Sensitization Of Anterior Cingulate Cortex In Visceral Hypersensitive Rats

Background & Aims: Visceral hypersensitivity is a characteristic of irritable bowel syndrome (IBS). The anterior cingulate cortex (ACC) is critically involved in processing of pain. Electrophysiological activity of the ACC with regard to visceral sensitization has not been characterized.Methods: Single ACC activities in response to colorectal distension (CRD) were recorded in normal rats and in viscerally hypersensitive rats that had been induced by intracolonic instillation of acetic acid (AC) or intraperitoneal injection of chicken egg albumin (EA). Reverse microdialysis of glutamate and glutamate receptor antagonists into the dendritic fields of the ACC was performed. Conditioned place avoidance (CPA) induced by CRD and focal field potential was tested in different groups. The quantities of different type of glutamate receptors was test by reverse transcription-polymerase chain reaction.Results: Spontaneous activity was significantly higher in sensitized rats than in normal rats. CRD produced greater pressure-dependent increases in ACC spike firing rates in the AC and EA rats compared to normal rats. Field potential induced by focal electrical stimuli increased in AC and EA rats. Pelvic nerve and splanchnic nerve section reduced ACC responses evoked by CRD. Reverse microdialysis of glutamate resulted in a higher increases in ACC neuronal discharges in the AC and EA rats. CPA induced by CRD was abolished by ACC lesion. Transcription of GluR2 and NR2B gene increased after sensitization.Conclusions: This study identifies neurons in the ACC response to CRD and establishes that persistence of a visceral afferent nociceptive input to the ACC induces...