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豚鼠黏膜下神经丛中对霍乱毒素敏感的神经元。

Cholera toxin-sensitive neurons in guinea pig submucosal plexus.

作者信息

Jiang M M, Kirchgessner A, Gershon M D, Surprenant A

机构信息

Vollum Institute, Oregon Health Sciences University, Portland 97201.

出版信息

Am J Physiol. 1993 Jan;264(1 Pt 1):G86-94. doi: 10.1152/ajpgi.1993.264.1.G86.

DOI:10.1152/ajpgi.1993.264.1.G86
PMID:8430809
Abstract

Cholera toxin (CT) increases intestinal secretions by direct stimulation of mucosal enterocytes; enteric neurons also may play a role. We tested the latter possibility by retrograde labeling of mucosal terminals in guinea pig small intestine with the B subunit of CT (B-CT) and by intracellular recordings from submucosal neurons during superfusion with CT. All vasoactive intestinal peptide (VIP)-positive neurons, and only VIP-positive neurons, were labeled with B-CT. Fluorogold (FG) was used to retrogradely label nerve terminals in submucosal arterioles in preparations in which B-CT labeled mucosal terminals; colocalization of B-CT with FG was observed in neurons up to 3 mm from the site of FG application. CT selectively depolarized neurons known to contain VIP. We conclude that all VIP-containing neurons, and only VIP neurons, in guinea pig submucosal plexus possess B-CT binding sites and can be activated by CT. Some of these neurons provide a dual innervation to both arterioles and mucosa. We suggest that one functional consequence of CT may be to activate vasodilator nerves, thus increasing vascular perfusion of the mucosa to further stimulate intestinal secretions.

摘要

霍乱毒素(CT)通过直接刺激黏膜肠上皮细胞增加肠道分泌;肠神经元也可能起作用。我们通过用CT的B亚基(B-CT)逆行标记豚鼠小肠黏膜终末以及在CT灌流期间对黏膜下神经元进行细胞内记录来检验后一种可能性。所有血管活性肠肽(VIP)阳性神经元,且只有VIP阳性神经元,被B-CT标记。在B-CT标记黏膜终末的标本中,用荧光金(FG)逆行标记黏膜下小动脉的神经终末;在距FG应用部位3毫米以内的神经元中观察到B-CT与FG的共定位。CT选择性地使已知含有VIP的神经元去极化。我们得出结论,豚鼠黏膜下神经丛中所有含VIP的神经元,且只有VIP神经元,具有B-CT结合位点,并且可被CT激活。其中一些神经元对小动脉和黏膜都提供双重神经支配。我们认为CT的一个功能后果可能是激活血管舒张神经,从而增加黏膜的血管灌注以进一步刺激肠道分泌。

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