Myenteric neurons activate submucosal vasodilator neurons in guinea pig ileum

2000 ◽  
Vol 279 (2) ◽  
pp. G380-G387 ◽  
Author(s):  
S. Vanner
Keyword(s):  
Blood Flow ◽  
Guinea Pig ◽  
Myenteric Plexus ◽  
Guinea Pig Ileum ◽  
Recording Site ◽  
Myenteric Neurons ◽  
Outside Diameter ◽  
Myenteric Ganglia ◽  
Double Chamber

This study examined whether myenteric neurons activate submucosal vasodilator pathways in in vitro combined submucosal-myenteric plexus preparations from guinea pig ileum. Exposed myenteric ganglia were electrically stimulated, and changes in the outside diameter of submucosal arterioles were monitored in adjoining tissue by videomicroscopy. Stimulation up to 18 mm from the recording site evoked large TTX-sensitive vasodilations in both orad and aborad directions. In double-chamber baths, which isolated the stimulating myenteric chamber from the recording submucosal chamber, hexamethonium or the muscarinic antagonist 4-diphenylacetoxy- N-(2-chloroethyl)-piperdine hydrochloride (4-DAMP) almost completely blocked dilations when superfused in the submucosal chamber. When hexamethonium was placed in the myenteric chamber ∼50% of responses were hexamethonium sensitive in both orad and aborad orientations. The addition of 4-DAMP or substitution of Ca2+-free, 12 mM Mg2+ solution did not cause further inhibition. These results demonstrate that polysynaptic pathways in the myenteric plexus projecting orad and aborad can activate submucosal vasodilator neurons. These pathways could coordinate intestinal blood flow and motility.

Properties of synaptic inputs from myenteric neurons innervating submucosal S neurons in guinea pig ileum

2000 ◽  
Vol 278 (2) ◽  
pp. G273-G280 ◽  
Author(s):  
B. A. Moore ◽  
S. Vanner
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Intracellular Recordings ◽  
Guinea Pig Ileum ◽  
Myenteric Neurons ◽  
Synaptic Inputs ◽  
Stimulus Train ◽  
Stimulation Of ◽  
Double Chamber

This study examined synaptic inputs from myenteric neurons innervating submucosal neurons. Intracellular recordings were obtained from submucosal S neurons in guinea pig ileal preparations in vitro, and synaptic inputs were recorded in response to electrical stimulation of exposed myenteric plexus. Most S neurons received synaptic inputs [>80% fast (f) excitatory postsynaptic potentials (EPSP), >30% slow (s) EPSPs] from the myenteric plexus. Synaptic potentials were recorded significant distances aboral (fEPSPs, 25 mm; sEPSPs, 10 mm) but not oral to the stimulating site. When preparations were studied in a double-chamber bath that chemically isolated the stimulating “myenteric chamber” from the recording side “submucosal chamber,” all fEPSPs were blocked by hexamethonium in the submucosal chamber, but not by a combination of nicotinic, purinergic, and 5-hydroxytryptamine-3 receptor antagonists in the myenteric chamber. In 15% of cells, a stimulus train elicited prolonged bursts of fEPSPs (>30 s duration) that were blocked by hexamethonium. These findings suggest that most submucosal S neurons receive synaptic inputs from predominantly anally projecting myenteric neurons. These inputs are poised to coordinate intestinal motility and secretion.

Somatostatin modulation of peptide-induced acetylcholine release in guinea pig ileum

1984 ◽  
Vol 246 (5) ◽  
pp. G509-G514 ◽  
Author(s):  
D. H. Teitelbaum ◽  
T. M. O'Dorisio ◽  
W. E. Perkins ◽  
T. S. Gaginella
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Longitudinal Muscle ◽  
Guinea Pig Ileum ◽  
Gut Motility ◽  
Release Of Acetylcholine

The peptides caerulein, neurotensin, somatostatin, and substance P modulate the activity of intestinal neurons and alter gut motility. We examined the effects of these peptides on acetylcholine release from the myenteric plexus and intestinal contractility in vitro. Caerulein (1 X 10(-9) M), neurotensin (1.5 X 10(-6) M), and substance P (1 X 10(-7) M) significantly enhanced the release of [3H]acetylcholine from the myenteric plexus of the guinea pig ileum. This effect was inhibited by tetrodotoxin (1.6 X 10(-6) M). Somatostatin (10(-6) M) inhibited caerulein- and neurotensin-evoked release of acetylcholine but did not inhibit release induced by substance P. Caerulein, neurotensin, and substance P caused contraction of the guinea pig ileal longitudinal muscle. Somatostatin inhibited the contractions induced by caerulein and neurotensin. In contrast, substance P-induced contraction was not inhibited significantly by somatostatin. Thus, in the guinea pig ileum, caerulein-, neurotensin-, and substance P-induced contractility is due, at least in part, to acetylcholine release from the myenteric plexus. The ability of somatostatin to inhibit peptide-induced contractility is selective, and its mechanism may be attributed to inhibition of acetylcholine release.

Synaptic behavior of myenteric neurons in guinea pig distal colon

1988 ◽  
Vol 255 (2) ◽  
pp. G184-G190 ◽  
Author(s):  
P. R. Wade ◽  
J. D. Wood
Keyword(s):  
Guinea Pig ◽  
Input Resistance ◽  
Distal Colon ◽  
Bathing Medium ◽  
Myenteric Neurons ◽  
Fiber Tracts ◽  
Slow Rise ◽  
Domain 3 ◽  
Myenteric Ganglia

Intracellular recording methods were used in vitro to analyze the synaptic behavior of neurons in myenteric ganglia of guinea pig distal colon. Fast excitatory postsynaptic potentials (EPSPs) were observed in a variety of types of colonic neurons. Both spontaneous and stimulus-evoked EPSPs were abolished or suppressed by addition of hexamethonium, tetrodotoxin, or elevation of Mg2+ and reduction of Ca2+ in the bathing medium. Individual neurons usually received inputs from several fiber tracts and multiple EPSPs were sometimes evoked by electrical stimulation of single-fiber tracts. Stimulus-evoked fast EPSPs were always of greater amplitude, longer duration, and longer decay time than were spontaneous fast EPSPs in the same neurons. No rundown of the fast EPSPs occurred during prolonged stimulation at frequencies up to 10 Hz. Repetitive stimulation evoked slow depolarizing potentials (slow EPSPs) in 25% of the neurons. Characteristics of the slow EPSPs were 1) slow rise times, 2) duration in the seconds time domain, 3) enhanced excitability, 4) increased input resistance, and 5) reduction of hyperpolarizing after-potentials. In general, the variety of synaptic potentials and the properties of the events were the same as found in myenteric neurons of the guinea pig small bowel. Compared with synaptic behavior of small intestinal myenteric neurons, the notable differences were absence of the rundown phenomenon for fast EPSPs in the colonic neurons and a greater incidence of spontaneously occurring fast EPSPs.

Neural circuitry of capsaicin-sensitive afferents innervating submucosal arterioles in guinea pig ileum

1996 ◽  
Vol 270 (6) ◽  
pp. G948-G955 ◽  
Author(s):  
S. Vanner ◽  
M. Bolton
Keyword(s):  
Guinea Pig ◽  
Neural Circuitry ◽  
Guinea Pig Ileum ◽  
Single Vessel ◽  
Opposite Chamber ◽  
Stimulation Of ◽  
Double Chamber

The circuitry of capsaicin-sensitive nerves innervating submucosal arterioles in the guinea pig ileum was examined. The orientation of in vitro submucosal preparations in a double-chamber bath was varied so that nerves on differing segments of arterioles could be stimulated with capsaicin. Capsaicin-evoked dilation of preconstricted arterioles was recorded using videomicroscopy. Superfusion of capsaicin onto either proximal or distal segments of a parent arteriole divided between the chambers evoked a dilation in the opposite chamber (63 and 58%, respectively) but had no effect on extrinsically denervated preparations. When the divider separated the vascular arcades joining the two parent arterioles on the opposite or same side of the intestine, capsaicin evoked little or no response (8 and 11%, respectively). Capsaicin stimulation confined to one branch of a single vessel dilated the opposite branch (42%). In preparations with adjacently attached mucosa, application of capsaicin to the mucosa dilated arterioles in the opposite chamber. These findings suggest that capsaicin stimulation of the mucosa evokes dilation of arterioles through a submucosal reflex and that both afferent and efferent elements are confined to the submucosa and mucosa.

Acute morphological changes in guinea-pig ileum myenteric neurons after ischemia in situ with superfusion in vitro

2008 ◽  
Vol 204 (2) ◽  
pp. 121-127 ◽  
Author(s):  
Rosa Ventura-Martinez ◽  
Jacinto Santiago-Mejia ◽  
Claudia Gomez ◽  
Rodolfo Rodriguez ◽  
Teresa I. Fortoul
Keyword(s):  
Guinea Pig ◽  
Morphological Changes ◽  
Guinea Pig Ileum ◽  
Myenteric Neurons

The action of substance P on neurons of the myenteric plexus of the guinea-pig small intestine

1979 ◽  
Vol 206 (1163) ◽  
pp. 191-208 ◽  
Keyword(s):  
Small Intestine ◽  
Substance P ◽  
Guinea Pig ◽  
Myenteric Plexus ◽  
Reversal Potential ◽  
Membrane Depolarization ◽  
Extracellular Potassium ◽  
Membrane Hyperpolarization ◽  
Myenteric Neurons

Extracellular and intracellular recordings were made in vitro from single neurons of the myenteric plexus of the guinea-pig small intestine. Synthetic substance P was applied to the neurons by means of the perfusing solution or by electrophoresis from micropipettes. Extracellular recording showed that substance P (100 pM-30 nM), applied by perfusion, increased the firing rate of myenteric neurons. Intracellular recording indicated that perfusion with substance P caused a dose-dependent membrane depolarization which was unaffected by hexamethonium, hyoscine, naloxone or baclofen. The depolarization was also evoked by electrophoretic application of substance P. It was associated with an increase in membrane resistance, augmented by membrane depolarization and reduced by membrane hyperpolarization. The relation between the substance P reversal potential and the logarithm of the extracellular potassium concentration was linear with a slope of 54 mV/log 10 [K + ], which indicates that substance P inactivates the resting potassium conductance of the myenteric neurons. This effect on ion conductance is the same as that of an unknown substance that mediates slow synaptic excitations with the myenteric plexus.

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