Endo Toshiki, Spenger Christian, Hao Jingxia, Tominaga Teiji, Wiesenfeld-Hallin Zsuzsanna, Olson Lars, Xu Xiao-Jun
Department of Neuroscience, Karolinska Institutet, Retzius vag 8, B2:4, Stockholm 171 77, Sweden Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Retzius vag 8, B2:4, Stockholm 171 77, Sweden Section of Clinical Neurophysiology, Department of Clinical Neuroscience, Karolinska Institutet, Retzius vag 8, B2:4, Stockholm 171 77, Sweden Department of Neurosurgery, School of Medicine, Tohoku University, Sendai 980-8574, Japan.
Pain. 2008 Aug 31;138(2):292-300. doi: 10.1016/j.pain.2007.12.017. Epub 2008 Feb 6.
Functional magnetic resonance imaging (fMRI) has been used to map cerebral activations related to nociceptive stimuli in rodents. Here, we used fMRI to investigate abnormally increased responses to noxious or innocuous stimuli, in a well-established rat model of chronic neuropathic pain induced by photochemical lumbar spinal cord injury. In this model, a subpopulation of rats exhibits allodynia-like hypersensitivity to mechanical and cold stimulation of the trunk area. In those rats that do not develop overt hypersensitivity after identical spinal cord injury (i.e. non-hypersensitive rats), touch evoked pain can be triggered by the opioid receptor antagonist, naloxone. We show that cerebral activations in contralateral primary somatosensory cortex (SI) are markedly correlated with different behavioural characteristics of these animals. Identical electrical stimulation, applied on trunks of spinally injured hypersensitive and non-hypersensitive rats, evoked significantly higher responses in SI of the former than the latter. Although levels of fMRI signals in SI of the trunk territory were not significantly different between normal and spinally injured non-hypersensitive rats, the administration of naloxone significantly increased fMRI signals in the non-hypersensitive rats, but not in the normal rats. We conclude that increased activation of contralateral SI is a key feature of behavioural neuropathic pain in spinally injured rats and that fMRI is an effective method to monitor experimental neuropathic pain in small animals.
功能磁共振成像(fMRI)已被用于绘制与啮齿动物伤害性刺激相关的大脑激活区域。在此,我们使用fMRI来研究在一种成熟的由光化学性腰段脊髓损伤诱导的慢性神经性疼痛大鼠模型中,对有害或无害刺激的异常增强反应。在该模型中,一部分大鼠对躯干区域的机械和冷刺激表现出类似痛觉过敏的超敏反应。在那些脊髓损伤后未出现明显超敏反应的大鼠(即非超敏大鼠)中,阿片受体拮抗剂纳洛酮可引发触摸诱发的疼痛。我们发现,对侧初级体感皮层(SI)的大脑激活与这些动物的不同行为特征显著相关。对脊髓损伤的超敏和非超敏大鼠的躯干施加相同的电刺激,前者的SI区诱发反应显著高于后者。虽然正常大鼠和脊髓损伤的非超敏大鼠躯干区域SI的fMRI信号水平无显著差异,但纳洛酮给药显著增加了非超敏大鼠的fMRI信号,而正常大鼠则未增加。我们得出结论,对侧SI激活增加是脊髓损伤大鼠行为性神经性疼痛的关键特征,且fMRI是监测小动物实验性神经性疼痛的有效方法。