双轴旋转运动刺激后大鼠中缝大核神经元活动分析（英文）

目的:分析大鼠经引发晕动病的双轴旋转运动刺激后,中缝背核(DR)内5-HT能神经元激活状况,以探讨5-HT水平与前庭刺激的关系。方法:将雄性SD大鼠随机分成两组:对照组和双轴旋转运动刺激组。所有动物装入定做的有机玻璃圆筒内,并于黑暗中进行如下处理2 h:运动刺激组动物以电动马达驱动的双轴旋转运动刺激;对照组动物放置在距刺激仪器20 cm的位置。应用包含DR的冠状脑切片,以双重免疫荧光标记技术标记5-HT和Fos蛋白,并对标记神经元进行计数和统计分析。结果:对照组和旋转运动刺激组的Fos阳性神经元、5-HT阳性神经元以及Fos/5-HT双标记神经元的数目分别是:93.4±12.0 vs 153.1±21.1、528.5±36.0 vs 531.1±23.4和15.1±11.3 vs 30.8±11.3。t检验分析显示两组Fos阳性神经元数目有显著性差异(P0.05);Fos/5-HT双标神经元数目在旋转运动刺激后有增加趋势。结论:引发晕动病的双轴旋转运动能激活中缝背核内的神经元,其中的5-HT能神经元也对刺激有反应。     

双轴旋转运动刺激后大鼠中缝大核神经元活动分析

目的:分析大鼠经引发晕动病的双轴旋转运动刺激后,中缝背核(DR)内5-HT能神经元激活状况,以探讨5-HT水平与前庭刺激的关系.方法:将雄性SD大鼠随机分成两组:对照组和双轴旋转运动刺激组.所有动物装入定做的有机玻璃圆筒内,并于黑暗中进行如下处理2h:运动刺激组动物以电动马达驱动的双轴旋转运动刺激;对照组动物放置在距刺激仪器20 cm的位置.应用包含DR的冠状脑切片,以双重免疫荧光标记技术标记5-HT和Fos蛋白,并对标记神经元进行计数和统计分析.结果:对照组和旋转运动刺激组的Fos阳性神经元、5-HT阳性神经元以及Fos/5-HT双标记神经元的数目分别是:93.4 ±12.0 vs 153.1 ±21.1、528.5±36.0vs 531.1±23.4和15.1 ±11.3 vs 30.8 ±11.3.t检验分析显示两组Fos阳性神经元数目有显著性差异(P＜0.05);Fos/5-HT双标神经元数目在旋转运动刺激后有增加趋势.结论:引发晕动病的双轴旋转运动能激活中缝背核内的神经元,其中的5-HT能神经元也对刺激有反应.     

前庭刺激激活大鼠内侧前额叶皮质神经元Fos表达

目的:分析对比加伐尼刺激(Galvanic stimulation)与双轴旋转运动分别作用于大鼠前庭器官对内侧前额叶皮质(mPFC)神经元活动的影响。方法:将雄性SD大鼠随机分为4组：电刺激组、对照组、双轴旋转运动组和对照组。电刺激组动物以100～200μA电流强度刺激前庭感受器1 h后休养1 h;双轴旋转组动物以双轴旋转运动刺激2 h。应用包含mPFC的25μm脑冠状切片,以免疫组织化学抗生物素蛋白-生物素复合物(ABC)技术进行Fos蛋白免疫反应并以3,3′-二氨基联苯胺(DAB)显色。最后,对mPFC内标记神经元进行计数和统计分析。结果:动物经两种类型分别刺激后,mPFC均见到大量Fos样免疫阳性反应神经元细胞核;曼-惠特尼U检验统计表明每种刺激条件下,刺激组较对照组动物mPFC内Fos阳性神经元数目都有显著增加(P<0.05)。半定量统计显示两种类型刺激后,接受刺激组和对照组动物mPFC内Fos阳性神经元数目激活的神经元数目分别是1053±240.50 vs 44.25±3.64和509.80±54.40 vs 128.30±7.66。结论:诱发晕动病的双轴旋转刺激和伽伐...     

后肢去负荷改变大鼠前庭复合体各亚核Fos表达(英文)

目的:以Fos蛋白表达为指标,分别研究后肢去负荷(hindlimb unloading,HU)以及去负荷一定时间后双轴旋转刺激对大鼠前庭核复合体(vestibular nucleus complex,VNC)各亚核神经元活动的影响。方法:动物分为后肢去负荷(即HU)组、HU处理后双轴旋转组(HU-R)和对照组(即假运动刺激组)。应用免疫组织化学ABC法,检查各组动物VNC各核团内Fos蛋白表达,统计Fos阳性神经元数目。结果:后肢去负荷1d可刺激VNC吻侧部前庭内侧核(MVe)、前庭下核(SpVe)两亚核内Fos阳性神经元数目较对照组有显著增加;但是,随后肢去负荷时间延长,VNC各核Fos阳性神经元数趋向于回到对照水平。2h双轴旋转刺激HU1d大鼠后,VNC所有核团内Fos阳性神经元数目都显著性增加;大鼠HU7d后再行双轴旋转刺激,MVe和SpVe内Fos阳性神经元数目有显著性增加。结论:地面模拟失重可刺激大鼠VNC神经元活动,随时间延长,模拟失重动物出现适应现象,前庭神经元活动减弱;运动刺激前庭感受器后,模拟失重动物VNC神经元活动显著增强。     

缺氧诱导大鼠中缝背核远位触液神经元表达Fos蛋白

本文旨在研究缺氧刺激条件下中缝背核内远位触液神经元Fos蛋白的表达情况。应用低压氧舱仿海拔8000米高空缺氧模型,采用侧脑室注射CB(霍乱毒素B亚单位)标记中缝背核内的远位触液神经元,并用Fos免疫组化和CB/Fos免疫组化双重染色方法显示Fos在中缝背核远位触液神经元内的表达情况。结果表明中缝背核内存在大量的CB标记神经元(31.16±3.36/每张切片)。缺氧实验组中缝背核内Fos阳性神经元数显著增加(40.28±2.17/每张切片,P<0.05),并可见CB/Fos双标神经元(2.00±0.39/每张切片)。对照组中缝背核内Fos阳性神经元数较少(5.55±0.81/每张切片),未见CB/Fos双标神经元。本文结果提示在缺氧刺激条件下,中缝背核内部分远位触液神经元在脑脑脊液之间的信息传递及功能调节中可能发挥一定作用。     

旋转运动刺激前庭感受器激活室旁核神经元活动的形态学证明

目的 探讨运动刺激前庭感受器后,下丘脑室旁核（Pa）神经元的反应,及Pa在前庭刺激引发机体自主反应中的作用和有关神经机制。 方法 将10只成年雄性SD大鼠平均分成两组,对照组和前庭损毁组,双侧鼓室内注射4-氨基苯砷酸钠（100 g/L）以损毁内耳迷路感受器。两组动物均经过2h双轴旋转运动刺激后,取含Pa的脑块并进行冠状切片（25μm）。以亲和素-生物素过氧化物酶体系（ABC）法对切片进行Fos蛋白免疫组织化学染色,观察和统计学分析Pa内Fos阳性神经元数量变化。 结果 药物损毁前庭后,动物头部有左右摇晃,运动时身体不稳或转圈等不平衡现象。免疫组织化学结果显示,两组动物下丘脑多个区域有大量Fos阳性神经元出现,其中Pa、室周核以及下丘脑外侧部等区域Fos阳性神经元密度更高。统计学分析表明,前庭损毁组动物Pa内Fos阳性神经元数目较正常组动物显著降低（P<0.05）,其中对照组为（104.00±7.00）个,前庭损毁组为（62.67±7.06）个。 结论 前庭信息传入能够激活Pa神经元,提示Pa神经元在前庭信息引发的自主反应中发挥一定的作用。     

大鼠前庭神经核复合体内5-HT能终末与表达5-HT1A受体的前庭-臂旁核投射神经元之间的联系

目的 观察大鼠前庭神经核复合体(VNC)内5-羟色胺(5-HT)样阳性终末与表达5-HT1A受体(5-HT1A R)的前庭-臂旁核投射神经元之间的联系.方法 运用逆行束路追踪和免疫荧光组织化学染色相结合的双重标记技术,在激光共焦显微镜下观察.结果 将四甲基罗达明(TMR)注入臂旁核后,在双侧VNC的各个核团内均可观察到许多TMR逆标神经元,但以同侧为主.免疫荧光组织化学染色结果显示,在前庭内侧核(MVe)、前庭下核(SpVe)、前庭上核(SuVe)、前庭外侧核(LVe)、X核以及Y核的一些区域内,许多神经元表达5-HT1A R样免疫阳性,并可观察到大量5-HT样阳性纤维和终末.激光共焦显微镜下可进一步观察到一些TMR逆标神经元同时呈5-HT1A R样免疫阳性,且有部分5-HT样阳性终末与TMR/5-HT1A R双标神经元的胞体或树突形成密切接触.结论 提示5-HT可能通过5-HT1A R对前庭神经核复合体-臂旁核间的信息传递发挥调控作用.     

大鼠前庭神经核复合体内5-羟色胺1A受体的分布

为了研究5-羟色胺1A受体(5-HT1AR)亚型在大鼠前庭神经核复合体(VNC)内的分布情况,本文采用免疫组织化学方法,在光学显微镜下对5-HT1AR亚型免疫阳性结构进行了观察。结果显示:5-HT1AR免疫阳性产物在VNC各个核团全长均有分布,主要定位于VNC神经元的胞体和近侧端树突,呈弥散分布,但在胞浆中也观察到许多染色深浅不同、分布不均匀的点状阳性结构。其中5-HT1AR样阳性神经元在前庭内侧核的全长呈密集分布,在前庭下核的尾段呈中等密度分布,在前庭上核、前庭外侧核和X核的全长、前庭下核的吻段和中段以及Y核的中、尾段均呈低密度分布,Y核的吻侧呈稀疏分布。本文结果提示,5-HT1AR阳性结构广泛地分布于大鼠VNC内,它们可能在介导5-HT对神经元活动的调节,参与前庭信息的整合与加工方面发挥重要作用。     

大鼠中缝背核向缰核投射的5-羟色胺能神经元对躯体伤害性刺激的fos表达

用WGA-HRP逆行追踪与抗FOS和抗5-羟色胺免疫组化的三重标记方法,观察向大鼠一侧有前跖部皮下注射8%福尔马林50μl后,中缝背核至缰核5-羟色胺能神经元的FOS表达.光镜下发现中缝背核内有七种阳性神经元.即HRP、FOS、5-HT单标细胞;FOS/HRP、FOS/5-HT、HRP/5-HT双标细胞;FOS/HRP/5-HT三标细胞.结果表明中缝背核至缰核的5-HT能投射神经元对躯体伤害性刺激起反应.     

双轴旋转运动刺激对大鼠前边缘皮质神经元放电的影响

目的:探索前庭信息是否调节前边缘皮质(prelimbic cortex,PrL)区神经元的活动。方法:体重130¹50 g雄性SD大鼠,分成两组:对照组和运动刺激组。运动刺激组动物接受2 h双轴旋转运动刺激,以刺激前庭感受器。采用全细胞脑片膜片钳技术,分别在电流钳和电压钳模式下,刺激PrL浅层(II/III层)并记录PrL深层(V/VI层)神经元,分析动作电位(action potential,AP)特性和诱发的兴奋性突触后电流(evoked excitatory postsynaptic current,eEPSC)。结果:2 h双轴旋转刺激没有改变PrL神经元AP阈值、幅值、半幅时程、峰值上升相最大斜率以及峰值下降相最大斜率等参数(P>0.05,n=10);但向神经元输入波宽180 ms,80150 g雄性SD大鼠,分成两组:对照组和运动刺激组。运动刺激组动物接受2 h双轴旋转运动刺激,以刺激前庭感受器。采用全细胞脑片膜片钳技术,分别在电流钳和电压钳模式下,刺激PrL浅层(II/III层)并记录PrL深层(V/VI层)神经元,分析动作电位(action potential,AP)特性和诱发的兴奋性突触后电流(evoked excitatory postsynaptic current,eEPSC)。结果:2 h双轴旋转刺激没有改变PrL神经元AP阈值、幅值、半幅时程、峰值上升相最大斜率以及峰值下降相最大斜率等参数(P>0.05,n=10);但向神经元输入波宽180 ms,80²80 pA的脉冲电流后,旋转刺激组PrL神经元放电数目显著增加(P<0.05,n=8)。结论:前庭信息可影响PrL神经元活动,故PrL很可能是接受和处理前庭信息的高级脑结构之一。     

Acid-sensing ionic-channel functional expression in the vestibular endorgans

In the vestibular system, the electrical discharge of the afferent neurons has been found to be highly sensitive to external pH changes, and acid-sensing ionic-channels (ASIC) have been found to be functionally expressed in afferent neurons. No previous attempt to assay the ASIC function in vestibular afferent neurons has been done. In our work we studied the electrical discharge of the afferent neuron of the isolated inner ear of the axolotl (Ambystoma tigrinum) to determine the participation of proton-gated currents in the postransductional information processing in the vestibular system. Microperfusion of FMRF-amide significantly increased the resting activity of the afferent neurons of the semicircular canal indicating that ASIC currents are tonically active in the resting condition. The use of ASIC antagonists, amiloride and acetylsalicylic acid (ASA), significantly reduced the vestibular-nerve discharge, corroborating the idea that the afferent neurons of the vestibular system express ASICs that are sensitive to amiloride, ASA, and to FMRF-amide. The sensitivity of the vestibular afferent-resting discharge to the microperfusion of ASIC acting agents indicates the participation of these currents in the establishment of the afferent-resting discharge.     

Acid-sensing ionic channels in the rat vestibular endorgans and ganglia

Acid-sensing ionic channels (ASICs) are members of the epithelial Na+ channel/degenerin (ENaC/DEG) superfamily. ASICs are widely distributed in the central and peripheral nervous system. They have been implicated in synaptic transmission, pain perception, and the mechanoreception in peripheral tissues. Our objective was to characterize proton-gated currents mediated by ASICs and to determine their immunolocation in the rat vestibular periphery. Voltage clamp of cultured afferent neurons from P7 to P10 rats showed a proton-gated current with rapid activation and complete desensitization, which was carried almost exclusively by sodium ions. The current response to protons (H+) has a pH0.5 of 6.2. This current was reversibly decreased by amiloride, gadolinium, lead, acetylsalicylic acid, and enhanced by FMRFamide and zinc, and negatively modulated by raising the extracellular calcium concentration. Functional expression of the current was correlated with smaller-capacitance neurons. Acidification of the extracellular pH generated action potentials in vestibular neurons, suggesting a functional role of ASICs in their excitability. Immunoreactivity to ASIC1a and ASIC2a subunits was found in small vestibular ganglion neurons and afferent fibers that run throughout the macula utricle and crista stroma. ASIC2b, ASIC3, and ASIC4 were expressed to a lesser degree in vestibular ganglion neurons. The ASIC1b subunit was not detected in the vestibular endorgans. No acid-pH-sensitive currents or ASIC immunoreactivity was found in hair cells. Our results indicate that proton-gated current is carried through ASICs and that ionic current activated by H+ contributes to shape the vestibular afferent neurons' response to its synaptic input.     

Intracranial self-stimulation induces Fos expression in GABAergic neurons in the rat mesopontine tegmentum

The cholinergic neurons which originate in the mesopontine tegmentum and innervate the midbrain ventral tegmental area have been proposed to play a key role in intracranial self-stimulation reward. This mesopontine area also contains GABA neurons. Detailed information is still lacking, however, about the relationship of cholinergic and GABAergic neurons in this region to self-stimulation reward. Therefore, using double immunostaining for Fos as a marker of neuronal activity and choline acetyltransferase as a marker of cholinergic neurons, or for Fos and GABA, we investigated whether self-stimulation of the medial forebrain bundle induces Fos expression within cholinergic and GABAergic neurons in two regions of the mesopontine tegmentum, i.e., pedunculopontine tegmental nucleus and laterodorsal tegmental nucleus. Self-stimulation of the medial forebrain bundle for 1 h induced a large increase in the number of cells expressing Fos in both the pedunculopontine tegmental nucleus and laterodorsal tegmental nucleus, when compared to control brains. However, the self-stimulation-induced expression of Fos was restricted mostly to GABA-, but not choline acetyltransferase-, immunostained cells. We also examined, using microdialysis, whether self-stimulation increases acetylcholine efflux in the ventral tegmental area, a terminal region of the mesopontine tegmentum cholinergic pathway. One hour of self-stimulation significantly increased acetylcholine efflux from this terminal area.These results indicate that intracranial self-stimulation of the medial forebrain bundle may increase acetylcholine release without affecting expression of Fos in cholinergic neurons, while the same stimulation may induce Fos expression in GABAergic neurons of the mesopontine tegmentum. GABAergic as well as cholinergic neurons in this area appear to be activated by self-stimulation reward in the medial forebrain bundle.     

Decreased Fos protein expression in rat caudal vestibular nucleus is associated with motion sickness habituation

We investigated the temporal change of Fos protein expression in the caudal vestibular nucleus of rats exposed to daily 2-h Ferris-wheel like (FWL) rotation. Repeated rotation (2 h daily for 14 consecutive days) caused an initial increase in defecation, followed by a gradual decline back to the baseline level after 8 rotation sessions. Unlike defecation, the Kaolin consumption of rats showed a bitonic function during the daily rotation sessions (2 h daily for 33 consecutive days) and finally recovered to the baseline after about 31 sessions. Immunohistochemistry study revealed increased Fos immunolabeled (Fos-LI) neurons in the medial vestibular nucleus and spinal vestibular nucleus during the initial 7 rotation sessions, and it decreased to the baseline level after 10 rotation sessions. There was a strong linear relationship between the amount of Fos-LI neurons and rat defecation level throughout the whole rotation sessions. These results suggest that the change of neuronal plasticity in the caudal vestibular nucleus might contribute to attenuation of gastrointestinal symptoms during motion sickness habituation process.     

Treadmill running induces striatal Fos expression via NMDA glutamate and dopamine receptors

 Several non-physiological stimuli (i.e. pharmacological or electrical stimuli) have been shown to induce Fos expression in striatal neurons. In this work, striatal Fos (i.e. Fos-like) expression was studied after physiological stimulation, i.e. motor activity (treadmill running at 36 m/min for 20 min). In rats killed 2 h after the treadmill session, Fos expression was observed in the medial region of the rostral and central striatum, and in the dorsal region of the caudal striatum. Fos expression was prevented by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK-801 (0.1 mg/kg) or the D₁ dopamine receptor antagonist SCH-23390 (0.1 mg/kg), but not by pretreatment with the D₂ receptor antagonist eticlopride (0.5 mg/kg). Thirty-six hours after 6-hydroxydopamine lesion, a considerable reduction in treadmill-induced Fos expression was observed in both sides; however, Fos expression in the lesioned striatum was higher than in the contralateral intact striatum. Several weeks after unilateral 6-hydroxydopamine lesion of the nigrostriatal system, treadmill-induced Fos expression was significantly, but not totally, reduced in the lesioned striatum. Corticostriatal deafferentation also led to considerable reduction in treadmill-induced Fos expression. The present results indicate that exercise induces striatal Fos expression and that, under physiological stimulation, concurrent activation of D₁ and NMDA receptors is necessary for such expression to occur. Reduction of Fos expression is practically absolute after acute blockage of these receptors, but not after lesions, possibly due partially to compensatory changes. Received: 5 November 1996 / Accepted: 17 January 1997     

D-Fenfluramine induces serotonin-mediated Fos expression in corticotropin-releasing factor and oxytocin neurons of the hypothalamus, and serotonin-independent Fos expression in enkephalin and neurotensin neurons of the amygdala

The neurotransmitters expressed by neurons activated by D-fenfluramine (5 mg/kg, i.p.) were identified in the hypothalamus, amygdala and bed nucleus of the stria terminalis. Induction of Fos immunoreactivity following D-fenfluramine injection was used as an index of neuronal activation. To test whether D-fenfluramine activated neurons by releasing serotonin from the serotonergic nerve terminals, rats were pretreated with fluoxetine (10 mg/kg, i.p.), a serotonin reuptake inhibitor that prevents the release of serotonin stimulated by D-fenfluramine, 12 h before D-fenfluramine injection. The approximate percentages of peptidergic neurons that contained Fos immunoreactivity after D-fenfluramine administration were 94% of corticotropin-releasing factor and 22% of oxytocin cells in the paraventricular nucleus of the hypothalamus, 6% of oxytocin cells in the supraoptic nucleus of the hypothalamus, 36% of enkephalin and 15% of neurotensin cells in the central amygdaloid nucleus, and 19% of enkephalin and 9% of neurotensin cells in the bed nucleus of the stria terminalis. Fluoxetine pretreatment blocked Fos expression in corticotropin-releasing factor- and oxytocin-expressing cells in the hypothalamus, but not in enkephalin-and neurotensin-expressing cells located in the bed nucleus of the stria terminalis and central amygdaloid nucleus. D-Fenfluramine did not induce Fos immunoreactivity in vasopressin-, thyrotropin-releasing hormone-, somatostatin- and tyrosine hydroxylase-containing cells in the hypothalamus, and corticotropin-releasing factor-expressing cells in the central amygdaloid nucleus and bed nucleus of the stria terminalis. These results show that D-fenfluramine stimulates corticotropin-releasing factor- and oxytocin-expressing cells in the hypothalamus via serotonin release. The enkephalin- and neurotensin-expressing cells in the amygdala are activated by D-fenfluramine via non-serotonergic mechanisms. Induction of Fos expression by D-fenfluramine in restricted populations of cells suggests a selective activation of neuronal circuitry that is likely to be involved in the appetite suppressant effects of D-fenfluramine.     

Immunoreactivity for calretinin and calbindin in the vestibular nuclear complex of the monkey

Immunoreactivity to calcium-binding proteins has been a useful extension to cytoarchitectonics in defining the organization of many central nervous system regions. Previously we found subdivisions of the cat medial vestibular nucleus (MVe) defined by immunoreactivity to the calcium-binding proteins, calretinin and calbindin. Here we report similar subdivisions in both the squirrel and the macaque monkey. Calretinin immunoreactivity reveals a small area of cells and processes located dorsally in the MVe. In the anterior–posterior direction these cells extend over less than half of the nucleus. This area is not distinct in Nissl-stained sections. Elsewhere in the vestibular nuclear complex (VNC) and in the nucleus prepositus hypoglossi (PrH) there are scattered labeled cells. Immunoreactivity for calbindin shows a small patch of dense fiber label at the border of MVe and PrH, and a patchy distribution in the rest of the VNC that changes at different anterior–posterior levels. There are also calbindin-labeled cells in the underlying reticular formation over a very restricted anterior–posterior extent in both squirrel and macaque monkey. The dendrites of some of these cells can be followed into PrH, and data from other studies suggests that they may contribute to vestibular–oculomotor function. Scattered cells in the VNC are densely outlined by calbindin-labeled terminals, suggesting a major drive from the calbindin-labeled fiber input. These findings, along with observations from rodents and cats, suggest that there are subdivisions of the MVe defined by calcium-binding proteins that are homologous across rodents, cats, and New World and Old World monkeys.     

双轴旋转刺激后模拟失重大鼠前扣带回皮质内Fos表达(英文)

目的:研究动物接受不同实验方式重力刺激后,前扣带回皮质(ACC)这一可能与空间飞行后心血管功能紊乱有关的前庭功能区中神经元活动变化。方法:该研究采用卵白素-生物素复合物(ABC)、3,3’-二氨基联苯胺四盐酸盐水合物(DAB)为呈色剂的免疫组织化学方法。大鼠随机分为三组:正常对照组(Con);后肢去负荷(HU)组(动物吊尾7d)和后肢去负荷-旋转组(HU-R)(动物后肢去负荷7d后进行2h双轴旋转刺激)。结果:(1)HU组动物ACC内Fos阳性神经元的数目(199.8±44.8)比Con组(365.0±135.6)显著降低(P0.05);(2)双轴旋转刺激显著可增加7d吊尾大鼠ACC内Fos免疫阳性神经元数量(491.6±229.3,P0.05)。这些结果提示模拟失重和双轴旋转都可影响ACC神经元活动。结论:ACC受模拟失重的影响,7d吊尾刺激使ACC内Fos表达水平下降可能是一种适应的表现。     

Changes in protein expression in the rat medial vestibular nuclei during vestibular compensation

The molecular mechanisms of neural and synaptic plasticity in the vestibular nuclei during 'vestibular compensation', the behavioural recovery that follows deafferentation of one inner ear, are largely unknown. In this study we have used differential proteomics techniques to determine changes in protein expression in ipsi-lesional and contra-lesional medial vestibular nuclei (MVN) of rats, 1 week after either sham surgery or unilateral labyrinthectomy (UL). A systematic comparison of 634 protein spots in two-dimensional electrophoresis gels across five experimental conditions revealed 54 spots, containing 26 proteins whose level was significantly altered 1 week post-UL. The axon-guidance-associated proteins neuropilin-2 and dehydropyriminidase-related protein-2 were upregulated in the MVN after UL. Changes in levels of further specific proteins indicate a coordinated upregulation of mitochondrial function, ATP biosynthesis and phosphate metabolism in the vestibular nuclei 1 week post-UL. These may reflect the metabolic energy demands of processes such as gliosis, neuronal outgrowth and synaptic remodelling that occur after UL. Our findings suggest novel roles for axon elaboration and guidance molecules, as well as mitochondrial and metabolic regulatory proteins, in the post-lesional physiology of the MVN during vestibular system plasticity.