Investigation of the possible role of TRP channels in Schizophrenia

Abstract

Schizophrenia is a debilitating psychiatric disorder. The limitations of current treatments for schizophrenia have led to an ongoing search for new drug targets. The observations that subjects with schizophrenia have impaired thermoregulation, are less sensitive to pain than normal subjects, and exhibit reduced niacin flare responses suggested that TRPV1 channels, and possibly also other temperature-sensitive TRPs that are co-expressed with TRPV1 on sensory neurons, might be linked with schizophrenia. In order to model deficit in function of TRP channels in animals, capsaicin treatment of neonatal rats was used to induce lifelong loss of a high proportion of primary afferent neurons that co-express TRPV1 and related TRP channels. The methods used to test the proposal that TRPV1 deficit induces brain and behavioral changes expected in an animal model of schizophrenia are described. © 2012 Springer Science+Business Media, LLC.