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第四脑室注射辣椒素可减轻肠道营养物质诱导的假饲抑制。

Fourth ventricular capsaicin attenuates suppression of sham feeding induced by intestinal nutrients.

作者信息

Yox D P, Stokesberry H, Ritter R C

机构信息

Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman 99164-6520.

出版信息

Am J Physiol. 1991 Apr;260(4 Pt 2):R681-7. doi: 10.1152/ajpregu.1991.260.4.R681.

DOI:10.1152/ajpregu.1991.260.4.R681
PMID:2012240
Abstract

Systemic treatment with capsaicin, a neurotoxin that destroys small unmyelinated primary sensory neurons, causes degeneration of vagal sensory fibers and attenuates suppression of sham feeding by exogenous cholecystokinin (CCK) or intraintestinally infused nutrients. To determine whether capsaicin-sensitive neurons or fibers in the hindbrain mediate suppression of feeding by intestinal nutrients, we examined nutrient-induced suppression of sham feeding in rats pretreated with fourth ventricular capsaicin. Capsaicin treatment abolished the suppression of sham feeding induced by intraperitoneal injection of CCK octapeptide or by intraintestinal maltose. Oleate-induced suppression of sham feeding also was significantly attenuated in capsaicin-treated rats. Capsaicin treatment, however, did not attenuate suppression of sham feeding by intraintestinal L-phenylalanine. These results indicate that capsaicin-sensitive substrates, located near the fourth ventricle, participate in the suppression of sham feeding by CCK and by some intestinal stimuli. Taken together with previously reported data, these results suggest that suppression of sham feeding by some intestinal nutrients is mediated by a neuronal substrate similar or identical to one that mediates suppression of feeding by exogenous CCK.

摘要

用辣椒素进行全身治疗,辣椒素是一种能破坏无髓鞘初级感觉神经元的神经毒素,会导致迷走神经感觉纤维退化,并减弱外源性胆囊收缩素(CCK)或肠道内注入营养物质对假饲的抑制作用。为了确定后脑中对辣椒素敏感的神经元或纤维是否介导肠道营养物质对进食的抑制作用,我们研究了用第四脑室注射辣椒素预处理的大鼠中营养物质诱导的假饲抑制情况。辣椒素处理消除了腹腔注射CCK八肽或肠道内麦芽糖诱导的假饲抑制作用。在经辣椒素处理的大鼠中,油酸诱导的假饲抑制作用也显著减弱。然而,辣椒素处理并未减弱肠道内L-苯丙氨酸对假饲的抑制作用。这些结果表明,位于第四脑室附近的对辣椒素敏感的底物参与了CCK和某些肠道刺激对假饲的抑制作用。结合先前报道的数据,这些结果表明,某些肠道营养物质对假饲的抑制作用是由一种与介导外源性CCK对进食抑制作用相似或相同的神经元底物介导的。

相似文献

1
Fourth ventricular capsaicin attenuates suppression of sham feeding induced by intestinal nutrients.第四脑室注射辣椒素可减轻肠道营养物质诱导的假饲抑制。
Am J Physiol. 1991 Apr;260(4 Pt 2):R681-7. doi: 10.1152/ajpregu.1991.260.4.R681.
2
Capsaicin attenuates suppression of sham feeding induced by intestinal nutrients.辣椒素可减轻肠道营养物质诱导的假饲抑制。
Am J Physiol. 1988 Oct;255(4 Pt 2):R569-74. doi: 10.1152/ajpregu.1988.255.4.R569.
3
Vagotomy attenuates suppression of sham feeding induced by intestinal nutrients.迷走神经切断术可减弱肠道营养物质对假饲的抑制作用。
Am J Physiol. 1991 Mar;260(3 Pt 2):R503-8. doi: 10.1152/ajpregu.1991.260.3.R503.
4
CCK-receptor antagonists attenuate suppression of sham feeding by intestinal nutrients.
Am J Physiol. 1992 Apr;262(4 Pt 2):R554-61. doi: 10.1152/ajpregu.1992.262.4.R554.
5
Intestinal capsaicin transiently attenuates suppression of sham feeding by oleate.肠道辣椒素可短暂减轻油酸对假饲的抑制作用。
Am J Physiol. 1994 Aug;267(2 Pt 2):R561-8. doi: 10.1152/ajpregu.1994.267.2.R561.
6
Capsaicin pretreatment attenuates suppression of food intake by cholecystokinin.辣椒素预处理可减轻胆囊收缩素对食物摄入的抑制作用。
Am J Physiol. 1985 Apr;248(4 Pt 2):R501-4. doi: 10.1152/ajpregu.1985.248.4.R501.
7
Capsaicin application to central or peripheral vagal fibers attenuates CCK satiety.将辣椒素应用于中枢或外周迷走神经纤维可减弱胆囊收缩素的饱腹感。
Peptides. 1988 May-Jun;9(3):601-12. doi: 10.1016/0196-9781(88)90171-4.
8
Suppression of sham feeding by intraintestinal nutrients is not correlated with plasma cholecystokinin elevation.肠内营养对假饲的抑制作用与血浆胆囊收缩素升高无关。
Am J Physiol. 1993 May;264(5 Pt 2):R972-6. doi: 10.1152/ajpregu.1993.264.5.R972.
9
Capsaicin attenuates hindbrain neuron responses to circulating cholecystokinin.辣椒素可减弱后脑神经元对循环胆囊收缩素的反应。
Am J Physiol. 1989 Nov;257(5 Pt 2):R1162-8. doi: 10.1152/ajpregu.1989.257.5.R1162.
10
Intracerebroventricular cholecystokinin A-receptor antagonist does not reduce satiation by endogenous CCK.脑室内胆囊收缩素A受体拮抗剂不会因内源性胆囊收缩素而降低饱腹感。
Physiol Behav. 1998 Feb 15;63(4):711-6. doi: 10.1016/s0031-9384(97)00519-2.

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