Guinea Pig Myenteric Plexus Neurons Research Articles

Evidence for a neurotransmitter role of glutamate in guinea pig myenteric plexus neurons

Longitudinal muscle-myenteric plexus strips of the guinea pig ileum were used to investigate a possible transmitter role of glutamate (Glu) in the enteric nervous system. Glu was released from this nerve muscle preparation by high K +-depolarization in a Ca 2+-dependent manner, by electrical field stimulation and by the ganglionic stimulant dimethylphenylpiperazinium which indicates its neural origin. Contractions of the longitudinal muscle evoked by electrical stimulation of the myenteric nerves or by Glu, were significantly reduced by the N-methyl- d-aspartate (NMDA)-receptor antagonist FR115427 (9 and 18 μM), whereas contractions induced by histamine were unaffected. The results show that the amino acid Glu is likely to play an excitatory neurotransmitter role via NMDA receptors in the myenteric plexus of the guinea pig.

Prostaglandin E 2 stimulation of acetylcholine release from guinea pig myenteric plexus neurons

Prostaglandins are widely distributed within the gastrointestinal tract and have important effects on gastrointestinal motility. Although actions upon gastrointestinal smooth muscle have been demonstrated for prostaglandins (PG), neural mechanisms may also be important. The effects of PGE2 on acetylcholine (ACh) release were studied using guinea pig myenteric plexus neurons in primary culture. PGE stimulated the release of ACh in a dose-dependent manner, with a median effective dose (ED50) of 0.8 x 10(-6) M. Involvement of L-type calcium channels was implied by the sensitivity of PGE2-stimulated ACh release to omega conotoxin or diltiazem. In addition, ACh release stimulated by PGE2 could be inhibited by co-incubation with dideoxyadenosine or Rp-cAMPS, agents that act upon cyclic adenosine monophosphate (cAMP)-dependent signaling pathways. PGE2 has direct effects upon myenteric neurons to stimulate cholinergic transmission.

Bombesin-Stimulated Acetylcholine Release from Myenteric Plexus Neurons

The ability of bombesin to stimulate acetylcholine release from guinea pig myenteric plexus neurons was studied using a primary neuronal culture system. Bombesin caused dose-dependent increases in [3H]acetylcholine (ACh) release from guinea pig myenteric plexus neurons. ACh release in response to 0.5 mM bombesin (160 ± 12% of control) was blocked by exposure to a calcium-free medium (116 ± 13%) by nifedipine (101 ± 11%) and by omega conotoxin (107 ± 10%). Bombesin-stimulated ACh release was inhibited the protein kinase C inhibitor, H7, but was not affected by inhibitors of the cAMP signaling pathway. Interactions with inhibitory neuropeptides was implied by sensitivity of bombesin-stimulated ACh release to neuropeptide Y and galanin. The findings suggest that bombesin activation of protein kinase C in myenteric neurons resuits in increased acetylcholine release.

Stimulation of acetylcholine release in myenteric plexus by calcitonin gene-related peptide

The effects of calcitonin gene-related peptide (CGRP) on acetylcholine (ACh) release from myenteric plexus neurons in primary culture were investigated. CGRP (10(-12) to 10(-6) M) produced a dose-dependent increase in [3H]ACh release. The ACh release caused by CGRP was significantly inhibited (74 +/- 24%) by preincubation with dideoxyadenosine but was increased more than threefold by preincubation with theophylline. Incubation of myenteric plexus neurons with CGRP (10(-8) M) in the presence of diltiazem (10(-5) M) or in a calcium-free medium markedly reduced [3H]ACh release. CGRP potentiated [3H]ACh release stimulated by potassium or substance P but not by cholecystokinin octapeptide or forskolin. The results demonstrate that CGRP cause release of ACh from guinea pig myenteric plexus neurons and suggest that the peptide acts through an adenosine 3',5'-cyclic monophosphate-dependent mechanism that involves neuronal calcium channels.

Slow synaptic potentials in AH-type myenteric plexus neurons.

Two types of slow depolarization were recorded in AH-type guinea pig myenteric plexus neurons when the myenteric plexus-longitudinal muscle preparation was stimulated transmurally with external electrodes. One depolarization was associated with a fall and the other with a rise in membrane resistance, the latter type (slow EPSP) being encountered about six times more commonly than the former. In some instances both types of potential were recorded in the same AH neuron. When this occurred the amplitude and duration of the slow EPSP was attenuated if it was timed to occur at about the same time as the other slow synaptic potential.