蛋白激酶A参与介导大鼠受损背根节神经元的自发放电

目的在背根节(DRG)慢性压迫模型上,采用单纤维记录神经元自发放电和生化检测受损组织中蛋白激酶A(protein kinase,PKA)活性的方法,研究PKA在DRG压迫损伤后感觉神经元中自发放电的作用.结果压迫损伤侧DRG组织中的PKA磷酸化PepTag肽百分数为25.51±2.62%,较未受压迫侧和正常组DRG组织明显增加(P＜0.05).PKA催化亚单位抑制剂H-89(10μM)可以明显抑制受损DRG神经元的自发放电,抑制百分数为76.91±13.79%.结论受损DRG组织中PKA活性上调,高活性的PKA参与介导受损DRG神经元的自发放电.     

瞬时感受器电位离子通道4在大鼠背根神经节持续受压后异位放电中的作用

目的:利用在体神经纤维电生理技术记录大鼠背根神经节(DRG)持续受压(CCD)后的异位放电情况,明确瞬时感受器电位离子通道4(TRPV4)是否参与了CCD后受损DRG的异位放电。方法:共采用35只Wistar大鼠。制备大鼠DRG的CCD模型,分别于术前和术后测量损伤侧的机械痛阈和热辐射刺激缩爪反应潜伏期。利用在体神经纤维电生理技术分别记录正常组大鼠DRG及CCD组、CCD+钌红(RR)组、CCD+佛波醇(4α-PDD)组受损DRG神经元的异位放电情况。结果:持续压迫明显降低大鼠损伤侧的机械痛阈和热辐射刺激缩爪反应潜伏期(n=30,P0.05);CCD组可以记录到受损DRG神经元的异位放电,放电率约为67%,而正常组DRG的异位放电率约为4.5%;以TRP家族阻断剂钌红(RR)100μm孵育受损DRG,较CCD组受损DRG神经元异位放电的频率和波幅均明显下降(n=10,P0.05);以TRPV4特异性激动剂佛波醇(4α-PDD)10μm孵育受损DRG,较CCD组受损DRG异位放电频率和波幅均明显增加(n=10,P0.05)。结论:CCD后受损DRG可出现异位放电,TRPV4参与了CCD后受损DRG的异位放电。     

受损背根节A类神经元的阈下膜电位振荡

目的：研究慢性压迫大鼠背根神经节(dorsal root ganglion，DRG)神经元阈下膜电位振荡(subthreshold membrane potential oscillation，SMPO)的特征及其与异位自发放电的关系。方法：采用在体DRG神经元细胞内记录。结果：在慢性压迫的650例DRG神经元，93例A类神经元出现具有特定频率及幅值的SMPO。对其进行研究发现，异位自发放电起始于SMPO的上升相，SMPO的规则、梭形及不规则形式分别决定了异位自发放电的周期／整数倍、阵发及不规则放电模式。有SMPO的神经元，其兴奋性高于没有SMPO的神经元。此外，低浓度河豚毒可以阻断SMPO的产生，进而消除异位自发放电。结论：阈下膜电位振荡是产生异位自发放电的基础，反映了初级感觉神经元超兴奋的基本电生理变化。     

兔腰神经根慢性压迫和炎症刺激后背根神经节的形态学变化研究

目的 分别经光镜和电镜观察兔腰神经根经慢性压迫和炎症刺激后背根神经节(dorsalrootganglion，DRG)的形态学变化。方法 纯种新西兰大白兔20只，随机分为对照组(5只)和实验组(15只)，实验组又分为损伤后10d、30d和90d组。取兔尾部的自体髓核组织放入内径1．5mm、外径2．5mm、管壁带孔的硅胶管内，压迫左侧L，神经根，实验组各亚组分别于造模后10d、30d、90d取材，作光镜及电镜观察。结果 10d组中，经压迫和炎症刺激后神经根与DRG胞膜水肿，内膜间隙明显充血、水肿，大量炎性细胞浸润，出现变性、坏死及小胶质细胞“嗜神经”现象；DRG胞质内粗面内质网及线粒体等细胞器含量减少，粗面内质网核糖体脱落，线粒体肿胀；细胞核常染色质淡染且分布不均匀，核膜皱褶。30d组DRG胞膜稍增厚，节细胞染色不均，部分神经元出现变性、坏死，DRG溶酶体与滑面内质网含量增多，线粒体肿胀，嵴部分消失，核仁浓缩偏向一侧。90d组DRG胞膜明显增厚，节细胞内纤维样改变：溶酶体及滑面内质网含量增多，线粒体肿胀、嵴消失，核仁浓缩居中。结论 神经根慢性压迫和自体髓核刺激可导致神经组织出现水肿、炎性细胞浸润以及神经纤维增生等神经变性改变。     

兔腰神经根慢性炎性压迫后的行为学改变及超短波疗效观察

目的 通过观测模拟腰椎间盘突出动物模型的神经行为学改变，探讨超短波治疗对神经源性疼痛的疗效。方法 从椎间外孔赛入带髓核的有孔硅胶管，建立兔腰神经根慢性炎性压迫模型。测定动物的运动功能，热辐射刺激缩腿反应的潜伏期及电刺激痛阈值，观察空白对照组，损伤模型组和超短波治疗组在损伤后不同时间(10d,30d和90d)时的动物神经行为改变情况。结果 损伤模型组动物患肢的热痛阈和电痛阈发生改变，出现明显痛觉过敏的现象；超短波治疗组动物在损伤后10d时患肢亦出现痛觉过敏的现象，但在损伤后30d时已基本恢复正常。结论 兔腰神经根受到慢性压迫和自体髓核刺激后可引起痛觉过敏，而超短波治疗对兔腰神经根慢性炎性压迫后产生的神经源性疼痛具有积极的治疗作用。     

慢性间歇性缺氧对幼年大鼠认知功能的影响及机制研究

目的 观察慢性间歇性缺氧对幼年大鼠认知功能的影响并探讨其发生机制.方法 （20±2）日龄SD雄性大鼠40只,随机分为正常组和慢性间歇性缺氧组.将慢性间歇性缺氧组幼鼠置入自制缺氧舱内每天缺氧8h,连续缺氧2周,建立模型后,利用Morris水迷宫检测认知功能的变化,记录海马CA1区神经元自发放电频率和幅度,利用HE染色和免疫组化法观察海马结构改变和GAP-43的表达情况.结果 与正常组比较,慢性间歇性缺氧组体重较轻（P＜0.05）,在Morris水迷宫测试中逃避潜伏期明显延长（P＜0.05）,穿越平台次数明显减少（P＜0.05）;海马CA1区神经元自发放电频率、波幅减小（P＜0.05）,海马CA1区出现明显的损伤,GAP-43表达增高（P＜0.05）.结论 慢性间歇性缺氧可引起幼年大鼠认知功能损伤,而海马神经元突触可塑性的改变可能是认知功能损伤的机制.     

海洛因依赖对大鼠杏仁核神经元自发放电的影响

目的：观察海洛因依赖SD大鼠杏仁核神经元自发放电及伤害性刺激对神经元自发放电的影响。 方法：实验于2004-12／2005-02在贵阳医学院生理教研室完成。选择健康SD大鼠45只，随机分为海洛因依赖组（n=25）和对照组（n=20）。海洛因依赖组按剂量（13mg/kk曲逐日递增原则，2次／d，连续9d皮下注射海洛因，首日剂量3mg／kg。对照组以同样方法注射等量生理盐水。第10天用5mg／kg纳洛酮腹腔注射催促戒断，确定海洛因依赖模型的建立成瘾后的大鼠从第10天起，给予海洛因维持剂量27mg／kg，1次／d。对照组同样方法注射等量生理盐水。给药12d后用玻璃微电极细胞外记录两组大鼠杏仁核神经元自发放电及鼠尾伤害性刺激对自发放电的影响。 结果：纳入大鼠45只，实验组在建立模型过程中有2只死亡，另外随机选取大鼠补充，最终进入结果分析大鼠保持为45只。①海洛因依赖组记录到114个单位神经元放电，对照组记录到80个。②两组大鼠杏仁核神经元可观察到单个不匀、束簇状和混合型3种放电形式，海洛因依赖组和对照组杏仁核神经元自发放电均以单个不匀为主，对照组中束簇状（7．5％）和混合型（13．8％）放电所占比例高于海洛因依赖组（1．8％和7．0％），组间差异有显著性意义（P〈0．05）。③海洛因依赖组大鼠杏仁核自发放电以低频为主（57．9％），而对照组则以低频（46.3％）和中频（47．5％）为主（P〈0．05）。④给予伤害性刺激后，大鼠杏仁核神经元自发放电表现为激活、抑制和无影响3种效应。实验组大鼠杏仁核神经元中频放电以抑制（45％）和无影响（40％）为主，而对照组以无影响为主（70％）。组间差异有显著性意义（P〈0．05）。⑤伤害性刺激后两组大鼠杏仁核神经元低频放电无变化。 结论：海洛因对大鼠杏仁核神经元自发放电的形式和频率产生影响，海洛因对伤害性刺激后大鼠杏仁核神经元中频放电产生影响。     

大鼠背根节慢性压迫对行为和电生理反应的影响

在麻醉消毒手术条件下，经大鼠Ｌ５椎间孔插入长４ｍｍ，直径０．５￣０．８ｍｍ的不锈钢线，可以形成对背根节及邻近神经根慢性稳定的压迫。经热痛缩腿反射潜伏期检测，术后５￣４２天，受损侧后肢足底的潜伏期显著缩短，表明持续的痛觉过敏。受损背根节与Ａ类纤维连接的神经元，自发放电的发生率明显增高，并显示多种放电的节律形式，该类神经元对背根节的机械压力刺激非常敏感，后放电过程显著延长；对局部浸浴ＴＥＡ也产生相对特     

兔腰神经根慢性压迫后超短波的治疗作用

目的　观察兔腰神经根慢性压迫后次日开始应用超短波共治疗 1 0次的效果。方法　纯种新西兰成年兔 2 8只 ,4只作神经定位解剖 ,其余 2 4只全部做手术造成腰神经慢性压迫 ,随机分成 2组 ,未处理组和超短波组 ,每组又分 1 0d组、30d组和 1 80d组。压迫模型 :将硅胶管从椎间外孔缓慢塞入椎间管内 ,压迫腰 6和腰 7左侧神经根直到实验兔被处死 ,右侧为自身对照侧。电生理测定潜伏时 (latency,Lat)和神经传导速度 (nerveconductionvelocity,NCV)。脉冲超短波于手术后的次日开始应用 ,无热量 ,1 0min,对置 ,治疗间隙 3cm ,每日一次 ,共 1 0次。结果　未处理组中 1 0d组神经根手术侧与非手术侧比较 ,潜伏时和神经传导速度均无差异 ;而 30d组与 1 80d组的潜伏时显著延长、神经传导速度显著减慢。超短波治疗的神经传导速度 1 0d组的 1 2 .31± 2 .41m/s逐渐恢复到 1 80d组的 1 6.78± 1 .36m/s(t=3 .2 4 ,P <0 .0 5) ,与非手术侧的 1 7.69± 1 .2 4m/s基本无差异 (t=0 .1 8,P <0 .0 5)。而未处理组的神经传导速度为 1 1 .2 6±1 .2 5m/s,虽有逐渐恢复的趋势但仍明显慢于非手术侧的1 8.0 7± 1 .36m/s(t=3 .65,P <0 .0 5)。结论　腰神经根慢性受压后 ,由于其可塑性 ,存在自行恢复的能力。若早期应用超短波治疗能及     

氟桂利嗪对缺血性神经元胞质内钙离子和细胞活性的影响

背景:神经元本身因缺血引起损伤以及缺血后再灌注导致神经元损伤是缺血性脑损伤的两大原因,二者均伴有神经元胞质内钙离子浓度增高,这种变化的重要意义备受研究者的关注,可能是各种损伤因素作用的结果,也可能是造成脑缺血损伤的各种因素最后作用的共同通路,即各种因素最后是通过增高的钙离子来产生神经毒性。目的:探讨缺血性神经元的损伤与细胞内钙离子的关系及氟桂利嗪的治疗意义。设计:完全随机设计,对照实验研究。地点和材料:解放军第四军医大学西京医院神经内科实验室和第四军医大学电镜中心。实验材料为孕15d昆明种二级孕鼠由本校实验动物中心提供,清洁级。干预:将培养的神经元随机分为缺血组,氟桂利嗪预处理组以及对照组,利用Ca2 指示剂Flu-3/AM作为细胞内钙离子的荧光探针负载培养的神经元,共聚焦技术检测细胞内荧光强度的变化,利用四唑蓝(四唑蓝)比色试验检测缺血性神经元的损伤程度。缺血组神经元给予类缺血处理10min,氟桂利嗪组2min预处理后,类缺血处理10min。对照组给予含糖的人工脑脊液,混合气体为50mL/LCO2的氧气,10min后进行实验。干预者为作者本人。主要观察指标:观察各组神经元经相应处理后,神经元胞浆内钙离子浓度的变化,细胞活性变化。结果:给予神经元类缺血处理10min后,缺血组神经元     

周围神经损伤后脊髓前角运动神经元内游离Ca~（2＋）的浓度

背景：神经损伤后可引起细胞膜上Ca2＋通道的开放,使细胞外Ca2＋内流,造成细胞内的钙超载。目的：观察臂丛神经根切断伤后相应脊髓前角运动神经元内游离Ca2＋浓度的变化。方法：健康成年雄性Wistar大鼠84只,分为3组：假手术组暴露臂丛神经不切断;对照组臂丛神经切断伤后不做其他处理;实验组臂丛神经切断伤后,给予腹腔注射Ca2＋阻带剂维拉帕米4mg/（kg？d）。于切断伤后12h,24h,48h,72h,1周,2周,4周每组随机以4只取材。结果与结论：周围神经损伤开始,对照组及实验组大鼠损伤侧脊髓前角运动神经元细胞内Ca2＋浓度开始升高,至伤后48h达高峰,此后逐渐下降,伤后1周,实验组已基本回至正常水平,但仍较假手术组高。说明神经损伤后相应神经元细胞膜上L型Ca2＋通道开放,Ca2＋内流进入细胞内,导致神经细胞内游离Ca2＋浓度增加,L型Ca2＋通道可以被维拉帕米阻断,减少神经损伤后的Ca2＋内流,减少神经细胞凋亡的数量。     

脑创伤后神经元细胞内游离钙的变化及其影响因素

目的研究液压冲击伤时体外培养的单个大鼠神经细胞内游离钙 ([Ca2+ ]i)的变化,探讨尼莫地平 D-2氨基戊酸 (D-2-amino-5-phosphonovaleric acid,D-AP-5)和亚低温对创伤后细胞内 [Ca2+ ]i的影响及其机制. 方法 以 Fluo-3/AM为细胞内钙离子的荧光指示剂,用激光共聚焦显微镜测定液压冲击伤时体外培养的单个大鼠神经细胞内游离钙 ([Ca2+ ]i)的变化. 结果 液压冲击伤后脑皮质细胞内游离 Ca2+迅速升高, 24 h达高峰,随后逐渐下降, 48 h仍维持较高水平 [(411.29± 52.46),(396.53± 51.32) nmol/L],尼莫地平, D-AP-5于各时相关均降低细胞内 [Ca2+ ]i,其中 Nimodipine 10 h内应用最佳 [6 h( 98.65± 15.65) nmol/L], D-AP-5于 1～ 10 h应用较好而亚低温 30 min内显著降低细胞内 [Ca2+ ]i(t=13.74, P< 0.001),最佳时机在伤后 15 min内,伤后 1 h以上无效. 结论 创伤后神经元细胞内钙超载,尼莫地平、 D-AP-5和亚低温均降低细胞内 [Ca2+ ]i,但各自最佳时间窗不同,揭示对创伤后神经细胞 Ca2+超载应注意综合治疗,并选定各自作用最佳时间窗.     

Axonal accumulation of hyperpolarization-activated cyclic nucleotide-gated cation channels contributes to mechanical allodynia after peripheral nerve injury in rat

Peripheral nerve injury causes neuropathic pain including mechanical allodynia and thermal hyperalgesia due to central and peripheral sensitization. Spontaneous ectopic discharges derived from dorsal root ganglion (DRG) neurons and from the sites of injury are a key factor in the initiation of this sensitization. Numerous studies have focused primarily on DRG neurons; however, the injured axons themselves likely play an equally important role. Previous studies of neuropathic pain rats with spinal nerve ligation (SNL) showed that the hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel in DRG neuronal bodies is important for the development of neuropathic pain. Here, we investigate the role of the axonal HCN channel in neuropathic pain rats. Using the chronic constriction injury (CCI) model, we found abundant axonal accumulation of HCN channel protein at the injured sites accompanied by a slight decrease in DRG neuronal bodies. The function of these accumulated channels was verified by local application of ZD7288, a specific HCN blocker, which significantly suppressed the ectopic discharges from injured nerve fibers with no effect on impulse conduction. Moreover, mechanical allodynia, but not thermal hyperalgesia, was relieved significantly by ZD7288. These results suggest that axonal HCN channel accumulation plays an important role in ectopic discharges from injured spinal nerves and contributes to the development of mechanical allodynia in neuropathic pain rats.     

Subthreshold membrane potential oscillation mediates the excitatory effect of norepinephrine in chronically compressed dorsal root ganglion neurons in the rat

Injured dorsal root ganglion (DRG) neurons often develop adrenergic sensitivity. To investigate the mechanisms of this phenomenon, the effects of norepinephrine (NE) on membrane potential of large- and medium-sized A-type neurons from chronically compressed DRG were recorded electrophysiologically in vitro. NE induced a depolarization in both control (26/36) and injured (56/62) neurons, whereas the incidence and amplitude of NE-induced depolarization in the injured neurons were significantly higher than that in controls. Following NE-induced depolarization, a subthreshold membrane potential oscillation (SMPO) was triggered or enhanced that initiated or increased repetitive firing in a fraction of injured neurons (15/56). After the SMPO was selectively abolished by application of tetrodotoxin (TTX), NE-induced depolarization failed to produce repetitive firing, even with a greater depolarization. Application of Rp-cAMPS (500 microM), a selective inhibitor of protein kinase A (PKA), decreased both SMPO and repetitive firing evoked by NE application or by intracellular current injection. Conversely, Sp-cAMPS (500 microM), a PKA activator, had a facilitating effect on both the SMPO and the repetitive firing. These results strongly suggest that a PKA mediated triggering and enhancement of SMPO may be responsible for the excitatory effects of NE on sensory neurons in neuropathic rats.     

大鼠受损背根节中型感觉神经元的温度敏感性

目的：观察大鼠损伤背根节（DRG）中型感觉神经元的热温度敏感性。方法：在急性离散的大鼠DRG中型神经元上,运用全细胞膜片钳技术,观察不同温度梯度刺激下受损DRG神经元的放电的特征。结果：大鼠损伤DRG中型神经元与热温度变化有一定的关系,它们根据放电模式可分为3型,其中62%（26/42）的中型神经元与热温度变化密切相关,随着温度的升高而引发的逐渐增强的膜电位去极化可引发频率由低到高的动作电位。随着温度的降低神经元又表现出频率由高到低的动作电位变化,放电后有规律的膜电位振荡,于较弱的超极化刺激可产生反跳动作电位,动作电位的幅值不一致。该类神经元具有电压依赖性。结论：大鼠受损DRG中型感觉神经元特别是紧张型放电的神经元对非伤害性刺激反应强烈,具有热温度敏感性。     

Tactile allodynia in the absence of C-fiber activation: altered firing properties of DRG neurons following spinal nerve injury

We examined the relation between ectopic afferent firing and tactile allodynia in the Chung model of neuropathic pain. Transection of the L5 spinal nerve in rats triggered a sharp, four- to six-fold increase in the spontaneous ectopic discharge recorded in vivo in sensory axons in the ipsilateral L5 dorsal root (DR). The increase, which was not yet apparent 16 h postoperatively, was complete by 24 h. This indicates rapid modification of the electrical properties of the neurons. Only A-neurons, primarily rapidly conducting A-neurons, contributed to the discharge. No spontaneously active C-neurons were encountered. Tactile allodynia in hindlimb skin emerged during precisely the same time window after spinal nerve section as the ectopia, suggesting that ectopic activity in injured myelinated afferents can trigger central sensitization, the mechanism believed to be responsible for tactile allodynia in the Chung model. Most of the spike activity originated in the somata of axotomized DRG neurons; the spinal nerve end neuroma accounted for only a quarter of the overall ectopic barrage. Intracellular recordings from afferent neuron somata in excised DRGs in vitro revealed changes in excitability that closely paralleled those seen in the DR axon recordings in vivo. Corresponding changes in biophysical characteristics of the axotomized neurons were catalogued. Axotomy carried out at a distance from the DRG, in the mid-portion of the sciatic nerve, also triggered increased afferent excitability. However, this increase occurred at a later time following axotomy, and the relative contribution of DRG neuronal somata, as opposed to neuroma endings, was smaller. Axotomy triggers a wide variety of changes in the neurochemistry and physiology of primary afferent neurons. Investigators studying DRG neurons in culture need to be alert to the rapidity with which axotomy, an inevitable consequence of DRG excision and dissociation, alters key properties of these neurons. Our identification of a specific population of neurons whose firing properties change suddenly and synchronously following axotomy, and whose activity is associated with tactile allodynia, provides a powerful vehicle for defining the specific cascade of cellular and molecular events that underlie neuropathic pain.     

丹参对兔脊髓损伤区钙、水含量的影响

背景脊髓损伤继发损伤机制是多种病理、生理、生化机制综合作用的结果.各国学者对脊髓损伤的早期治疗,抑制或阻止脊髓损伤继发损害的方面作了较多探索.目的探讨丹参对脊髓伤区水、钙含量的影响,分析丹参对脊髓的保护作用.设计随机分组实验研究.地点和对象实验在武汉大学人民医院骨科完成,对象为日本大耳白兔35只,雌雄不拘,均购自武汉大学医学院实验中心.干预按抽签法随机分成3组正常组5只,仅做L1椎板咬除而脊髓无损伤,对照组15只,治疗组15只.采用改良Allen氏法制作兔脊髓损伤模型.术后治疗组兔静注丹参注射液,对照组兔静注等量生理盐水.主要观察指标3组兔术后2,12,24h测量脊髓损伤段水、钙含量.结果脊髓损伤后,伤区水、钙含量增高,伤后12 h对照组水、钙含量分别为(77.34±2.16)%,(30.83±8.76)μmol/g,治疗组水、钙含量分别为(68.42±3.01)%,(19.32±2.79)μmol/g.丹参治疗后2,12,24 h水、钙含量均较对照组降低,趋近正常值.结论丹参可减轻脊髓伤区水、钙储留,对脊髓起保护作用.     

嗅鞘细胞条件培养液和星形胶质细胞条件培养液对受损海马神经元保护作用的对比研究

目的:观察嗅鞘细胞条件培养液(OECCM)和星形胶质细胞条件培养液(ACM)对受损海马神经元的保护作用。方法:分别采用2种胶质细胞条件培养液预处理受损海马神经元(谷氨酸诱导损伤),对比其对受损海马神经元活力、凋亡率和胞浆内游离钙离子浓度的影响。结果:与谷氨酸组相比,OECCM组神经元活力明显增高(P0.01),ACM组神经元活力增高(P0.05);与OECCM组相比,ACM组神经元活力降低(P0.05)。与谷氨酸组相比,ACM组神经元凋亡率和胞内游离钙浓度降低(P0.05),OECCM组明显降低(P0.01);OECCM组神经元凋亡率和胞内游离钙浓度低于ACM组(P0.05)。结论:OECCM和ACM均可明显提高受损海马神经元活力、降低凋亡率和胞浆内游离钙离子浓度,OECCM的保护作用优于ACM。     

The pattern of expression of the voltage-gated sodium channels Na(v)1.8 and Na(v)1.9 does not change in uninjured primary sensory neurons in experimental neuropathic pain models

A spared nerve injury of the sciatic nerve (SNI) or a segmental lesion of the L5 and L6 spinal nerves (SNL) lead to behavioral signs of neuropathic pain in the territory innervated by adjacent uninjured nerve fibers, while a chronic constriction injury (CCI) results in pain sensitivity in the affected area. While alterations in voltage-gated sodium channels (VGSCs) have been shown to contribute to the generation of ectopic activity in the injured neurons, little is known about changes in VGSCs in the neighboring intact dorsal root ganglion (DRG) neurons, even though these cells begin to fire spontaneously. We have now investigated changes in the expression of the TTX-resistant VGSCs, Nav1.8 (SNS/PN3) and Nav1.9 (SNS2/NaN) by immunohistochemistry in rat models of neuropathic pain both with an intermingling of intact and degenerated axons in the nerve stump (SNL and CCI) and with a co-mingling in the same DRG of neurons with injured and uninjured axons (sciatic axotomy and SNI). The expression of Nav1.8 and Nav1.9 protein was abolished in all injured DRG neurons, in all models. In intact DRGs and in neighboring non-injured neurons, the expression and the distribution among the A- and C-fiber neuronal populations of Nav1.8 and Nav1.9 was, however, unchanged. While it is unlikely, therefore, that a change in the expression of TTX-resistant VGSCs in non-injured neurons contributes to neuropathic pain, it is essential that molecular alterations in both injured and non-injured neurons in neuropathic pain models are investigated.