Migrating action-potential complex activity in absence of fluid production is produced by B subunit of cholera enterotoxin.

The myoelectric response and fluid output from in vivo rabbit ileal loops injected with B subunits of purified cholera enterotoxin are compared with the response to the purified cholera holotoxin. Migrating action-potential complex (MAPC) frequency is similar after injection of purified cholera toxin or B subunits. In contrast, fluid output after B-subunit injection is significantly (P less than 0.05) less than fluid output after purified cholera toxin injection. Specific antiserum to the holotoxin incubated with holotoxin at equivalence significantly decreased both MAPC activity (P less than 0.05) and fluid output (P less than 0.001) from the purified toxin. Purified cholera toxin and B subunits, modified by reaction with 2-nitrophenylsulfonyl chloride to produce monomeric B fractions with decreased GM1 ganglioside-binding properties, produced significantly (P less than 0.05) less fluid output and MAPC activity. Binding of the toxin or B subunits in the aggregated form is essential for the expression of MAPC activity or fluid output. These results suggest that the B subunit of cholera toxin produces MAPC activity in the rabbit ileum in the absence of fluid production. Furthermore, previous assumptions that MAPC activity is linked to fluid secretion should be reconsidered. It appears that the gut responses to cholera toxin, fluid production, or MAPC activity are produced by separate mechanisms.