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Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum

BACKGROUND: Adenosine is known to act as a neuromodulator by suppressing synaptic transmission in the central and peripheral nervous system. Both the release of adenosine within the small intestine and the presence of adenosine receptors on enteric neurons have been demonstrated. The aim of the pres...

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Autores principales: Storr, Martin, Thammer, Jutta, Dunkel, Ralf, Schusdziarra, Volker, Allescher, Hans-Dieter
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2002
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC139982/
https://www.ncbi.nlm.nih.gov/pubmed/12495441
http://dx.doi.org/10.1186/1471-2202-3-21
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author Storr, Martin
Thammer, Jutta
Dunkel, Ralf
Schusdziarra, Volker
Allescher, Hans-Dieter
author_facet Storr, Martin
Thammer, Jutta
Dunkel, Ralf
Schusdziarra, Volker
Allescher, Hans-Dieter
author_sort Storr, Martin
collection PubMed
description BACKGROUND: Adenosine is known to act as a neuromodulator by suppressing synaptic transmission in the central and peripheral nervous system. Both the release of adenosine within the small intestine and the presence of adenosine receptors on enteric neurons have been demonstrated. The aim of the present study was to characterize a possible involvement of adenosine receptors in the modulation of the myenteric reflex. The experiments were carried out on ileum segments 10 cm in length incubated in an single chambered organ bath, and the reflex response was initiated by electrical stimulation (ES). RESULTS: ES caused an ascending contraction and a descending relaxation followed by a contraction. All motility responses to ES were completely blocked by tetrodotoxin, indicating that they are mediated by neural mechanisms. Atropine blocked the contractile effects, whereas the descending relaxation was significantly increased. The A(1 )receptor agonist N6-cyclopentyladenosine increased the ascending contraction, whereas the ascending contraction was reduced by the A(1 )receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine. Activation of the A(1 )receptor further reduced the descending relaxation and the latency of the peristaltic reflex. The A(2B )receptor antagonist alloxazine increased ascending contraction, whereas descending relaxation remained unchanged. For A(2A )and A(3 )receptors, we found contradictory effects of the agonists and antagonists, thus there is no clear physiological role for these receptors at this time. CONCLUSIONS: This study suggests that the myenteric ascending and descending reflex response of the rat small intestine is modulated by release of endogenous adenosine via A(1 )receptors.
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spelling pubmed-1399822003-01-20 Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum Storr, Martin Thammer, Jutta Dunkel, Ralf Schusdziarra, Volker Allescher, Hans-Dieter BMC Neurosci Research Article BACKGROUND: Adenosine is known to act as a neuromodulator by suppressing synaptic transmission in the central and peripheral nervous system. Both the release of adenosine within the small intestine and the presence of adenosine receptors on enteric neurons have been demonstrated. The aim of the present study was to characterize a possible involvement of adenosine receptors in the modulation of the myenteric reflex. The experiments were carried out on ileum segments 10 cm in length incubated in an single chambered organ bath, and the reflex response was initiated by electrical stimulation (ES). RESULTS: ES caused an ascending contraction and a descending relaxation followed by a contraction. All motility responses to ES were completely blocked by tetrodotoxin, indicating that they are mediated by neural mechanisms. Atropine blocked the contractile effects, whereas the descending relaxation was significantly increased. The A(1 )receptor agonist N6-cyclopentyladenosine increased the ascending contraction, whereas the ascending contraction was reduced by the A(1 )receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine. Activation of the A(1 )receptor further reduced the descending relaxation and the latency of the peristaltic reflex. The A(2B )receptor antagonist alloxazine increased ascending contraction, whereas descending relaxation remained unchanged. For A(2A )and A(3 )receptors, we found contradictory effects of the agonists and antagonists, thus there is no clear physiological role for these receptors at this time. CONCLUSIONS: This study suggests that the myenteric ascending and descending reflex response of the rat small intestine is modulated by release of endogenous adenosine via A(1 )receptors. BioMed Central 2002-12-20 /pmc/articles/PMC139982/ /pubmed/12495441 http://dx.doi.org/10.1186/1471-2202-3-21 Text en Copyright © 2002 Storr et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
spellingShingle Research Article
Storr, Martin
Thammer, Jutta
Dunkel, Ralf
Schusdziarra, Volker
Allescher, Hans-Dieter
Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum
title Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum
title_full Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum
title_fullStr Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum
title_full_unstemmed Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum
title_short Modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum
title_sort modulatory effect of adenosine receptors on the ascending and descending neural reflex responses of rat ileum
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC139982/
https://www.ncbi.nlm.nih.gov/pubmed/12495441
http://dx.doi.org/10.1186/1471-2202-3-21
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