Babygirija Reji, Sood Manu, Kannampalli Pradeep, Sengupta Jyoti N, Miranda Adrian
Department of Pediatrics, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI, United States.
Department of Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI, United States.
Neuroscience. 2017 Jul 25;356:11-21. doi: 10.1016/j.neuroscience.2017.05.012. Epub 2017 May 17.
A non-invasive, auricular percutaneous electrical nerve field stimulation (PENFS) has been suggested to modulate central pain pathways. We investigated the effects of BRIDGE® device on the responses of amygdala and lumbar spinal neurons and the development of post-colitis hyperalgesia. Male Sprague-Dawley rats received intracolonic trinitrobenzene sulfonic acid (TNBS) and PENFS on the same day. Control rats had sham devices. The visceromotor response (VMR) to colon distension and paw withdrawal threshold (PWT) was recorded after 7days. A different group of rats had VMR and PWT at baseline, after TNBS and following PENFS. Extracellular recordings were made from neurons in central nucleus of the amygdala (CeA) or lumbar spinal cord. Baseline firing and responses to compression of the paw were recorded before and after PENFS. Sham-treated rats exhibited a much higher VMR (>30mmHg) and lower PWT compared to PENFS-treated rats (p<0.05). PENFS decreased the VMR to colon distension and increased the PWT compared to pre-stimulation (p<0.05). PENFS resulted in a 57% decrease in spontaneous firing of the CeA neurons (0.59±0.16 vs control: 1.71±0.32imp/s). Similarly, the response to somatic stimulation was decreased by 56% (3.6±0.52 vs control: 1.71±0.32 imps/s, p<0.05). Spinal neurons showed a 47% decrease in mean spontaneous firing (4.05±0.65 vs control: 7.7±0.87imp/s) and response to somatic stimulation (7.62±1.7 vs control: 14.8±2.28imp/s, p<0.05). PENFS attenuated baseline firing of CeA and spinal neurons which may account for the modulation of pain responses in this model of post-inflammatory visceral and somatic hyperalgesia.
一种非侵入性的耳穴经皮电神经场刺激（PENFS）已被认为可调节中枢疼痛通路。我们研究了BRIDGE®设备对杏仁核和腰脊髓神经元反应以及结肠炎后痛觉过敏发展的影响。雄性Sprague-Dawley大鼠在同一天接受结肠内三硝基苯磺酸（TNBS）和PENFS。对照大鼠安装假设备。7天后记录对结肠扩张的内脏运动反应（VMR）和爪部撤离阈值（PWT）。另一组大鼠在基线、TNBS后和PENFS后测量VMR和PWT。对杏仁核中央核（CeA）或腰脊髓中的神经元进行细胞外记录。记录PENFS前后的基线放电以及对爪部压迫的反应。与接受PENFS治疗的大鼠相比，假治疗大鼠表现出更高的VMR（>30mmHg）和更低的PWT（p<0.05）。与刺激前相比，PENFS降低了对结肠扩张的VMR并提高了PWT（p<0.05）。PENFS使CeA神经元的自发放电减少了57%（0.59±0.16对对照组：1.71±0.32次/秒）。同样，对躯体刺激的反应减少了56%（3.6±0.52对对照组：1.71±0.32次/秒，p<0.05）。脊髓神经元的平均自发放电减少了47%（4.05±0.65对对照组：7.7±0.87次/秒），对躯体刺激的反应也减少了（7.62±1.7对对照组：14.8±2.28次/秒，p<0.05）。PENFS减弱了CeA和脊髓神经元的基线放电，这可能解释了在这种炎症后内脏和躯体痛觉过敏模型中疼痛反应的调节机制。
