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Updated: May 29, 2026

A Novel Approach to Assess Motor Outcome of Deep Brain Stimulation Effects in the Hemiparkinsonian Rat: Staircase and Cylinder Test
Published on: May 31, 2016
Effect of unilateral subthalamic deep brain stimulation on rat digestive motor activity
S Derrey1, W Ouelaa, M Lecointre
1Appareil Digestif Environnement Nutrition (ADEN EA4311), Institute for Biomedical Research, European Institute for Peptide Research (IFR 23), Rouen University, France. stephane.derrey@chu-rouen.fr
Unlabelled:
A significant proportion of patients with Parkinson's disease suffers from digestive symptoms. Bilateral deep brain stimulation of the subthalamic nucleus has become a reliable therapeutic option for parkinsonian patients, but its effects on digestive motility remain poorly investigated. The aim of our study was to assess whether subthalamic stimulation could induce changes in gastric, colonic, and rectal motility and modulate brain centers involved in gut motility.
Methods:
In anesthetized rats, unilateral subthalamic nucleus stereotactic implantation was performed while intra-gastric, -colonic, and -rectal pressures were recorded during the ON and OFF periods of the stimulation. c-Fos protein expression was quantified by immunostaining in the nucleus of the solitary tract, the dorsal motor nucleus of the vagus nerve, the locus coeruleus, and the Barrington's nucleus.
Results:
Compared to baseline, sham stimulation did not change phasic gastric, colonic or rectal motor activity. Unilateral subthalamic stimulation increased colonic phasic motility (P<0.05) compared to baseline and the OFF period with no change in gastric and rectal motility. Pre-treatment with atropine, or specific D1 and D2 receptors antagonists prevented the rise in colonic motor activity. An increase in c-Fos protein-positive cells within all the studied nuclei was observed in the stimulated group compared to the sham group.
Conclusions:
Unilateral subthalamic stimulation impacts on gut motility in anesthetized rats with a significant increase in colonic motility probably via the modulation of several brain centers. These findings warrant further confirmation in parkinsonian rat models before being transposed to clinical conditions.
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