γ-氨基丁酸A受体α1亚基信使核糖核酸在硝酸甘油偏头痛大鼠模型脑干及三叉神经组织中的表达变化

目的 利用硝酸甘油所致偏头痛大鼠模型探讨γ-氨基丁酸A(GABAA)受体α1亚基mRNA在偏头痛大鼠脑干及三叉神经组织中的表达变化.方法 30只成年雌性SD大鼠按完全随机分组方法分为对照组、模型组和丙戊酸钠干预组,后两组又随机分发作期和间歇期两个亚组(每组各6只).模型组及丙戊酸钠干预组按Cristina法复制偏头痛大鼠模型(每周1次,连续5周),干预组于第2次造模后每天灌服0.5 g/L的丙戊酸钠2次,共10 mL/kg;对照组和模型组于第2次造模后每天灌服生理盐水2次,共10 ml/kg.第5次造模后用逆转录-聚合酶链反应法测定大鼠脑干及三叉神经组织中GABAA受体α1亚基mRNA的表达.结果 模型组发作期的GABAA受体α1亚基mRNA的表达(1.50±0.13)均高于其他各组(对照组1.01±0.24,模型组间歇期1.04±0.10,干预组发作期0.99±0.22,干预组间歇期0.72±0.03),但仅与模型组间歇期相比差异有统计学意义(x2=9.490,P =0.009);模型组与对照组、干预组的发作期及间歇期相比差异无统计学意义,干预组的发作期及间歇期与对照组相比差异无统计学意义.结论 偏头痛的发生可能与GABAA受体α1亚基在mRNA水平的表达上调有关.     

基质金属蛋白酶-9在偏头痛大鼠模型中的表达和意义

目的探讨基质金属蛋白酶-9（MMP-9）在偏头痛大鼠模型中的表达情况。方法 48只雄性SD大鼠随机分为正常对照组、阴性对照组和模型组,每组16只。正常对照组不作处理,模型组采用皮下注射硝酸甘油法制作大鼠偏头痛模型,阴性对照组注射生理盐水。应用免疫组化技术及Western blot,分别观察各组大鼠硬脑膜、三叉神经节及三叉神经颈复合体MMP-9蛋白的表达情况。结果 MMP-9在各组大鼠中均有不同程度表达,模型组中MMP-9表达明显高于阴性对照组及正常对照组（P〈0.05）。结论 MMP-9在偏头痛大鼠模型中表达增强,其可能在偏头痛发病机制中发挥重要的作用。     

缝隙连接蛋白43在偏头痛大鼠三叉神经颈髓复合体的表达及其对痛觉超敏的影响

目的 探讨三叉神经颈髓复合体内缝隙连接蛋白43(Cx43)对偏头痛大鼠痛觉超敏的影响. 方法 将SD大鼠随机数字表法分为空白组、假手术组、生理盐水组、改良致炎剂3d组、改良致炎剂7d组、甘珀酸(CBX)预防组、CBX预防对照组、CBX治疗组和CBX治疗对照组,每组6只.用改良致炎剂反复刺激硬脑膜法建立偏头痛大鼠模型.Von-Frey纤维丝测定眶周痛觉阈值,免疫荧光染色法观察大鼠三叉神经颈髓复合体内Cx43的表达. 结果 行为学结果显示,与对照组相比,改良致炎剂组大鼠眶周痛阈逐日下降,出现痛觉超敏表现;而CBX预防组大鼠未出现痛觉超敏表现;CBX治疗组大鼠给予CBX后痛阈上升.细胞核及Cx43免疫荧光染色显示:改良致炎剂组大鼠后角细胞数及Cx43表达较对照组增多,3d组以Ⅰ、Ⅱ层增多为主,7d组以Ⅰ～Ⅳ层增多为主;CBX预防组及治疗组Cx43平均吸光度值与其对照组相比,差异有统计学意义(P＜0.05). 结论 反复予硬脑膜改良致炎剂能有效诱导偏头痛大鼠产生眶周痛觉超敏表现,并能引起三叉神经颈髓复合体内Cx43表达上调.非特异性缝隙连接阻断剂CBX能有效抑制Cx43表达上调,缓解痛觉超敏,提示Cx43在偏头痛大鼠痛觉超敏形成和加重中起重要作用.     

罗格列酮对硝酸甘油诱导偏头痛大鼠的保护作用

目的观察罗格列酮对硝酸甘油诱导大鼠偏头痛模型的保护作用。方法 48只雄性SD大鼠随机分为模型组、罗格列酮组和对照组。模型组(按Tassorelli法皮下注射硝酸甘油复制大鼠偏头痛模型),罗格列酮组(于造模后30 min腹腔注射罗格列酮),对照组(不造模,皮下注射生理盐水)。观察大鼠行为学变化,采用免疫组化和Western blot法观察三叉神经颈复合体过氧化物酶体增殖物激活受体γ(PPARγ)及白介素-6(IL-6)、细胞间黏附分子-1(ICAM-1)、基质金属蛋白酶-9(MMP-9)表达。结果对照组三叉神经颈复合体中PPARγ为弱阳性表达,模型组为阳性表达,罗格列酮组为强阳性表达。模型组IL-6、ICAM-1和MMP-9表达高于对照组(P0.05)。罗格列酮组大鼠耳发红、肢频繁挠头、爬笼次数增多、烦躁不安等症状减轻,IL-6、ICAM-1、MMP-9表达较模型组明显下降(P0.05)。结论偏头痛时PPARγ表达增强;罗格列酮可通过活化PPARγ,下调IL-6、ICAM-1、MMP-9对偏头痛具有一定的保护作用。     

蛋白激酶Cγ亚型和N-甲基-天门冬氨酸受体1在硝酸甘油致偏头痛大鼠模型发病机制中的作用探讨

目的通过硝酸甘油致偏头痛大鼠模型,初步探讨蛋白激酶Cγ亚型(PKCγ)、N-甲基-天门冬氨酸受体1(NMDAR1)和磷酸化NMDAR1在偏头痛发病机制中的作用。方法将30只成年雌性SD大鼠随机分为对照组、模型组、干预组,后两组再各自分为发作期组和间歇期组,每组6只。模型组及干预组按Tassorelli Cristina法复制偏头痛大鼠模型,对照组用生理盐水造模。干预组每天灌服氟桂利嗪2 ml(0.5 mg/kg),对照组每天灌服生理盐水2 ml。受试动物于第5次造模后2 h(发作期组)或第4天(对照组及间歇期组)分别断头处死取脑干组织。RT-PCR法检测PKCγ及NMDAR1 mRNA,Western-Blot检测PKCγ、NMDAR1、磷酸化NMDAR1蛋白的表达。结果与对照组相比,无论是偏头痛发作期组和间歇期组,还是模型组和干预组大鼠脑干组织中PKCγ、NMDAR1 mRNA及蛋白的表达差异均无统计学意义(P0.05)。与对照组相比,模型组PKCγ依赖的磷酸化NMDAR1蛋白的表达明显上调(P0.05);干预组也稍有上调,但差异无统计学意义(P0.05)。模型组与干预组,以及发作期与间歇期相比,磷酸化NMDAR1蛋白的表达差异无统计学意义(P0.05)。结论偏头痛的发生发展可能与PKCγ依赖的磷酸化NMDAR1蛋白表达的上调有关,可能与PKCγmRNA及蛋白、NMDAR1 mRNA及蛋白(非磷酸化)的表达量无关。氟桂利嗪预防偏头痛发作的机制之一可能是打断了PKCNMDAR这一正反馈环路的恶性循环。     

小电导钙激活型钾通道SK3在大鼠偏头痛模型中脑干的表达变化

目的初步探讨小电导钙激活型钾通道SK3与大鼠偏头痛的关系,为研究偏头痛的发病机制,寻找新治疗靶点提供实验依据。方法 40只成年雌性SD大鼠随机分为对照组8只,模型组16只,干预组16只,后两组再随机分为发作期组和间歇期组,每组8只。按Tassorelli Cristina法复制偏头痛大鼠模型。对照组用生理盐水造模。干预组每天灌服氟桂利嗪2 ml(0.5 mg/kg),对照组每天灌服生理盐水2 ml。发作期组于第5次造模后3 h、间歇期组于第5次造模后4 d断头处死取脑干组织。RT-PCR法及Western法分别检测各组脑干SK3 mRNA及其蛋白的表达。结果模型组、干预组脑干SK3 mRNA及其蛋白的表达水平均较对照组下降(P0.05),且各发作期组均较相应间歇期组更低(P0.05);而模型发作期组与干预发作期组、模型间歇期组与干预间歇期组比较SK3 mRNA及其蛋白的表达水平无明显差异(P0.05)。结论脑干SK3表达的降低可能与偏头痛的发生发展有关;氟桂利嗪防治偏头痛可能不是通过影响脑干SK3的表达量实现的。     

通心络胶囊对实验性偏头痛大鼠CGRP及α-CGRP基因表达的影响

目的研究通心络胶囊对硝酸甘油性偏头痛大鼠模型血浆降钙素基因相关肽(CGRP)、脑干及三叉神经节αCGRP基因mRNA表达的影响,以探讨通心络治疗偏头痛的可能机制。方法50只SD大鼠随机分为空白对照组、生理盐水组、模型组、苯噻啶防治组、通心络防治组。模型组和药物干预组用硝酸甘油10mg/kg皮下注射造模,每周1次,连续4周,第2次造模后每天分别灌服通心络1.5g/kg/d(通心络组)或苯噻啶0.5mg/kg/d(苯噻啶组)进行干预。第4次造模后用放射免疫法测定血浆CGRP、RTPCR技术测定脑干及三叉神经节区αCGRP基因mRNA的表达。结果与空白对照组比较,反复硝酸甘油造模后,通心络组血浆CGRP水平明显升高(55.63±9.01ng/Lvs45.23±1.79ng/L,P<0.05);苯噻啶组和通心络组αCGRP基因mRNA表达分别为0.67±0.12和0.64±0.12,与空白对照组的0.88±0.09比较,明显下调(P<0.05)。结论通心络胶囊下调了脑干及三叉神经节αCGRP基因mRNA的表达,增加了血浆CGRP含量,提示通心络胶囊不是通过下调血浆CGRP含量而起到预防偏头痛的作用。     

偏头痛模型大鼠相关活性物质表达

目的研究磷酸化的细胞外信号调节激酶(the phosphorylated form of the extracellular signal-regulated kinase,p-ERK)、降钙素基因相关肽(calcitonin gene-related peptide,CGRP)及环氧化酶-2(cyclooxygenase-2,COX-2)在偏头痛模型大鼠硬脑膜、三叉神经节和三叉神经脊束尾核组织中的表达及其相关性,为探讨偏头痛发病机制提供依据。方法将60只雄性SD大鼠随机分为空白组、生理盐水组、硝酸甘油组和电刺激组;硝酸甘油组和生理盐水组根据注射后时间再分别分为30 min、1h和3h组;电刺激组再分为电刺激三叉神经节(ESTG)模型组、假手术组和尼美舒利干预组。采用免疫组化染色观察大鼠硬脑膜、三叉神经节和三叉神经脊束尾核p-ERK、CGRP、COX-2的表达。结果 (1)硝酸甘油组大鼠硬脑膜、三叉神经节和三叉神经脊束尾核的pERK、CGRP、COX-2表达均明显高于生理盐水组(均P0.01),ESTG大鼠不同部位组织的p-ERK、CGRP、COX-2表达均明显高于假手术组和空白组(均P0.01);(2)p-ERK表达在注射硝酸甘油后的30min组均高于1h组和3h组,后随时间增加其表达逐渐降低(均P0.01);(3)尼美舒利干预组大鼠不同组织中p-ERK、CGRP、COX-2的表达均低于ESTG模型组(P0.05)。结论 (1)p-ERK、CGRP、COX-2表达上调与偏头痛的炎性反应和疼痛敏化有关,其中p-ERK可能参与偏头痛早期过程;(2)偏头痛过程中,p-ERK、CGRP和COX-2蛋白之间有密切联系。     

大鼠疼痛模型中类固醇对c-fos mRNA和c-fos蛋白表达的调节

目的:探讨偏头痛三叉神经血管机制中,三叉神经疼痛刺激诱导c-fos mRNA、c-fos蛋白表达和类固醇激素之间的关系。方法:选择了与偏头痛发病机制相关的电刺激大鼠三叉神经根的疼痛模型。电刺激组:用电脉冲持续刺激三叉神经根10分钟(n=15)。然后分别在30(n=5),60(n=5),120(n=5)分钟后断头处死动物。类固醇治疗组:电刺激同时在颈动脉鞘旁注射强地松龙混悬液1.25mg/kg(n=5),对照组:仅做麻醉处理(n=4)。结果:中缝核和三叉神经脊束核神经元c-fos mRNA、c-fos的表达数量随时间的延长逐渐增加(P<0.01)。注射强地松龙混悬液120分钟后两者的表达细胞数量增多,(P<0.05)。结论:类固醇可以正向调节c-fos mRNA、和 c-fos表达。其原因可能由于激活了不同的c-fos mRNA、和c-fos表达通道所致,包括疼痛刺激反应和疼痛调节通道。这种作用可能是类固醇激素在临床上治疗偏头痛长期疗效的基础。     

替尼达普对慢性颞叶癫(癎)大鼠海马内向整流钾通道2.3亚单位表达的影响

目的 观察慢性颞叶癫(癎)(TEE)大鼠致(癎)后不同时点海马组织中内向整流钾通道(Kir)2.3亚单位mRNA和蛋白的表达变化规律及通道特异性开放剂替尼达普对其表达的影响,探讨Kir2.3通道与TLE发病机制的关系,并为临床应用钾通道开放剂作为抗癫(癎)药物提供依据.方法 匹罗卡品诱导大鼠产生癫(癎)持续状态(SE),持续观察2周,成模为慢性TLE大鼠.用逆转录PCR(RT-PCR)和Western blot方法检测对照组及致(癎)组大鼠SE终止后0、6、72 h和2周后海马组织中Kit2.3通道mRNA和蛋白表达变化趋势;随后以慢性期2周作为观察时间点,检测替尼达普对大鼠海马Kir2.3通道mRNA及蛋白表达变化的影响.结果 对照组、致(癎)组SE终止后0、6、72 h和2周时Kir2.3 mRNA/β-actin比值分别为0.080±0.030、0.103±0.045、0.164±0.026、0.132±0.024和0.011±0.008(F:23.684,P<0.01);各时间点Kir2.3蛋白/甘油醛-3磷酸脱氢酶(GAPDH)比值分别为0.305±0.030、0.263±0.028、0.767±0.167、0.498±0.077和0.176±0.026(F=44.183,P<0.05),其表达呈现急性期增高、慢性期明显降低的动态变化趋势.在慢性期,替尼达普给药组大鼠Kir2.3 mRNA/β-actin与Kir2.3蛋白/GAPDH比值分别为0.021±0.006和0.636±0.140,与未给药组相比表达增高,差异有统计学意义(F=25.216、47.355,P<0.05、0.01).结论 Kir2.3通道mRNA和蛋白在慢性期表达下调,可能是难治性癫(癎)发病的分子生物学机制之一.替尼达普通过增加Kir2.3通道的表达,最终可能减少(癎)样放电的产生.     

PKCepsilon upregulates voltage-dependent calcium channels in cultured astrocytes

Astrocytes express voltage-gated calcium channels (VGCCs) that are upregulated in the context of the reactive astrogliosis occurring in several CNS pathologies. Moreover, the ability of selective calcium channel blockers to inhibit reactive astrogliosis has been revealed in a variety of experimental models. However, the functions and regulation of VGCC in astrocytes are still poorly understood. Interestingly, protein kinase C epsilon (PKCepsilon), one of the known regulators of VGCC in several cell types, induces in astrocytes a stellated morphology similar to that associated to gliosis. Thereby, here we explored the possible regulation of VGCC by adenovirally expressed PKCepsilon in astrocytes. We found that PKCepsilon potently increases the mRNA levels of two different calcium channel alpha(1) subunits, Ca(V)1.2 (L-type channel) and Ca(V)2.1 (P/Q-type channel). The mRNA upregulation was followed by a robust increase in the corresponding peptides. Moreover, the new calcium channels formed as a consequence of PKCepsilon activation are functional, since overexpression of constitutively-active PKCepsilon increased significantly the calcium current density in astrocytes. PKCepsilon raised currents carried by both L- and P/Q-type channels. However, the effect on the P/Q-type channel was more prominent since an increase of the relative contribution of this channel to the whole cell calcium current was observed. Finally, we found that PKCepsilon-induced stellation was significantly reduced by the specific L-type channel blocker nifedipine, indicating that calcium influx through VGCC mediates the change in astrocyte morphology induced by PKCepsilon. Therefore, here we describe a novel regulatory pathway involving VGCC that participates in PKCepsilon-dependent astrocyte activation.     

川芎、白芷提取物对大鼠偏头痛模型脑膜肥大细胞和血浆组胺的影响

目的 探讨川芎、白芷提取物对大鼠偏头痛模型硬脑膜组织中肥大细胞及血浆组胺的影响,为都梁软胶囊治疗偏头痛提供实验依据.方法 实验分为三组：假手术组、偏头痛模型无干预组、偏头痛模型药物（川芎、白芷提取物）治疗组.电刺激三叉神经节建立偏头痛大鼠模型,镜下观察硬脑膜肥大细胞数量及脱颗粒现象.用酶联免疫吸附分析法（ELISA）测定大鼠血浆组胺含量.结果 偏头痛模型无干预组大鼠刺激侧硬脑膜高倍视野肥大细胞数、脱颗粒百分率及血浆组胺含量分别为（11.63±1.67）,（29.10±9.39）%,（11.59±1.20）ng/ml,与假手术组（15.46±2.40）,（14.09±4.53）%,（9.87±0.88）ng/ml相比,肥大细胞数下降,脱颗粒百分率及血浆组胺含量升高,差异有统计学意义（P〈0.05）.药物治疗组大鼠刺激侧硬脑膜高倍视野肥大细胞数、脱颗粒百分率及血浆组胺含量分别为（15.14±2.01）,（17.22±4.10）%,（10.00±0.81）ng/ml,与偏头痛模型无干预组相比,差异有统计学意义（P〈0.05）.结论 川芎、白芷提取物能有效地抑制肥大细胞脱颗粒、释放组胺,减轻偏头痛大鼠硬脑膜炎症反应,从而有效地控制疼痛.     

Neuronal P/Q-type calcium channel dysfunction in inherited disorders of the CNS

The past two decades have witnessed the emergence of a new and expanding field of neurological diseases--the genetic ion channelopathies. These disorders arise from mutations in genes that encode ion channel subunits, and manifest as paroxysmal attacks involving the brain or spinal cord, and/or muscle. The voltage-gated P/Q-type calcium channel (P/Q channel) is highly expressed in the cerebellum, hippocampus and cortex of the mammalian brain. The P/Q channel has a fundamental role in mediating fast synaptic transmission at central and peripheral nerve terminals. Autosomal dominant mutations in the CACNA1A gene, which encodes voltage-gated P/Q-type calcium channel subunit α(1) (the principal pore-forming subunit of the P/Q channel) are associated with episodic and progressive forms of cerebellar ataxia, familial hemiplegic migraine, vertigo and epilepsy. This Review considers, from both a clinical and genetic perspective, the various neurological phenotypes arising from inherited P/Q channel dysfunction, with a focus on recent advances in the understanding of the pathogenetic mechanisms underlying these disorders.     

偏头痛大鼠硬脑膜肥大细胞脱颗粒与神经源性炎症相关因子的变化

目的 观察偏头痛大鼠硬脑膜肥大细胞脱颗粒与神经源性炎症相关因子的变化,探讨偏头痛疼痛产生的可能机制.方法 64只SD大鼠随机分为刺激组(32只)和假手术组(32只).电刺激大鼠单侧三叉神经节建立偏头痛模型,放射免疫法测定刺激侧颈静脉血中降钙素基因相关肽(CGRP)的含量.酶联免疫吸附法测定刺激侧颈静脉血中组胺和硬脑膜中前列腺素E2(PGE2)的含量,甲苯胺蓝染色观察硬脑膜肥大细胞的数量及脱颗粒百分率,免疫组织化学染色法、免疫蛋白质印迹技术观察硬脑膜中环氧化酶-2(COX-2)的阳性细胞数及蛋白表达.结果 假手术组和刺激组颈静脉血中CGRP含量分别为(59.20±11.66)pg/ml和(82.84±16.24)pg/ml(t=-3.34);组胺含量分别为(9.87±0.88)ng/ml和(11.59±1.20)ng/ml(t=-3.27);硬脑膜中肥大细胞数量分别为15.46±2.40和11.63±1.67(t=3.71),脱颗粒百分率分别为14.09%±4.53%、29.10%±9.39%(t=-4.07).两组硬脑膜中PGE2的含量分别为(80.70±10.60)pg/ml和(382.30±20.90)pg/ml(t=-16.674);硬脑膜中COX-2阳性细胞数分别为42.00±18.40和139.00±20.50(t=-7.994),COX-2蛋白表达(吸光度值)分别为19.50±9.20和359.20±21.90(t=-5.190).两组间比较,上述指标差异均有统计学意义(P＜0.05).结论 电刺激单侧三叉神经节可诱导硬脑膜肥大细胞脱颗粒及神经源性炎症的产生,相关炎症因子的改变可能是偏头痛疼痛发生的重要病理生理基础.     

Calcium channels control tDCS-induced spontaneous vesicle release from axon terminals

BackgroundTranscranial direct current stimulation (tDCS) is a subthreshold neurostimulation therapeutic method that ameliorate neuropsychiatric impairments. The most sensitive subcellular compartment for tDCS are the axons that polarize. However, how these relatively small polarizations significantly alter synaptic dynamics is still unknown.Objective/Hypothesis: We hypothesized that tDCS-induced axonal polarization modulates calcium channel activity at the presynaptic compartment, thus playing a crucial role in synaptic vesicle release.MethodsFor this aim, we examined how different DCS conditions and orientations affect the spontaneous excitatory post synaptic currents (sEPSCs) recorded from hippocampal CA1 pyramidal neurons. Since P/Q-type calcium-channels are the main presynaptic voltage-dependent calcium-channels in the hippocampus, we further examined the DCS effects while applying a P/Q-type calcium channels blocker, ω-agatoxin. Additionally, to explain the DCS-induced calcium channel-regulated vesicle release dynamics, we developed a simplified model to complement our experimental results.ResultsWe demonstrated that anodal-DCS application in a dorso-ventral orientation, similar to that of in-vivo experiments, enhanced the sEPSCs frequency, while cathodal-DCS was ineffective. Moreover, DCS application in parallel to the Schaffer collaterals (medio-lateral orientation), showed both anodal and cathodal significant effects. Furthermore, the ω-agatoxin application occluded the DCS-induced modulation of sEPSC frequencies in any orientation. The model showed the interaction between DCS-induced membrane polarization, calcium channel activation and presynaptic vesicle release.ConclusionUsing experiments and modeling we show that DCS induces a small variation in terminal membrane potential sufficient to activate P/Q type voltage-gated calcium channels, and that this is sufficient to modify presynaptic calcium concentration, subsequently altering spontaneous vesicle release.     

N‐Methyl‐d‐aspartate receptor open‐channel blockers memantine and magnesium modulate nociceptive trigeminovascular neurotransmission in rats

Experimental and clinical studies suggest that the low‐affinity N‐methyl‐d ‐aspartate (NMDA) receptor open‐channel blockers Mg²⁺ and memantine are effective in reducing trigeminal nociceptive activation. The aim of this study was to investigate the apparent effectiveness of these channel blockers using a model of trigeminal activation in vivo. Rats were anaesthetized before electrically stimulating the dura mater adjacent the middle meningeal artery. Neurons responding to stimulation were recorded extracellularly using electrophysiological methods. l ‐Glutamate or NMDA, and Mg²⁺, memantine, or sodium controls were applied locally using microiontophoresis. Microiontophoretic application of Mg²⁺ or memantine into the trigeminocervical complex inhibited mechanically and electrically stimulated craniovascular afferents,  and l ‐glutamate or NMDA‐evoked neuronal activity at the second‐order trigeminal synapse of craniovascular afferents. By contrast, intravenous administration of MgSO₄ (100 mg/kg) or memantine (10 mg/kg) did not significantly affect electrically stimulated afferent‐evoked activity within the trigeminocervical complex. The Mg²⁺ and memantine concentrations achieved after systemic administration may not effectively inhibit activation of the trigeminocervical complex, perhaps providing an explanation for the relatively poor efficacy of these NMDA receptor open‐channel blockers for headache treatment in clinical studies. Nevertheless, the present results suggest blocking of NMDA‐receptor open channels inhibits nociceptive activation of the trigeminocervical complex. Further exploration of such channel blockers as a therapeutic strategy for primary head pain is warranted.     

Up-regulation of class A Ca2+ channels in trigeminal ganglion after pulp exposure

We have studied changes in the level of calcium channel expression in the cell bodies of neurons located in the maxillary division of the trigeminal ganglion following induction of persistent pulpitis by pulp exposure in the right maxillary molars. Using anti-peptide antibodies to the alpha1 subunit of class A (P-/Q-type) voltage-gated calcium channels, we observed slight increases in the expression level three days following surgery and approximately 4 fold increase by eight days following the lesion. These changes in the expression of the alpha1 subunit of class A calcium channels may have functional implications in the responses of nociceptive neurons to chronic inflammation.