天麻素对单侧前庭功能丧失大鼠前庭内侧核中GLU-IR、GFAP、GABA B2表达及疗效的影响

目的 本研究观察单侧前庭功能丧失大鼠及经不同剂量天麻素治疗后前庭内侧核中GLU-IR、GFAP、GABA B2表达的变化.方法 将99只SD大鼠随机分为空白对照组(KBDZ组,n=9)、假手术对照组(JSSDZ组,n=18)、模型对照组(MXDZ组,n=18)、模型治疗组(MXZL组,n=54),KBDZ组正常饲养,J...     

前庭代偿过程中前庭传出性和传入性神经系统的相互作用

目的 通过前庭代偿的动物模型，了解在前庭病变的情况下，前庭传出性和传入性神经系统的相互作用。方法 动物模型：A组(16只)为正常大鼠。B组(15只)左侧前庭损毁术后7d。C组(7只)术后3个月。D组(7只)前庭代偿后。检测两侧头长肌静息状态的肌电图。检测传出性前庭神经系统降钙素基因相关肽免疫组化。检测传出性前庭神经系统胆硷乙酰转移酶(choline acetyltransferase，AChT)免疫组化。检测传入性前庭神经系统Na-K-ATP酶活性。结果 损伤同侧肌群肌电活动减弱、对侧肌群增强，前庭代偿期恢复对称性。急性期传出性前庭神经系统降钙素基因相关肽阳性细胞双侧性增多，活性增高。传出性前庭神经系统损伤同侧AChT阳性反应细胞减少，两侧反应程度增加。前庭代偿期对侧反应程度显著增加。急性期同侧Na-K-ATP酶mRNA表达水平低，对侧前庭信号增强，在前庭代偿期，同侧Na-K-ATP酶mRNA表达水平增强，与对侧一致或略强。结论 传出性前庭神经系统可能抑制对侧前庭传入信息，调整同侧前庭中枢兴奋性，在前庭代偿的复杂机制中发挥作用。     

新霉素对大鼠前庭的损伤及复制缺陷型腺病毒前庭导入的研究

目的 研究新霉素对大鼠前庭毛细胞的毒性作用并探索前庭基因导入的方法和途径,为药物性前庭功能损伤动物模型的制备和基因治疗的相关研究提供参考.方法 将25只成年Wistar大鼠分为正常对照组、新霉素鼓阶给药组、新霉素前庭阶给药组、腺病毒(缺失E1、E3基因且构建有绿色荧光蛋白报告基因的复制缺陷型腺病毒,Ad-EGFP)鼓阶导入组、腺病毒(Ad-EGFP)前庭阶导入组,每组各5只动物.新霉素组大鼠在右耳通过耳蜗底回鼓阶(鼓阶组)或前庭阶打孔(前庭组)的方法在耳蜗内注入0.1%新霉素5 μl,Ad-EGFP组则以同法导入物理滴度为2.1×1011vp/ml的Ad-EGFP 5 μl,正常对照组大鼠不做任何处理.处理3天后对动物进行颈髓硬膜外短声诱发电位(click- evoked potentials on the surface of the cervical dura mater,CDM-CEP)检查和游泳试验,评价前庭功能,然后将动物处死,进行组织学和形态学观察.结果 3天后新霉素组大鼠的前庭毛细胞即出现严重破坏,并出现严重的前庭功能损伤.正常对照组、新霉素鼓阶给药组、新霉素前庭阶给药组、Ad-EGFP鼓阶导入组、Ad-EGFP前庭阶导入组的游泳时间分别为4.0±0.71、10.2±1.64、9.8±1.48、4.8±0.84、5.0±0.71 s;正常对照组CDM-CEP的阈值为85±3.54 dB SPL,潜伏期为6.59±0.41 s;新霉素组120 dB SPL未引出CDM-CEP;Ad-EGFP鼓阶导入组CDM-CEP阈值为91±5.48 dB SPL,潜伏期为6.76±0.26 s,Ad-EGFP新霉素前庭阶导入组CDM-CEP的阈值为89±6.52 dB SPL,潜伏期为6.78±0.26 s.3天后,Ad-EGFP前庭阶导入组的前庭终末器官均出现Ad-EGFP的转染;而Ad-EGFP鼓阶导入组未见前庭终末器官的表达.结论 新霉素对前庭毛细胞具有极强的破坏作用,新霉素耳蜗内注射的方法可以制备理想的前庭功能障碍动物模型,耳蜗底回前庭阶打孔可以作为基因导入前庭的有效途径.     

新霉素对大鼠前庭毛细胞损伤作用的实验研究

目的 研究新霉素对大鼠前庭毛细胞的毒性作用,为药物性前庭功能障碍动物模型的制备和相关研究提供参考.方法 将15只成年Wistar大鼠分为正常对照组(n=5)、新霉素组(n=5)和人工外淋巴液组(n=5),新霉素组大鼠在右耳通过耳蜗底转鼓阶打孔的方法在耳蜗内注入0.1%(g/100ml)新霉素5μl,人工外淋巴液组按同样方法注入人工外淋巴液5μl.正常对照组大鼠不做任何处理.处理3天后对动物进行颈髓硬膜外短声诱发电位(click-evoked potential on the surface of the cervical dura mater,CDM-CEP)检查和游泳试验以评价前庭功能;然后将动物处死,进行形态学观察.结果 3天后新霉素组大鼠的前庭毛细胞即出现严重破坏,并出现严重的前庭功能损伤.正常对照组大鼠的游泳时间为(4.0±0.71)8(3～5s,n=5),新霉素组大鼠的游泳时间为(10.2±1.64)8(8～12s,n=5),人工外淋巴液组大鼠的游泳时间为(4.4±1.14)s(3～6s,n=5);在短音(click)刺激下,正常大鼠引出CDM-CEP的阈值为(85±3.54)dB SPL(80-90 dB SPL,n=5),阈值时的潜伏期为(6.59±0.41)8(6.05～7.05s,12=5);新霉素组大鼠120dB SPL仍无法引出CDM-CEP;人工外淋巴液组大鼠引出CDM-CEP的阈值为(90±5.0)dB SPL(85-95 dB SPL,n=5),阈值时的潜伏期为(6.68±0.31)s(6.35～7.02s,n=5).结论 新霉素对大鼠前庭毛细胞具有极强的破坏作用,新霉素耳蜗内注射的方法可以制备理想的前庭功能障碍动物模型.     

前庭性偏头痛患者前庭功能分析及治疗效果评估北大核心CSCD

目的分析前庭性偏头痛(vestibular migrain,VM)患者的前庭功能并评估其治疗效果。方法对40例前庭性偏头痛患者(VM组)及40例健康志愿者(对照组)分别进行前庭功能相关检查,包括冷热试验、摇头试验、前庭自旋转试验,并分析比较两组的检查结果;对VM患者给予药物治疗及预防,并以视觉评分量表(visual analogue scale,VAS)对VM患者治疗前后进行评分,评估治疗效果。结果VM组患者冷热试验异常15例(37.5%),摇头试验异常13例(32.5%),前庭自旋转异常10例(25%),其中32例(80%)患者至少一项前庭功能试验结果异常;对照组冷热试验异常2例(5%),摇头试验异常1例(2.5%),前庭自旋转异常1例(2.5%);VM组水平半规管功能异常发生率明显高于对照组,差异有统计学意义(P<0.05)。VM患者用药后头痛、头晕的VAS评均分较治疗前明显降低,差异有统计学意义(P<0.05)。结论本组80%VM患者出现前庭功能异常,前庭外周功能及前庭中枢功能均有损害,前庭低频功能损伤较高频功能受损多见;药物治疗可明显缓解VM患者症状。     

前庭性偏头痛患者前庭功能的临床研究

目的通过实验室检查来评估前庭性偏头痛(vestibular migrain,VM)患者的前庭功能,探寻该疾病的前庭功能特点。方法对37例确诊为前庭性偏头痛的患者及30例健康志愿者分别行冷热试验(caloric test)、摇头试验(head-shaking nystagmus,HNS)、速度阶梯试验及颈肌性前庭诱发电位(cervical Vestibular-Evoked Myogenic Potentials,cVEMP)检查,对两组冷热试验、摇头试验及速度阶梯试验的异常结果进行分析,对100dB的短音刺激情况下cVEMP不对称性进行分析。结果前庭性偏头痛患者水平半规管功能的异常率显著高于对照组,差异有统计学意义(P<0.05)。37例VM患者中,有11例(29.7%)出现冷热试验异常,14例(37.8%)出现摇头试验异常,7例(18.9%)出现速度阶梯试验异常。30例健康志愿者中,有2例(6.7%)出现冷热试验异常,1例(3.3%)出现摇头试验异常,无患者出现速度阶梯试验异常。总体而言,28例(76%)VM患者至少在一个水平半规管功能试验中出现异常,异常率最高的是摇头试验,其次是冷热试验和速度阶梯试验。前庭性偏头痛患者的cVEMP异常率(21.6%)要显著高于对照组(3.3%),差异有统计学意义(P<0.05)。结论 76%的前庭性偏头痛患者被发现存在前庭功能异常,在冷热试验的基础上加用摇头试验和旋转试验,可以提高VM患者前庭功能异常的检出率。前庭性偏头痛患者显示的cVEMP结果,反映了球囊功能的异常及VM患者在球囊-颈反射通路上有所损害。前庭性偏头痛患者存在不同程度的前庭功能异常。     

单侧前庭功能丧失大鼠患侧前庭内侧核及小脑绒球中GLU-IR、GFAP、GABA B2的表达

目的 探讨单侧前庭功能丧失大鼠中枢代偿的机制.方法 将45只成年健康SD大鼠随机分为空白对照组(n=9)、生理盐水注射组(n=18)、模型组(n=18).每组大鼠随机确定实验耳侧别,空白对照组正常饲养,生理盐水注射组鼓室内一次性注射生理盐水0.1～0.2毫升/耳,模型组鼓室内一次性注射50％ 氯仿0.1～0.2毫升/耳...     

前庭代偿过程中GABAA受体α1亚型在前庭内侧核中的变化

目的 观察单侧迷路破坏术后前庭内侧核(medial vestibular nuclei, MVN)内γ-氨基丁酸A受体(gamma-aminobutyric acid A receptor, GABAA receptor)α1亚型的表达变化.方法 将24只大鼠随机分为术后1、3、7天组和假手术组,每组6只,前三组切除大鼠一侧迷路,第4组行假手术,利用免疫组织化学、原位杂交组织化学的方法,观察术后1、3、7天组前庭内侧核区GABAA受体α1亚型表达的变化,及其在前庭代偿中可能的作用 ,并与假手术组进行比较.结果 手术后1天、3天、7天组行为学上开始均有前庭静态症状,术后7天时前庭静态症状均消失,假手术组无相关症状出现.免疫组织化学、原位杂交组织化学方法前庭内侧核中各组手术侧与对侧比较及术后1天、3天、7天组与假手术组比较,GABAA受体α1亚型表达差异均无统计学意义(P>0.05).结论 在前庭代偿的早期,GABAA受体α1亚型表达的变化可能没有涉及前庭代偿.     

前庭康复治疗对平衡障碍患者的疗效分析

目的探讨前庭康复治疗(vestibular rehabilitation therapy,VRT)对平衡障碍患者的疗效。方法对76例平衡障碍患者根据单、双侧及针对性康复原则随机分为四组,A组(单侧)29例为单纯药物组,B组(单侧)29例为药物联合前庭康复组;C组(双侧)9例为单纯药物组,D组(双侧)9例为药物联合前庭康复组,分别给予药物联合前庭康复训练治疗或单纯药物治疗,疗程4周,采用前庭症状指数(vestibular symptom index,VSI)主观评估,Berg平衡量表(Berg balance scale,BBS)、功能性伸手试验及Fukuda踏步试验评估平衡功能,比较各组的疗效。结果 4组患者治疗后VSI评分均明显低于治疗前(P<0.01);无论单侧或双侧平衡障碍患者,药物联合前庭康复治疗组患者治疗后BBS评分、功能性伸手试验、Fukuda踏步等平衡功能均明显优于单纯药物治疗组(均为P<0.01)。结论前庭康复训练联合药物治疗平衡障碍患者的效果优于单纯药物治疗,前庭康复训练可作为前庭功能减退平衡功能障碍患者的辅助疗法。     

前庭损伤后脑干相关神经元C-FOS的表达

目的观察大鼠内耳前庭损伤后，在静止和角加速度刺激状态下双侧前庭神经核C—FOS阳性表达的改变，初步探讨前庭代偿机制。方法将60只SD大鼠分为5组（12只，组）：（1）无手术组；（2）单耳前庭神经切断手术组；（3）单耳前庭神经切断手术对照组；（4）双耳前庭神经切断手术组；（5）双耳前庭神经切断手术对照组，每组一半动物给予角加速度刺激。用免疫组化ABC法观察C—FOS在前庭神经核、舌下神经前置核的神经元表达的改变。结果在静止状态下，正常鼠和手术对照组鼠的双侧前庭神经核、舌下神经前置核无C—FOS阳性神经元；给予旋转刺激后，双侧前庭神经核、舌下神经前置核皆有C—FOS阳性神经元。单耳手术组术后24小时．同侧前庭神经内核、对侧舌下神经前置核有C—FOS阳性神经元，旋转刺激后双侧前庭神经核、舌下神经前置核皆有C—FOS阳性神经元。双耳手术组24小时，在静止状态和角加速度刺激状态下，双侧前庭神经核、舌下神经前置核皆无C—FOS阳性神经元。结论一侧前庭损伤后，同侧前庭神经内核、对侧舌下神经前置核C—FOS阳性神经元在前庭代偿早期可能起启动突触联系的作用。     

天麻素对单侧前庭功能丧失大鼠绒球中谷氨酸免疫反应物、胶质纤维酸性蛋白、γ-氨基丁酸B2型受体表达及疗效的影响

目的　探讨天麻素促进前庭功能恢复及中枢代偿的机制。方法　成年健康SD大鼠随机分组,空白对照组（n=9）正常饲养,假手术对照组（n=18）鼓室内注射生理盐水,模型对照组（n=18）、模型治疗组（n=54）鼓室内注射氯仿。造模成功后,对照组肌肉注射生理盐水;模型治疗组再随机分为天麻素低、中、高剂量组（每组n=18）,每日分别肌肉注射低、中、高剂量天麻素,连续注射3d。观察绒球中谷氨酸免疫反应物（glutamate immunoreactivity,GLU-IR）、胶质纤维酸性蛋白（giial fibrillary acid protein,GFAP）、γ-氨基丁酸B2型受体（gamma-aminobutyric acid B2,GABA B2）表达。结果　模型对照组、模型治疗组GLU-IR表达明显下调,GFAP、GABA B2表达明显上调。经天麻素治疗后,模型治疗组与模型对照组比较,GLU-IR、GABAB2表达明显上调,GFAP表达明显下调,天麻素高剂量组均最为明显。结论　天麻素能够对中枢进行多靶点调控,加速代偿的进程与程度。     

Role of Histamine H1 Receptors in Vestibular Nucleus in Motion Sickness

Objectives To investigate the expression of histamine H1 receptors (H1R) in the vestibular nucleus of brainstem in rats and the role of H1R in motion sickness (MS). Methods A total of 24 healthy Sprague-Dawley rats were divided randomly into four groups (n=6 each) which determined if the animals would receive induction of MS or drug (promethazine) treatment: MS(-)/Drug(-); MS(+)/Drug(-); MS(-)/Drug(+ at 0.25 mg); and MS(+)/Drug(+). MS was induced by complex motion stimulation and the conditioned taste aversion was used as a behavioral indicator of MS. The volume of 0.15% sodium saccharin solution (SS) intake within 45 minutes after motion stimulation was measured. H1R in the vestibular nucleus was examined by immunofluorescence staining. The expression of H1R protein in brainstem tissue at vestibular nucleus level was detected by western blot. Results The mean SS intake volume in the MS(+)/Drug(-) group (8.8 ml) was significantly less than that of the MS(-)/Drug(-) group (15.1 ml) (P < 0.01). The mean SS intake volume of the MS(-)/Drug(+) group (14.8 ml) was similar to that of the MS(-)/Drug(-) group. The mean SS intake volume (9.6 ml) of the MS(+)/Drug(+) group was more than that of the MS(+)/Drug(-)group (P < 0.01), but less than that of the MS(-)/Drug(-) group or MS(-)/Drug(+) group (P < 0.01). Immunofluorescence staining showed positive expression of H1R in the vestibular nucleus of brainstem and the expression was enhanced by motion stimulation. Western blot analysis showed that H1R protein expressed in the brainstem tissue at vestibular nucleus level and the expression also increased significantly after motion stimulation. The MS-induced increase of H1R was not affected significantly by promethazine. Conclusions H1Rs exist in the vestibular nucleus in rats and H1R expression is up-regulated by motion stimulation, but not affected by promethazine. The findings indicate that the histaminergic system is involved in MS. Promethazine, as an H1R blocker, may play its anti-MS role by competing the binding site on H1Rs with histamine rather than inhibiting H1R expression.     

Localization of histamine (H1, H2, H3 and H4) receptors in mouse inner ear

Conclusion The present findings show that all four types of histamine receptors (H1R, H2R, H3R, and H4R) are present in the inner ear, thus supporting the hypothesis that histamine plays a physiological role in the inner ear. Objective To analyse the presence of histamine receptors in the normal mouse inner ear. Methods CBA/J mice were used in this study. The localization of H1R, H2R, H3R, and H4R in the inner ear, i.e. cochlea, vestibular end organs, vestibular ganglion, and endolymphatic sac, was studied by real-time PCR and immunohistochemistry. Results The mRNA for each receptor sub-type was detected in the inner ear. In the immunohistochemical study, the organ of Corti, spiral ganglion, vestibular ganglion, vestibular sensory epithelium, and endolymphatic sac cells showed an immunofluorescent reaction to all histamine receptors.     

前庭代偿过程中Ⅰ组代谢性谷氨酸受体亚型在前庭内侧核中的变化

目的观察单侧迷路破坏术后前庭内侧核(medialvestibular nuclei,MVN)内I组代谢性谷氨酸受体亚型(group I metabotropic glutamate receptors,mGluR1)的表达变化。方法成年雄性Wistar大鼠28只,分为迷路破坏组(20只)和对照组(8只),前者破坏单侧迷路,对照组手术方式相同但保持迷路完好。单侧迷路破坏术后,通过免疫组织化学、原位杂交组织化学法检测不同存活时间(术后12h、36h、7d、30d)两组动物MVN内mGluR1的表达变化。结果单侧迷路破坏术后可诱导同侧MVN区I组代谢性谷氨酸受体亚型mGluR1减少,术后12h最少,术后36h开始增加,至术后7d和30d后和对照组差异无统计学意义;对侧和术侧的变化趋势相同。结论单侧迷路破坏术后可诱导MVN区I组代谢性谷氨酸受体亚型mGluR1减少。初级前庭传入或中枢前庭神经元的静息放电降低可能与I组代谢性谷氨酸受体亚型mGluR1减少有关,但其在前庭代偿中的作用尚有待研究。     

Immunocytochemical and stereological study of glucocorticoid receptors in rat medial vestibular nucleus neurons and the effects of unilateral vestibular deafferentation

CONCLUSION: The results of this study suggest that neither the number of medial vestibular nucleus (MVN) neurons expressing cytosolic glucocorticoid receptors nor blood corticosterone levels change significantly during the development of vestibular compensation. OBJECTIVE: Vestibular compensation is a process of partial behavioral recovery that occurs following damage to the vestibular labyrinth. It has been suggested that this compensation process might be dependent on the release of glucocorticoids such as corticosterone at the time of unilateral vestibular deafferentation (UVD) and that changes in glucocorticoid receptors in the MVN might contribute to the initiation of the compensation process. MATERIAL AND METHODS: We compared the number of MVN neurons expressing cytosolic glucocorticoid receptors in rats at 10 h and 2 weeks following UVD, and in sham and anesthetic control animals; we also measured blood corticosterone levels. RESULTS: Using immunocytochemistry and stereology, we found that the majority of MVN neurons expressed glucocorticoid receptors, but there were no significant differences in the number of glucocorticoid receptor-expressing neurons in the ipsilateral or contralateral MVNs at 10 h or 2 weeks post-UVD; furthermore, corticosterone levels did not vary significantly between the UVD and control groups.     

Immunocytochemical and stereological study of glucocorticoid receptors in rat medial vestibular nucleus neurons and the effects of unilateral vestibular deafferentation

Conclusion. The results of this study suggest that neither the number of medial vestibular nucleus (MVN) neurons expressing cytosolic glucocorticoid receptors nor blood corticosterone levels change significantly during the development of vestibular compensation. Objective. Vestibular compensation is a process of partial behavioral recovery that occurs following damage to the vestibular labyrinth. It has been suggested that this compensation process might be dependent on the release of glucocorticoids such as corticosterone at the time of unilateral vestibular deafferentation (UVD) and that changes in glucocorticoid receptors in the MVN might contribute to the initiation of the compensation process. Material and methods. We compared the number of MVN neurons expressing cytosolic glucocorticoid receptors in rats at 10 h and 2 weeks following UVD, and in sham and anesthetic control animals; we also measured blood corticosterone levels. Results. Using immunocytochemistry and stereology, we found that the majority of MVN neurons expressed glucocorticoid receptors, but there were no significant differences in the number of glucocorticoid receptor-expressing neurons in the ipsilateral or contralateral MVNs at 10 h or 2 weeks post-UVD; furthermore, corticosterone levels did not vary significantly between the UVD and control groups.     

Comparison of protein kinase activity and protein phosphorylation in the medial vestibular nucleus and prepositus hypoglossi in labyrinthine-intact and labyrinthectomized guinea pigs

The aim of the present study was to compare in vitro protein expression, protein kinase activity and protein phosphorylation in the medial vestibular nucleus (MVN) and prepositus hypoglossi (PH) from labyrinthine-intact guinea pigs and from guinea pigs at various stages of vestibular compensation following unilateral labyrinthectomy (UL). The ipsilateral (I-MVN) and contralateral (C-MVN) MVN, and the ipsilateral (I-PH) and contralateral (C-PH) PH, were dissected from 3 naive labyrinthine-intact guinea pigs and 55 guinea pigs at 10 hs or 53 hs following a surgical UL or sham operation. Tissue extracts were incubated with [gamma-33P]ATP+/-Ca2+, phorbol 12, 13 dibutyrate and phosphatidylserine or +/- Ca2+ and calmodulin, to enhance protein kinase C (PKC) or calcium calmodulin kinase (CaMK) activity, respectively. Data were analysed as the ratio of activated to basal 33P incorporation detected by phosphorimaging. There were similar total protein and phosphoprotein profiles in the MVN and PH, as well as both PKC and CaMKII activity, suggesting that the MVN and PH are similar in the way that proteins undergo rapid modification by phosphorylation. During the development of vestibular compensation, a 46 kDa band in C-PH displayed higher PKC-mediated phosphorylation from 10 hs post-UL compared to sham controls. Significantly greater PKC-mediated phosphorylation of proteins of approximately 18, 46 and 75 kDa was observed in C-PH at 10 hs compared to 53 hs post-UL and in most cases the phosphorylation was greater in C-PH than in the C-MVN. These results suggest that between 10 and 53 hs post-UL, PKC-mediated phosphorylation changes mainly in the C-PH rather than the ipsilateral or contralateral MVN.     

糖尿病大鼠颈性前庭诱发肌源性电位的观察

目的：观察糖尿病大鼠不同时期的颈性前庭诱发肌源性电位（cervical vestibular evoked myogenic potential ,cVEMP）的变化及意义。方法将220只雄性SD大鼠随机分为对照组（20只）及糖尿病组（200只）,应用链脲佐菌素（streptozotocin ,STZ）诱导糖尿病大鼠模型,再按照造模的时间将糖尿病组分为糖尿病4、6、8、10、12周组,每组40只,观察各组大鼠的一般情况及血糖、ABR、cVEM P检测结果。结果糖尿病组大鼠造模后出现多饮、多食、多尿等典型糖尿病症状,与对照组比较,血糖升高（P＜0．01）、体重下降（P＜0．01）;糖尿病组从第6周开始出现ABR反应阈值升高（P＜0．05）;糖尿病组cVEMP阈值第8周（53．87±11．16 dB nHL）、第10周（67．00±12．74 dB nHL）、第12周（67．00±9．23 dB nHL）升高（P＜0．01）,P1波潜伏期第8周（5．01±0．33 ms）、第10周（5．37±0．45 ms）、第12周（5．39±0．24 ms）延长（P＜0．01）,N1波潜伏期第10周（8．98±0．86 ms）、第12周（9．08±0．45 ms）延长（P＜0．01）,但糖尿病组P1－N1波间振幅与对照组比较差异无统计学意义（P＞0．05）。结论糖尿病大鼠从造模成功第8周开始,cVEMP阈值开始升高、P1波及N1波潜伏期延长,出现不同程度的前庭终器损伤,提示cV EM P可作为早期诊断前庭功能损害的方法之一。     

Effect of baclofen on neuronal activity in the medial vestibular nucleus after unilateral surgical labyrinthectomy in rats

Conclusions: Ipsilateral and contralateral medial vestibular nuclei (MVN) neurons respond differently to systemic injection of baclofen (4-amino-3-(4-chlorophenyl)-butanoic acid), illustrating the plastic changes of the type B γ-aminobutyric acid (GABA_B) receptor during vestibular compensation. Objectives: To investigate the responsiveness of MVN neurons to baclofen during the early, partially compensated period after unilateral surgical labyrinthectomy. Materials and methods: MVN were localized using field potentials evoked by electrical stimulation, along with a stereotaxic atlas of rat brain. Neuronal activity in MVN was recorded and analyzed in rats that had undergone labyrinthectomy with and without administration of baclofen. Results: After left labyrinthectomy the mean discharge rate in ipsilesional MVN decreased, but it was nearly restored by postoperative day 8. Baclofen (3 mg/kg) reversed the mean discharge rates between bilateral MVN at days 4 and 8 after surgical labyrinthectomy. In addition, the reduction ratio of the right MVN neurons was higher than that of the left MVN neurons.