Panteleev S, Grundy D
Laboratory of Cortico-visceral Physiology, I.P. Pavlov Institute of Physiology, n. Makarova, 6, St-Petersburg 199034, Russia.
Auton Neurosci. 2000 Dec 28;86(1-2):78-83. doi: 10.1016/S1566-0702(00)00249-6.
In experiments on urethane anaesthetised rats the influence of electrical stimulation of ventral areas of the medial prefrontal cortex (mPFC) on spontaneous and vagally-mediated gastric motility were studied. Stimulation of the mPFC resulted in gastric relaxation manifested as a fall in intragastric pressure from a baseline value of 5.0 +/- 0.5 cm H2O. These were most prominent following a short latency when the infralimbic cortex (IL) was stimulated (27.4 +/- 2.5% fall in gastric pressure). Electrical stimulation of the central end of one cervical vagus nerve caused a comparable decrease in gastric pressure (27.1 +/- 2.9%). The cortical mediated relaxation was reduced by atropine and abolished by vagotomy. The cortically induced gastric relaxation followed a shorter latency (5.9 +/- 1.0 s), time to nadir (20.1 +/- 2.7 s) and the half recovery time (21.5 +/- 4.0 s) than vagally mediated-relaxations (9.9 +/- 2.3, 56.0 +/- 5.3 and 83.4 +/- 9.5 s, respectively). Vagally mediated relaxations were inhibited by simultaneous stimulation of the infralimbic cortex. In this case the decrease of gastric pressure, the time to nadir and the half recovery time were significantly decreased in comparison with the gastric relaxatory responses to vagal stimulation alone (P < 0.05). We conclude that one way in which the mPFC influences gastric motility is via corticofugal projections from the infralimbic cortex to the brain-stem which modulate transmission of vago-vagal reflexes.
