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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Anandamide-evoked activation of vanilloid receptor 1 contributes to the development of bladder hyperreflexia and nociceptive transmission to spinal dorsal horn neurons in cystitis.
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Anandamide-evoked activation of vanilloid receptor 1 contributes to the development of bladder hyperreflexia and nociceptive transmission to spinal dorsal horn neurons in cystitis.

机译：花生四烯酸诱发的类香草酸受体1的激活有助于膀胱反射亢进的发展，并伤害性传递至膀胱炎中的脊髓背角神经元。

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摘要

The role of anandamide in the development of inflammatory hyperalgesia and visceral hyperreflexia was studied in the rat urinary bladder. Animals were given intraperitoneal cyclophosphamide injection, which evokes painful hemorrhagic cystitis accompanied by increased bladder reflex activity. The vanilloid receptor 1 [transient receptor potential vanilloid 1 (TRPV1)] antagonist capsazepine, applied onto the serosal surface of bladders, significantly reduced the hyperreflexia. Mass spectrometric analysis revealed that cyclophosphamide injection significantly and persistently increased the anandamide content of bladder tissues. The increase in the anandamide content paralleled the development of reflex hyperactivity. Anandamide (1-100 microm), applied onto the serosal surface of naive bladders, increased the reflex activity in a concentration-dependent manner. Repeated anandamide applications did not produce desensitization of the response. The anandamide-evoked effect was blocked by capsazepine or by instillation of resiniferatoxin, the ultrapotent TRPV1 agonist, into the bladders 24 hr before the anandamide challenge. The cannabinoid 1 receptor antagonist SR141716A [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3 -carboxamide] significantly increased the potency of anandamide in enhancing bladder reflex activity in naive but not in cyclophosphamide-injected animals. Application of the fatty acid amide hydrolyze inhibitor palmitoylisopropylamine onto the serosal surface of bladders also increased the reflex activity both in naive and cyclophosphamide-injected rats. This latter effect in naive animals was blocked by capsazepine and by resiniferatoxin pretreatment. Finally, intravesical instillation of anandamide (50 microm) increased c-fos expression in the spinal cord, which was reduced by capsazepine or by resiniferatoxin pretreatment. These results suggest that anandamide, through activating TRPV1, contributes to the development of hyperreflexia and hyperalgesia during cystitis.
机译：在大鼠膀胱中研究了anandamide在炎症性痛觉过敏和内脏高反射性反应中的作用。给动物腹膜内注射环磷酰胺，这会引起痛苦的出血性膀胱炎，并伴有膀胱反射活性的增加。施用在膀胱浆膜表面的类香草酸受体1 [transient receptor potential Vanilloid 1（TRPV1）]拮抗剂卡塞平显着降低了反射亢进。质谱分析表明，环磷酰胺注射显着并持续增加了膀胱组织中的anandamide含量。阿南酰胺含量的增加与反射亢进的发展平行。应用于幼稚膀胱浆膜表面的Anandamide（1-100微米）以浓度依赖性方式增加了反射活性。重复使用anandamide不会导致反应减敏。在辣椒素攻击前24小时，辣椒碱或超强TRPV1激动剂树酯毒素被滴注到膀胱中，从而阻断了腺苷酰胺引起的作用。大麻素1受体拮抗剂SR141716A [N-哌啶子基-5-（4-氯苯基）-1-（2,4-二氯苯基）-4-甲基吡唑-3-羧酰胺]显着提高了大麻素在增强幼稚期膀胱反射活性方面的功效。但不是在注射环磷酰胺的动物中。将脂肪酸酰胺水解抑制剂棕榈酰异丙基胺施用于膀胱的浆膜表面，还可以提高幼稚和环磷酰胺注射大鼠的反射活性。后者在幼稚动物中的作用被辣椒碱和树脂毒素预处理所阻断。最后，囊腔内滴入anandamide（50微米）可增加脊髓中c-fos的表达，但卡扎西平或resiniferatoxin预处理可降低c-fos的表达。这些结果表明，阿南酰胺通过激活TRPV1，在膀胱炎期间促进反射亢进和痛觉过敏的发展。

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