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首页> 外文期刊>Pain. >Bilateral behavioral and regional cerebral blood flow changes during painful peripheral mononeuropathy in the rat.
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Bilateral behavioral and regional cerebral blood flow changes during painful peripheral mononeuropathy in the rat.

机译:大鼠疼痛性周围性单神经病期间,双侧行为和局部脑血流量发生变化。

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摘要

A unilateral chronic constriction injury (CCI) of the sciatic nerve produced bilateral effects in both pain related behaviors and in the pattern of forebrain activation. All CCI animals exhibited spontaneous pain-related behaviors as well as bilateral hyperalgesia and allodynia after CCI. Further, we identified changes in baseline (unstimulated) forebrain activation patterns 2 weeks following CCI by measuring regional cerebral blood flow (rCBF). Compared to controls, CCI consistently produced detectable, well-localized and typically bilateral increases in rCBF within multiple forebrain structures in unstimulated animals. For example, the hindlimb region of somatosensory cortex was significantly activated (22%) as well as multiple thalamc nuclei, including the ventral medial (8%), ventral posterior lateral (10%) and the posterior (9%) nuclear groups. In addition, several forebrain regions considered to be part of the limbic system showed pain-induced changes in rCBF, including the anterior dorsal nucleus of the thalamus (23%), cingulate cortex (18%), retrosplenial cortex (30%), habenular complex (53%), interpeduncular nucleus (45%) and the paraventricular nucleus of the hypothalamus (30%). Our results suggest that bilateral somatosensory and limbic forebrain structures participate in the neural mechanisms of prolonged persistent pain produced by a unilateral injury.
机译:坐骨神经的单侧慢性压迫性损伤(CCI)在疼痛相关行为和前脑激活模式方面均产生了双侧影响。 CCI后,所有CCI动物均表现出自发的疼痛相关行为以及双侧痛觉过敏和异常性疼痛。此外,我们通过测量局部脑血流量(rCBF)确定了CCI 2周后基线(未刺激)前脑激活模式的变化。与对照相比,CCI持续在未受刺激的动物的多个前脑结构内产生可检测的,定位良好的且典型地双向增加的rCBF。例如,躯体感觉皮层的后肢区域被显着激活(22%)以及多个丘脑核,包括腹内侧(8%),腹后外侧(10%)和后核(9%)。此外,一些被认为是边缘系统一部分的前脑区域显示了rCBF的疼痛诱发变化,包括丘脑的前背背核(23%),扣带状皮层(18%),脾后皮层(30%),ha状复合体(53%),椎弓根间核(45%)和下丘脑室旁核(30%)。我们的结果表明,双侧体感和边缘前脑结构参与了由单侧损伤产生的持续持续疼痛的神经机制。

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