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Spontaneous hypersensitivity in mesenteric afferent nerves of mice deficient in the sst2 subtype of somatostatin receptor
Ist Teil von
The Journal of physiology, 2007-06, Vol.581 (2), p.779-786
Ort / Verlag
Oxford, UK: The Physiological Society
Erscheinungsjahr
2007
Link zum Volltext
Quelle
Free E-Journal (出版社公開部分のみ)
Beschreibungen/Notizen
Somatostatin is an inhibitory peptide present in abundance in the gastrointestinal (GI) tract. The effects of somatostatin
are mediated through its interaction with a family of G-protein-coupled receptors, namely sst1â5. Previous evidence suggested
that the sst2 receptor mediates an inhibitory role of somatostatin on GI afferent nerve sensitivity. In the present study
we further evaluated mechanical and chemical sensitivity of mesenteric afferents in mice deficient in the sst2 receptor. Multi-unit
recordings were made from mesenteric afferents from mouse jejunal segments perfused in vitro . Ramp distension of the jejunum up to 60 mmHg induced biphasic increases in afferent activity in both wild-type (WT) and
sst2 gene knock-out (KO) mice. However, the level of afferent activity was significantly higher in the KO ( n
= 15) compared to the WT ( n
= 16) mice across the entire pressure range. The mesenteric afferent sensitivity to acid was evaluated by intraluminal
infusion of hydrochloric acid (HCl 20 m m ) for 2 min. Peak afferent discharge rate following acid infusion was significantly greater in KO (36.76 ± 6.47 impulses s â1 , n
= 7) than in WT preparations (16.53 ± 3.91 impulses s â1 , n
= 5, P < 0.01). The response to bath-applied bradykinin (1 μ m , 3 ml) was not significantly different in the KO and the WT preparations. It is interesting that in the WT preparations,
octreotide inhibited both low- and high-threshold mechanosensory responses, whereas in the sst2 KO group it appeared to inhibit the low-threshold responses preferentially and failed to affect the high-threshold responses.
The results of the present investigation demonstrate that sst2 deficiency is associated with exaggerated jejunal afferent sensitivity to both mechanical and chemical stimulations, suggesting
that somatostatin plays an important inhibitory role in the control of visceral sensitivity by interacting with the sst2 receptor.