Sellers et al. (1979, Am. J. Phys., 237
: E457-E464) proposed a pelvic flexure pacemaker mechanism to account for the bidirectional contraction waves needed to both retain ingesta within the right ventral colon for cellulose digestion and terminal fermentation and to transport the digesta distad once the process has been completed. To corroborate the presence of a pelvic flexure pacemaker, we prepared whole mount samples of the tunica muscularis from 23 horses at ten sites along the large colon, cecum and jejunum. Following smooth muscle enzymatic digestion, somata of the myenteric plexus were stained with an RNAspecific agent, Cuprolinic blue. These somata were quantified at each site to establish any regional variations in neuronal density. Results indicated an increased neuronal density a t the level of the pelvic flexure, especially in the region of the left dorsal colon. The increased neuronal density at the left dorsal colon compared to the other sampling sites was statistically significant (Wilcoxon signed rank test, P<.Ol at each sampling site). There was remarkable size variation (from 10-60 pm) among neurons a t the individual sampling sites. However, no statistically significant size discrepancy existed between sampling sites (Friedman's rank test, P= .lo). The 23 horses ranged from 6 months to 15 years of age. No age-related differences in neuronal density was discovered (Kruskal-Wallis ANOVA test, P>.05). Neuronal densities did not vary on the basis of sex (Wilcoxon signed pairs test, P>.05). These neuronal counts serve both as corroborative evidence for the pelvic flexure pacemaker hypothesis and as standard values for neuronal density at each of our sampling sites. These standards will provide an important foundation for future studies in gastrointestinal motility and enteric pathology.