电解损毁杏仁中央核对大鼠牙移动疼痛的影响研究(3)
影像学、药理学及生理学等多种学科均证实杏仁核参与了疼痛的调控。Helmstette等发现杏仁核在应激镇痛时主要是通过激活脑干的下行抗伤害系统发挥作用的,损伤杏仁核可减弱应激的镇痛作用。利用功能磁共振成像(fMRI)的方法发现,当给予伴有能够引起强烈情绪反应的疼痛刺激时,杏仁核的信号增强。由于在fMRI实验中,杏仁核在疼痛时的激活为双侧性,因此Bingel等[14]认为杏仁核负责处理与疼痛情感成分有关的信息,但也有实验表明在给予伤害性热刺激时杏仁核信号降低[15]。
本研究发现,与假损毁对照组相比,双侧损毁CeA组大鼠的牙移动痛觉行为学减弱,尤其在4h~5d时间段内最为明显,而在7d和14d时间点上,与对照组无明显差异。单侧损毁CeA组大鼠的牙移动痛觉行为学也有明显的减弱,其变化规律与双侧损毁CeA组近似,但减弱程度比双侧损毁要更弱,差异均有统计学意义。而在其余时间点上,与对照组相比差异无统计学意义(P>0.05)。以上结果表明损毁杏仁中央核可显著减弱大鼠牙移动疼痛的程度,主要原因可能为为杏仁中央核参与了牙移动疼痛的中枢调控,如痛觉的编码和调制过程,故将该核团损毁后可起到阻断痛觉传导的效果,因此大鼠的牙移动疼痛症状可获得改善。
, 百拇医药
综上所述,杏仁中央核在牙移动疼痛调控中扮演重要角色,起着正性调控作用,有助于更深入理解正畸疼痛反应的机制,并将为正畸疼痛的治疗提供新的方法。
[参考文献]
[1]Asiry MA,Albarakati SF,Almarwan MS,et al.Perception of pain and discomfort from elastomeric separators in Saudi adolescents[J].Saudi Med J,2014,35(35):504-507.
[2]Hussain AS,Al MT,Elias WY.Methodologies in orthodontic pain management:a review[J].Open Dent J,2017,11:492-497.
[3]Larrea M,Salvador R,Cibrian R,et al.A new equation for predicting evolution of oral pain in orthodontic treatment:a longitudinal,prospective cohort study[J].J Oral Facial Pain Headache,2017,31(2):172-179.
, 百拇医药
[4]Thompson JM,Neugebauer V.Amygdala plasticity and pain[J].Pain Res Manag,2017,2017(2):1-12.
[5]Shinohara K,Watabe AM,Nagase M,et al.Essential role of endogenous calcitonin gene-related peptide in pain-associated plasticity in the central amygdala[J].Eur J Neurosci,2017,46(6):2149-2160.
[6]Brügger M,Lutz K, Br?nnimann B,et al.Tracing toothache intensity in the brain[J].J Dent Res,2012,91(2):156-160.
, 百拇医药
[7]Brugger M,Ettlin DA,Meier M,et al.Taking sides with pain- lateralization aspects related to cerebral processing of dental pain[J].Front Hum Neurosci,2011,5(1):12.
[8]Novaes AP,da Rocha MJ,Leite-Panissi CR.Tooth movement activates the central amygdala and the lateral hypothalamus by the magnitude of the force applied[J].Angle Orthod,2010,80(1):111-115.
[9]Qiao H,Gao Y,Zhang C,et al.Increased expression of TRPV1 in the trigeminal ganglion is involved in orofacial pain during experimental tooth movement in rats[J].Eur J Oral Sci,2015,123(1):17-23.
, 百拇医药
[10]Yang Z,Wang Y,Luo W,et al.Trigeminal expression of N-methyl-D-aspartate receptor subunit 1 and behavior responses to experimental tooth movement in rats[J]. Angle Orthod,2009,79(5):951-957.
[11]Yang Z,Cao Y,Wang Y,et al.Behavioural responses and expression of P2X receptor in trigeminal ganglion after experimental tooth movement in rats[J].Archives of Oral Biology,2009,54(1):63-70.
[12]Pannese E.The structure of the perineuronal sheath of satellite glial cells (SGCs) in sensory ganglia[J].Neuron Glia Biol,2010,6(1):3-10.
, 百拇医药
[13]Frühholz S,Schlegel K,Grandjean D.Amygdala structure and core dimensions of the affective personality[J].Brain Struct Funct,2017,222(9):3915-3925.
[14]Bingel U,Quante M,Knab R,et al.Subcortical structures involved in pain processing:evidence from single-trial fMRI[J].Pain,2002,99(1-2):313-321.
[15]Becerra LR,Breiter HC,Stojanovic M,et al.Human brain activation under controlled thermal stimulation and habituation to noxious heat:an fMRI study[J].Magn Reson Med,1999,41(5):1044-1057.
[收稿日期]2018-07-15 [修回日期]2018-10-31
編辑/贾敏, 百拇医药(乔虎 黄倩倩 周洪)
本研究发现,与假损毁对照组相比,双侧损毁CeA组大鼠的牙移动痛觉行为学减弱,尤其在4h~5d时间段内最为明显,而在7d和14d时间点上,与对照组无明显差异。单侧损毁CeA组大鼠的牙移动痛觉行为学也有明显的减弱,其变化规律与双侧损毁CeA组近似,但减弱程度比双侧损毁要更弱,差异均有统计学意义。而在其余时间点上,与对照组相比差异无统计学意义(P>0.05)。以上结果表明损毁杏仁中央核可显著减弱大鼠牙移动疼痛的程度,主要原因可能为为杏仁中央核参与了牙移动疼痛的中枢调控,如痛觉的编码和调制过程,故将该核团损毁后可起到阻断痛觉传导的效果,因此大鼠的牙移动疼痛症状可获得改善。
, 百拇医药
综上所述,杏仁中央核在牙移动疼痛调控中扮演重要角色,起着正性调控作用,有助于更深入理解正畸疼痛反应的机制,并将为正畸疼痛的治疗提供新的方法。
[参考文献]
[1]Asiry MA,Albarakati SF,Almarwan MS,et al.Perception of pain and discomfort from elastomeric separators in Saudi adolescents[J].Saudi Med J,2014,35(35):504-507.
[2]Hussain AS,Al MT,Elias WY.Methodologies in orthodontic pain management:a review[J].Open Dent J,2017,11:492-497.
[3]Larrea M,Salvador R,Cibrian R,et al.A new equation for predicting evolution of oral pain in orthodontic treatment:a longitudinal,prospective cohort study[J].J Oral Facial Pain Headache,2017,31(2):172-179.
, 百拇医药
[4]Thompson JM,Neugebauer V.Amygdala plasticity and pain[J].Pain Res Manag,2017,2017(2):1-12.
[5]Shinohara K,Watabe AM,Nagase M,et al.Essential role of endogenous calcitonin gene-related peptide in pain-associated plasticity in the central amygdala[J].Eur J Neurosci,2017,46(6):2149-2160.
[6]Brügger M,Lutz K, Br?nnimann B,et al.Tracing toothache intensity in the brain[J].J Dent Res,2012,91(2):156-160.
, 百拇医药
[7]Brugger M,Ettlin DA,Meier M,et al.Taking sides with pain- lateralization aspects related to cerebral processing of dental pain[J].Front Hum Neurosci,2011,5(1):12.
[8]Novaes AP,da Rocha MJ,Leite-Panissi CR.Tooth movement activates the central amygdala and the lateral hypothalamus by the magnitude of the force applied[J].Angle Orthod,2010,80(1):111-115.
[9]Qiao H,Gao Y,Zhang C,et al.Increased expression of TRPV1 in the trigeminal ganglion is involved in orofacial pain during experimental tooth movement in rats[J].Eur J Oral Sci,2015,123(1):17-23.
, 百拇医药
[10]Yang Z,Wang Y,Luo W,et al.Trigeminal expression of N-methyl-D-aspartate receptor subunit 1 and behavior responses to experimental tooth movement in rats[J]. Angle Orthod,2009,79(5):951-957.
[11]Yang Z,Cao Y,Wang Y,et al.Behavioural responses and expression of P2X receptor in trigeminal ganglion after experimental tooth movement in rats[J].Archives of Oral Biology,2009,54(1):63-70.
[12]Pannese E.The structure of the perineuronal sheath of satellite glial cells (SGCs) in sensory ganglia[J].Neuron Glia Biol,2010,6(1):3-10.
, 百拇医药
[13]Frühholz S,Schlegel K,Grandjean D.Amygdala structure and core dimensions of the affective personality[J].Brain Struct Funct,2017,222(9):3915-3925.
[14]Bingel U,Quante M,Knab R,et al.Subcortical structures involved in pain processing:evidence from single-trial fMRI[J].Pain,2002,99(1-2):313-321.
[15]Becerra LR,Breiter HC,Stojanovic M,et al.Human brain activation under controlled thermal stimulation and habituation to noxious heat:an fMRI study[J].Magn Reson Med,1999,41(5):1044-1057.
[收稿日期]2018-07-15 [修回日期]2018-10-31
編辑/贾敏, 百拇医药(乔虎 黄倩倩 周洪)
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