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.

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.

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.

Actions of nitric oxide-generating sodium nitroprusside in myenteric plexus of guinea pig small intestine

1993 ◽  
Vol 265 (5) ◽  
pp. G887-G893 ◽  
Author(s):  
K. Tamura ◽  
M. Schemann ◽  
J. D. Wood
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Guinea Pig ◽  
Sodium Nitroprusside ◽  
Myenteric Plexus ◽  
Membrane Properties ◽  
Dependent Manner ◽  
Membrane Excitability ◽  
Concentration Dependent Manner ◽  
Myenteric Neurons

Sodium nitroprusside (NaNP) was used as a donor of nitric oxide (NO) to investigate actions of NO on electrical and synaptic behavior of single myenteric neurons in guinea pig small intestine. NaNP (10 microM-1 mM) did not affect resting membrane properties of the neurons, except for an occasional decrease in input resistance and hyperpolarization attributable to suppression of excitatory transmitter release. NaNP did not alter fast nicotinic neurotransmission but suppressed noncholinergic slow excitatory postsynaptic potentials (slow EPSPs) in a concentration-dependent manner. Pretreatment with either methylene blue or oxyhemoglobin reduced the inhibitory action of NaNP on the slow EPSPs. Slow EPSP-like responses to microejected substance P or 5-hydroxytryptamine were unaffected by NaNP. The nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester, did not affect resting membrane excitability or excitatory synaptic events in any of the myenteric neurons. The results suggest that NO may not be released extensively as a neurotransmitter at synapses within the myenteric plexus. If myenteric neurons are exposed to NO released from nonneural sources, then the principal action is expected to be presynaptic inhibition of slow synaptic excitation.

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.

Noradrenergic modulation of firing pattern in guinea pig and cat thalamic neurons, in vitro

1988 ◽  
Vol 59 (3) ◽  
pp. 978-996 ◽  
Author(s):  
D. A. McCormick ◽  
D. A. Prince
Keyword(s):  
Guinea Pig ◽  
Potassium Conductance ◽  
Reversal Potential ◽  
Extracellular Potassium ◽  
Thalamic Nuclei ◽  
Extracellular Potassium Concentration ◽  
Single Spike ◽  
Medial Geniculate ◽  
Slow Depolarization

1. The electrophysiological actions of norepinephrine (NE) in the guinea pig and cat thalamus were investigated using intracellular recordings from neurons of in vitro thalamic slices. 2. Application of NE to neurons of the lateral and medial geniculate nuclei, nucleus reticularis, anteroventral nucleus, and the parataenial (PT) nucleus resulted in a slow depolarization associated with a 2- to 15-nS decrease in input conductance and an increase in the slow membrane time constant from an average of 27.7 to 37.7 ms. The slow depolarization was not abolished by blockade of synaptic transmission, indicating that it was a direct (postsynaptic) effect. 3. The reversal potential of the NE-induced slow depolarization varied as a Nernstian function of extracellular potassium concentration ([K]o), indicating that it is due to a decrease in potassium conductance. This conclusion was supported by the finding that the amplitude of the NE-evoked depolarization was affected by changes in [K]o between 0.5 and 5.0 mM as expected for a K-mediated response. 4. Neurons of the PT nucleus displayed unusually large afterhyperpolarizations (AHPs) in comparison to cells in other thalamic nuclei. NE application to PT neurons caused not only a marked slow depolarization and decreased conductance, but also selectively reduced the slow AHP. 5. The NE-induced slow depolarization effectively suppressed burst firing and promoted the occurrence of single spike activity. NE-induced reduction of the slow AHP in PT neurons was accompanied by a decrease in spike frequency accommodation and the emergence of a slow afterdepolarization. 6. We suggest that through these electrophysiological actions, NE can effectively inhibit the generation of thalamocortical rhythms and greatly facilitate the faithful transfer of information through the thalamus to the cerebral cortex.

Actions of reactive oxygen species on AH/type 2 myenteric neurons in guinea pig distal colon

2000 ◽  
Vol 279 (5) ◽  
pp. G893-G902 ◽  
Author(s):  
S. Wada-Takahashi ◽  
K. Tamura
Keyword(s):  
Reactive Oxygen Species ◽  
Guinea Pig ◽  
Late Onset ◽  
Reactive Oxygen ◽  
Distal Colon ◽  
Membrane Depolarization ◽  
Oxygen Species ◽  
Membrane Hyperpolarization ◽  
Myenteric Neurons

With conventional intracellular recording methods, we investigated the mechanism of actions of reactive oxygen species (ROS) derived from hypoxanthine and xanthine oxidase (HX/XO) reactions on AH/type 2 myenteric neurons in the guinea pig distal colon. Of the 54 neurons to which HX/XO was applied, 32 neurons showed a transient membrane hyperpolarization(s) followed by a long-lasting membrane depolarization. Two additional groups of 10 myenteric neurons exhibited only a membrane hyperpolarization(s) or a late-onset membrane depolarization, respectively, and the remaining two neurons did not show any response to HX/XO. Analysis of changes of the input resistance induced by HX/XO indicated that suppression and augmentation of the conductance of Ca2+-dependent K+ channels are the ionic mechanisms underlying the membrane hyperpolarization and depolarization, respectively. The effects of HX/XO on myenteric neurons were mimicked by application of caffeine or H2O2. The results suggest that OH·, but neither H2O2 nor O2 · −, is responsible for HX/XO-induced responses. The intracellular Ca2+ store may be the acting site of ROS in colonic AH/type 2 neurons.

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