Pharmacological characterization of rat jejunal contractility after chronic ablation of the myenteric plexus.

The authors have pharmacologically characterized longitudinal muscle contractility of the isolated rat jejunum chronically devoid of myenteric neurons. The myenteric plexus of a 3- to 4-cm segment of rat jejunum was ablated by serosal application of the cationic surfactant benzalkonium chloride (BAC). Fifteen days after treatment, both BAC-treated and untreated control jejunal segments were removed from each animal for pharmacological studies. BAC-treated tissues did not respond to the ganglionic stimulants nicotine, 1,1-dimethyl-4-phenylpiperazinium iodide and McN-A-343 or to the acetylcholinesterase inhibitor physostigmine. Short-pulse duration transmural electrical stimulation (0.1 msec) caused a frequency-dependent, tetrodotoxin-sensitive contraction in control but not BAC-treated tissues. Long-pulse duration transmural electrical stimulation (5.0 msec) contracted both control and BAC-treated jejunum. These contractions were partially reduced but not completely blocked by tetrodotoxin. To assess smooth muscle function, the mechanical responses to the muscarinic receptor agonist carbachol were examined. Carbachol contracted both control and BAC-treated tissues with maximal responses and ED50 values that were not significantly different. In addition, the maximal tension development produced by 10(-2) M barium chloride in similar lengths of control and BAC-treated jejunal segments was not significantly different. These studies demonstrate that chronic ablation of the myenteric plexus by serosal application of BAC essentially eliminates neuronally mediated responses without a concomitant alteration in longitudinal muscle contractility. Because nerve-mediated longitudinal muscle responses are lost despite the presence of an intact submucosal plexus in the BAC-treated jejunum, our data suggest that the motor neurons innervating the rat jejunal longitudinal muscle are located in the myenteric plexus.