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This Article Full Text Full Text (PDF) All Versions of this Article: 297/4/G655    most recent 00128.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Mueller, M. H. Articles by Kreis, M. E. PubMed PubMed Citation Articles by Mueller, M. H. Articles by Kreis, M. E.

NEUROREGULATION AND MOTILITY

Extrinsic afferent nerve sensitivity and enteric neurotransmission in murine jejunum in vitro

¹Department of Surgery and ²Walter-Brendel Institute of Surgical Research, Ludwig-Maximilian's University, Munich; ³Department of Surgery, University of Tuebingen, Tuebingen Germany; ⁴Department of Biomedical Science, University of Sheffield, Sheffield, United Kingdom

Submitted April 1, 2009 ; accepted in final form July 23, 2009

Enteric and extrinsic sensory neurons respond to similar stimuli. Thus they may be activated in series or in parallel. Because signal transmission via synapses or mediator release would depend on calcium, we investigated its role for extrinsic afferent sensitivity to chemical and mechanical stimulation. Extracellular multiunit afferent recordings were made in vitro from paravascular nerve bundles supplying the mouse jejunum. Intraluminal pressure and afferent nerve responses were recorded under control conditions and under four conditions designed to interfere with enteric neurotransmission. We found that phasic intestinal contractions ceased after switching perfusion to Ca²⁺-free buffer with or without a purinergic P2 receptor antagonist, pyridoxal phosphate-6-azo(benzene-2,4-disulfonic acid) (PPADS) or cadmium (blocking all Ca²⁺-channels) but not following -conotoxin GVIA (N-type Ca²⁺-channel blocker). Luminal HCl (pH 2) and 5-HT (500 µM) evoked peak firing of 17 ± 4 impulses per second (imp/s) (n = 10) and 21 ± 4 imp/s (n = 13) under control conditions. These responses were reduced to 4 ± 2 imp/s and 5 ± 2 imp/s by cadmium (n = 7, P < 0.05), to 7 ± 2 imp/s and 6 ± 1 imp/s by Ca²⁺-free perfusion (n = 6, P < 0.05), and to 3 ± 1 imp/s and 4 ± 1 imp/s by Ca²⁺-free perfusion with PPADS (n = 6, P < 0.05). Responses were unchanged by -conotoxin GVIA. Mechanical ramp distension of the intestinal segment to 60 cmH₂O was not altered by any of the experimental conditions. We concluded that HCl and 5-HT activate extrinsic afferents via a calcium-dependent mechanism, which is unlikely to involve enteric neurons carrying N-type calcium channels. Extrinsic mechanosensitivity is independent of enteric neurotransmission. It appears that cross talk from the enteric to the extrinsic nervous system does not mediate extrinsic afferent sensitivity.

HCl; 5-HT; mouse