suggest that circulating glucocorticoids may influence the encoding and processing of sensory stimuli. The current study investigated this hypothesis by measuring the generation (amplitude), gating (recovery cycle), and sensitivity (intensity function) of auditory evoked responses in C57BL/6 mice treated with chronic corticosterone (0, 1, 5, 15, or 30 mg/kg/day for 14 days). We found that low-dose corticosterone (5 but not 1 mg/kg/day) enhanced the amplitude and improved gating of evoked potentials without affecting the intensity function. In comparison, higher doses (15 and 30 mg/kg/day) decreased the amplitude and impaired gating of evoked potentials, also without altering the stimulus intensity function. At all doses, lower amplitudes of evoked potentials were significantly correlated with higher circulating corticosterone levels. These data highlight the need to consider serum glucocorticoid levels when assessing human disease states associated with aberrations of information processing such as schizophrenia and depression.