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新生儿膀胱炎症改变成年大鼠脊髓内脏伤害感受神经元的活动。

Neonatal bladder inflammation alters activity of adult rat spinal visceral nociceptive neurons.

机构信息

Department of Anesthesiology, University of Alabama at Birmingham, 1530 Third Avenue South, BMR2-270, Birmingham, AL 35294-0006, USA.

出版信息

Neurosci Lett. 2010 Mar 26;472(3):210-4. doi: 10.1016/j.neulet.2010.02.007. Epub 2010 Feb 10.

Abstract

PURPOSE

This investigation examined the effect of inflammation produced by intravesical zymosan during the neonatal period on spinal dorsal horn neuronal responses to urinary bladder distension (UBD) as adults.

METHODS

Female rat pups (P14-P16) were treated with intravesical zymosan or with anesthesia-only. These groups of rats were subdivided forming four groups: half received intravesical zymosan as adults and half received anesthesia-only. One day later, rats were anesthetized, the spinal cord was transected at a cervical level and extracellular single-unit recordings of L6-S1 dorsal horn neurons were obtained. Neurons were classified as Type I--inhibited by heterotopic noxious conditioning stimuli (HNCS) or as Type II--not inhibited by HNCS--and were characterized for Spontaneous Activity and responses to graded UBD (20-60 mm Hg).

RESULTS

227 spinal dorsal horn neurons excited by UBD were characterized. In rats treated as neonates with anesthesia-only, Type II neurons demonstrated increased spontaneous and UBD-evoked activity following adult intravesical zymosan treatment whereas Type I neurons demonstrated decreased spontaneous and UBD-evoked activity relative to controls. In rats treated as neonates with intravesical zymosan, the spontaneous and UBD-evoked activity of both Type I and Type II neurons increased following adult intravesical zymosan treatment relative to controls.

CONCLUSIONS

Neonatal bladder inflammation alters subsequent effects of acute bladder inflammation on spinal dorsal horn neurons excited by UBD such that overall there is greater sensory neuron activation. This may explain the visceral hypersensitivity noted in this model system and suggest that impaired inhibitory systems may be responsible.

摘要

目的

本研究旨在探讨新生期膀胱内酵母聚糖引起的炎症对成年后膀胱扩张(UBD)时脊髓背角神经元反应的影响。

方法

对雌性幼鼠(P14-P16)进行膀胱内酵母聚糖或仅麻醉处理。将这些大鼠分为四组:一半在成年时接受膀胱内酵母聚糖处理,另一半接受仅麻醉处理。一天后,对大鼠进行麻醉,在颈段切断脊髓,记录 L6-S1 背角神经元的细胞外单细胞记录。将神经元分为 I 型-被异位伤害性条件刺激(HNCS)抑制或 II 型-不受 HNCS 抑制-并对其自发性活动和对分级 UBD(20-60mmHg)的反应进行特征描述。

结果

对 227 个由 UBD 兴奋的脊髓背角神经元进行了特征描述。在仅麻醉处理的新生期大鼠中,接受成年期膀胱内酵母聚糖处理后,II 型神经元的自发性和 UBD 诱发活动增加,而 I 型神经元的自发性和 UBD 诱发活动相对于对照组减少。在接受膀胱内酵母聚糖处理的新生期大鼠中,接受成年期膀胱内酵母聚糖处理后,I 型和 II 型神经元的自发性和 UBD 诱发活动均相对于对照组增加。

结论

新生儿膀胱炎症改变了随后急性膀胱炎症对 UBD 兴奋的脊髓背角神经元的影响,使得总的感觉神经元激活增加。这可能解释了该模型系统中观察到的内脏高敏性,并提示受损的抑制系统可能是原因。

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