Transcranial direct current stimulation relieves visceral hypersensitivity via normalizing GluN2B expression and neural activity in anterior cingulate corter.

Irritable bowel syndrome (IBS) is one of the most common clinical diseases with treatment for which being challenging. The aim of this study is to investigate whether transcranial direct current stimulation (tDCS) has analgesic effect on visceral hypersensitivity (VH) in an animal model of IBS as well as the underlying mechanism. Since the activation of GluN2B in anterior cingulate cortex (ACC) takes part in VH, we examined whether and how GluN2B in ACC take part in the effect of tDCS. Neonatal maternal deprivation (NMD), a valuable experimental model to study the IBS pathophysiology, was used to induce visceral hypersensitivity of rats. We quantified VH as colorectal distention threshold and performed patch clamp recordings of ACC neurons. The expression of GluN2B were determined by RT-qPCR and western blotting. The GluN2B antagonist Ro 25-6981 was microinjected into the rostral and caudal ACC. tDCS was performed for 7 consecutive days. It was found that NMD decreased expression of GluN2B, which could be obviously reversed by tDCS. Injection of Ro 25-6981 into rostral and caudal ACC of normal rats induced VH and also reversed the analgesic effect of tDCS. Our data sheds light on the non-pharmacological therapy for chronic VH in pathological states such as IBS.