Brain-gut interactions: brain stem neuronal response to local gastric effects of substance P

Abstract

Single-unit activity that responded to phasic gastric distension was recorded extracellularly from neurons in brain stem of anesthetized cats during local substance P chemically induced changes in wall tension. Local gastric intra-arterial administration of substance P via splenic artery often produced a triphasic gastric response. Gastric changes were characterized by 1) an initial brief increase in distension of corpus immediately after peptide and 2) a subsequent contraction that gave way to 3) a prolonged late increase in distension exceeding control levels. The contraction phase was atropine sensitive, suggesting that one mechanism of action during this phase was linked to cholinergic enteric nerves. Distension phases were unaffected by atropine, suggesting a different mechanism of action. Increase in gastric wall tension after peptide resulted in 1) onset of or enhanced activity of brain stem unit during nondistending phase and 2) greater spike discharge per unit change in volume during distending phase in many neurons. Some neurons showed a brief flurry of tonic activity during distending and nondistending phases of the cycle after local gastric injection of peptide with no observable change in wall tension. This suggests that the peptide may also act on chemoreceptors served by vagal primary afferents, which impinge on this neuronal population in the brain stem. Less than 10% of the neurons showed no change in discharge rate after a significant increase in wall tension, which occurred after local gastric injection of substance P, suggesting a mechanism of action involving input from primary vagal afferent fibers serving mucosal receptors unaffected by this level of change in wall tension.(ABSTRACT TRUNCATED AT 250 WORDS)