Depolarization-evoked GABA release from myenteric plexus is partially coupled to L-, N-, and P/Q-type calcium channels.

1. There are many evidences suggesting that gamma-aminobutyrate (GABA) is an important neurotransmitter and/or neuromodulator in the gut. 2. Using the myenteric plexus-longitudinal muscle preparation from the guinea pig ileum, we investigated the evoked release of [3H] GABA from enteric neurons by electrical pulses or high KCl, which occurs in a calcium-dependent and -independent way. In addition, using selective calcium channel blockers, we report the participation of distinct subtypes of calcium channels in the evoked release, showing a minor participation of L- and Q-type calcium channels, while N- and P-type have a participation of approximately 15%, each. However, regardless of the combination of Ca2+ channel blockers, we did not observe an inhibition greater than 50% of the calcium-dependent component of [3H] GABA release. 3. Thus, while the observed Ca2+-independent release mostly probable occur via reversal of the membrane GABA transporter, in our conditions, a considerable portion of the Ca2+-dependent evoked release of [3H] GABA is not coupled to L-, N-, or P/Q-type calcium channels, suggesting the involvement of intracellular calcium stores or other ways of getting calcium across the membrane.