Dekkers J A, Akkermans L M, Kroese A B
Department of Human and Animal Physiology, Agricultural University, Wageningen, The Netherlands.
Am J Physiol. 1997 Jun;272(6 Pt 1):G1451-6. doi: 10.1152/ajpgi.1997.272.6.G1451.
The effects of the inflammatory mediator prostaglandin E2 (PGE2) on myenteric neurons were investigated by intracellular recordings in a conventional plexus preparation. Bath application of PGE2 (1-1,000 nM) evoked a concentration-dependent and reversible slow depolarization and an augmentation of excitability in 23 of 26 AH and 12 of 13 S neurons. The amplitude of the slow depolarization ranged from 4 +/- 1 mV at 1 nM to 13 +/- 3 mV at 1 microM in S and AH neurons. In AH neurons, PGE2 evoked an increase in membrane resistance and a reduction of afterhyperpolarization. In S neurons, PGE2 evoked either an increase or a decrease in membrane resistance. PGE2 slightly reduced the amplitude of electrically evoked fast excitatory postsynaptic potentials and had no effect on slow excitatory postsynaptic potentials. Moreover, PGE2 evoked bursts of fast excitatory postsynaptic potentials and action potentials in S neurons, indicative of cyclical neural activity in the myenteric plexus. It is concluded that the inflammatory mediator PGE2 can act as an excitatory neuromodulator of gastrointestinal motility through direct action on neurons in the myenteric plexus.
