Mouse model of Bell's palsy induced by reactivation of herpes simplex virus type 1

In order to investigate the mechanism of Bell's palsy, we developed an animal model of facial nerve paralysis induced by the reactivation of herpes simplex virus type 1 (HSV-1). Eight weeks after recovery from facial nerve paralysis caused by inoculation with HSV-1, the mice were treated with auricular skin scratch at the site of the previous inoculation, or with intraperitoneal injection of anti-CD3 monoclonal antibody (mAb), or combination of both procedures. No mice developed facial nerve paralysis when they were treated with either auricular scratch or mAb injection alone. In contrast, 20% of mice developed facial nerve paralysis with the combined treatment. With one exception, no mouse treated with either auricular scratch or mAb injection showed HSV-I DNA in their facial nerve tissue, whereas 4 out of 6 mice receiving both treatments showed HSV-1 DNA on day 10 after treatment. Histopathological findings showed neuronal degeneration in the geniculate ganglion and demyelination of the facial motor nerve in paralyzed mice. These findings suggest that a combination of stimuli, local skin irritation, and general immunosuppression is essential for successfully inducing facial nerve paralysis in mice with latent HSV-1 infection.     

The Alterations of Matrix Metalloproteinase-9 in Mouse Brainstem During Herpes Simplex Virus Type 1-Induced Facial Palsy

The aim of this study is to explore the changes of matrix metalloproteinase-9 (MMP9) in the mouse brainstem during the development of facial paralysis induced by herpes simplex virus type 1 (HSV-1) and the inhibitory effect of methylprednisolone sodium succinate (MPSS) on MMP9 expression. HSV-1 was inoculated into the surface of posterior auricle of mouse to establish a paralyzed animal model. The paralyzed mice were divided randomly into three groups. In one group without any treatment, mice were killed at different time points of 6 h, 1, 2, 3, and 7 days post-induction of facial paralysis; in the other two groups, mice were injected daily with MPSS and a combination of MPSS and glucocorticoid receptor blocker (RU486) for 2 days, respectively. The expression of MMP9 in the facial nucleus of brainstem was detected by Western blot, quantitative real-time polymerase chain reaction, and immunofluorescence technique. A total of 52.07 % of mice developed unilateral facial paralysis after inoculated with HSV-1. Both mRNA and protein expression of MMP9 were present at low levels in normal facial nucleus of brainstem and were increased significantly after facial paralysis with its peak time at 2 days post-induction of facial paralysis. Expression of MMP9 of paralyzed mice was inhibited by MPSS, and the inhibition could be blocked by RU486. Our findings suggest that MMP9 in mouse brainstem is involved in the evolution of facial palsy induced by HSV-1 and may play an important role in the pathogenesis of this disease. MPSS might effectively relieve HSV-1-mediated damages by inhibitory effect on expression of MMP9 in HSV-1-induced facial paralysis.     

The sensory component of the facial nerve of a reptile (Lacerta viridis).

The sensory fibers of the facial nerve in Lacerta viridis have been studied with a silver impregnation method to follow the course of axonal degeneration. Destruction of the geniculate ganglion demonstrated the degenerated sensory component of the facial nerve adjacent to the anterior vestibular root. Within the lateral vestibular area the facial sensory fibers consist of numerous rootlets separated by vestibular fibers and cells. These rootlets may join to form a main or paired sensory tract that passes through the vestibular nuclei to enter the tractus solitarius and divide into a small ascending prefacial component and a major descending prevagal division. A few fibers continue into the postvagal part of tractus solitarius and extend caudally to terminate in the nucleus commissura infima. Prefacial fibers terminate along the periventricular gray while prevagal fibers terminate within the tractus solitarius on the dendrites of cells of nucleus tractus solitarius and near the periphery of the dorsal motor nucleus of X. There was no noticeable degeneration in the descendens tractus trigemini. Terminal degeneration to descendens nucleus trigemini and motor nucleus of VII followed the tractus solitarius course. Most facial sensory fibers are probably related to taste and other visceral information.     

An HRP study of the central course of sensory intermediate and vagal fibers in peripheral facial nerve branches in the cat

Previous studies have shown that sensory fibers of intermediate and vagal nerve origin are present in facial nerve branches to the mimetic muscles in the cat. In the present study the central course of these fibers has been examined by transganglionic transport of horseradish peroxidase (HRP). In some of these experiments the facial nerve proper was transected central to the site of HRP application. In this way, the central course of the vagal fibers could be studied separately. For comparison HRP-conjugated wheat germ agglutinin was injected into the geniculate ganglion, revealing the central course of the entire afferent component of the intermediate nerve. The results show that labeled sensory intermediate nerve fibers, at their level of entrance in the brainstem, form a tract at the dorsal margin of the spinal trigeminal tract (5T). While some fibers ascend from this level to terminate in the main sensory trigeminal nucleus, and a few fibers terminate in the rostral part of the solitary tract nucleus, the majority take a descending course. The main site of termination for these descending fibers is in the medial part of the C2 dorsal horn. Terminal labeling is also seen in the ventrolateral part of the cuneate nucleus (CUN) and in a small area of gray substance between CUN and trigeminal nucleus caudalis. After entering the brainstem some sensory vagal fibers project to the trigeminal nucleus interpolaris and to an interstitial nucleus within the 5T, but the larger part joins the descending tract of intermediate nerve fibers. These descending vagal fibers have a terminal distribution pattern similar to the intermediate nerve fibers.     

Demyelination can proceed independently of axonal degradation during Wallerian degeneration in wlds mice

Peripheral nerve injury induces axonal degeneration and demyelination, which are collectively referred to as Wallerian degeneration. It is generally assumed that axonal degeneration is a trigger for the subsequent demyelination processes such as myelin destruction and de-differentiation of Schwann cells, but the detailed sequence of events that occurs during this initial phase of demyelination following axonal degeneration remains unclear. Here we performed a morphological analysis of injured sciatic nerves of wlds mice, a naturally occurring mutant mouse in which Wallerian degeneration shows a significant delay. The slow Wallerian degerenation phenotype of the wlds mutant mice would enable us to dissect the events that take place during the initial phase of demyelination. Ultrastrucural analysis using electron microscopy showed that the initial process of myelin destruction was activated in injured nerves of wlds mice even though they exhibit morphologically complete protection of axons against nerve injury. We also found that some intact axons were completely demyelinated in degenerating nerves of wlds mice. Furthermore, we observed that de-differentiation of myelinating Schwann cells gradually proceeded even though the axons remained morphologically intact. These data suggest that initiation and progression of demyelination in injured peripheral nerves is, at least in part, independent of axonal degeneration.     

An autopsied case of the Crow-Fukase syndrome: a neuropathological study with emphasis on spinal roots

Summary An autopsied case of the Crow-Fukase syndrome is reported. Neuropathological findings were as follows: (1) in the sural nerve, there was marked decrease of large and small myelinated fibers. Myelinated fibers showing axonal degeneration and segmental demyelination and remyelination were moderately increased. (2) In the lumbar spinal roots, myelinated fibers showing segmental demyelination and remyelination were frequently observed. The density of myelinated fibers of the ventral root was less at the dural site than the spinal site, while that of the dorsal roots was less at the spinal site than the dural site. (3) In the dorsal root ganglion, there were Nageotte's residual nodules and satellitosis; (4) in the lumbar and thoracic spinal cord, there was pallor of the dorsal column; and (5) nerve cells showing central chromatolysis were frequently observed in the spinal anterior horn cells. Segmental demyelination and remyelination in the spinal roots and loss of myelinated fibers with axonal degeneration in the sural nerve are fibers with axonal degeneration in the sural nerve are main neuropathological features of this syndrome.     

Enhanced adenoviral gene delivery to motor and dorsal root ganglion neurons following injection into demyelinated peripheral nerves

Injection of viral vectors into peripheral nerves may transfer specific genes into their dorsal root ganglion (DRG) neurons and motoneurons. However, myelin sheaths of peripheral axons block the entry of viral particles into nerves. We studied whether mild, transient peripheral nerve demyelination prior to intraneural viral vector injection would enhance gene transfer to target DRG neurons and motoneurons. The right sciatic nerve of C57BL/6 mice was focally demyelinated with 1% lysolecithin, and the left sciatic nerve was similarly injected with saline (control). Five days after demyelination, 0.5 μl of Ad5‐GFP was injected into both sciatic nerves at the site of previous injection. The effectiveness of gene transfer was evaluated by counting GFP⁺ neurons in the DRGs and ventral horns. After peripheral nerve demyelination, there was a fivefold increase in the number of infected DRG neurons and almost a 15‐fold increase in the number of infected motoneurons compared with the control, nondemyelinated side. Focal demyelination reduced the myelin sheath barrier, allowing greater virus–axon contact. Increased CXADR expression on the demyelinated axons facilitated axoplasmic viral entry. No animals sustained any prolonged neurological deficits. Increased gene delivery into DRG neurons and motoneurons may provide effective treatment for amyotrophic lateral sclerosis, pain, and spinal cord injury. © 2010 Wiley‐Liss, Inc.     

Long-term consequences of impaired regeneration on facial motoneurons in the C57BL/Ola mouse

Peripheral nerves of the C57BL/Ola mouse mutant undergo markedly slowed Wallerian degeneration following injury. This is associated with impaired regeneration of both sensory and motor axons. Following a crush lesion of the facial nerve, there was no cell loss in facial nuclei of normal (C57BL/6J) adult mice, but 40% cell loss occurred in Ola mice and the survivors increased in size during the period when functional reinnervation was established. These results are interpreted as a result, first, of prolonged deprivation of target-derived trophic factor in the slowly regenerating Ola motoneurons and second, increased peripheral field size of the survivors. Within the regenerated facial nerve, there was marked heterogeneity of myelinated fibre size in Ola mice. Some Ola axons, both proximal and distal to the lesion site, had areas over twice as great as the largest 6J axons when measured 1 year following injury. A population of small diameter fibres, not observed in 6J nerves, persisted distal to the crush site in Ola nerves, and this was associated with an increase in the total number of myelinated axons in the distal nerve: on average, each parent Ola axon retained three persistent daughter axons. The delayed Wallerian degeneration in Ola mice not only impairs immediate axon regrowth, but also results in a breakdown of the normal mechanisms which regulate axon number and size in regenerating nerve.     

HSV-2感染小鼠导致脊髓白质髓鞘脱失的研究

该实验为了解人类Ⅱ型单纯疮疹病毒（HSV－2）所致中枢神经系统（CNS）白质的脱髓鞘机制,将病毒经阴道感染小鼠。在感染前用环磷酸胺腹腔注射抑制小鼠免疫力,在病毒感染后第8天取小鼠脊髓制作样本分别进行光镜和电镜观察。结果显示,在机体免疫力抑制的条件下,病毒引起的髓鞘脱失率高于单独病毒感染所致。认为髓鞘脱失是由于病毒直接作用于少突胶质细胞及与其有关的髓鞘所致,而非自身免疫所引起。在讨论中认为由于免疫力降低,增加了病毒对少突胶质细胞及与其有关的髓鞘的毒性攻击能力,以致脱髓鞘频率增高。本实验的电镜中观察显示了少突细胞线粒体变性及髓鞘水肿变性,此时神经纤维轴索未受损伤。随后纤维断裂、崩解、被吞噬细胞吞噬,其时胞浆中内含有大量的次级溶酶体,其中的变性髓鞘处于不同的消化阶段。     

Brainstem facial-motor pathways from two distinct groups of stapedius motoneurons in the cat

To determine the brainstem origins and axonal routes of stapedius motoneurons, we labeled motoneurons by injecting cat stapedius muscles with horseradish peroxidase. Some injections were made in normal cats and some in cats in which the middle segment of the internal facial genu had been cut. By tracing labeled axons and by comparing the locations of labeled cell bodies in normal and lesioned cats, we divided stapedius motoneurons into two groups: "perifacial" and "accessory." Perifacial stapedius motoneurons have cell bodies located around the motor nucleus of the facial nerve and axons which follow the classical course of facial motor axons through the internal genu of the facial nerve. Accessory stapedius motoneurons have cell bodies near the descending facial motor root and axons which ascend to the rostral tip of the internal facial genu, abruptly reverse direction, and then join the descending facial motor root. The sharply hooked course of axons of accessory stapedius motoneurons is similar to the course of axons from other accessory nuclei of cranial nerves V-VII. Our present results, with those of McCue and Guinan (J. Neurophysiol. 60:1160-1180, '88), demonstrate that cats have two groups of stapedius motoneurons which can be separated anatomically by the locations of their cell bodies or by the courses of their axons, and which, on the average, have different response properties.     

Promyelocytic leukemia nuclear bodies provide a scaffold for human polyomavirus JC replication and are disrupted after development of viral inclusions in progressive multifocal leukoencephalopathy

Progressive multifocal leukoencephalopathy is a fatal demyelinating disorder due to human polyomavirus JC infection in which there are viral inclusions in enlarged nuclei of infected oligodendrocytes. We report that the pathogenesis of this disease is associated with distinct subnuclear structures known as promyelocytic leukemia nuclear bodies (PML-NBs). Postmortem brain tissues from 5 patients with the disease were examined. Affected cells with enlarged nuclei contained distinct dot-like subnuclear PML-NBs that were immunopositive for PML protein and nuclear body protein Sp100. Major and minor viral capsid proteins and proliferating cell nuclear antigen, an essential component for DNA replication, colocalized with PML-NBs. By in situ hybridization, viral genomic DNA showed dot-like nuclear accumulation, and by electron microscopy, virus-like structures clustered in subnuclear domains, indicating that PML-NBs are the site of viral DNA replication and capsid assembly. Molecules involved in the ubiquitin proteosome pathway (i.e. ubiquitin and small ubiquitin-like modifier 1) did not accumulate in the nuclei with viral inclusions, indicating that cell degeneration may not be dependent on this pathway. When viral progeny production was advanced, PML-NBs were disrupted. These data suggest that: 1) PML-NBs allow for efficient viral propagation by providing scaffolds, 2) disruption of PML-NBs is independent of the ubiquitin-proteasome pathway, and 3) this disruption probably heralds oligodendrocyte degeneration and the resulting demyelination.     

Preservation of Facial Nerve Function Repaired by Using Fibrin Glue-Coated Collagen Fleece for a Totally Transected Facial Nerve during Vestibular Schwannoma Surgery

Recently, the increasing rates of facial nerve preservation after vestibular schwannoma (VS) surgery have been achieved. However, the management of a partially or completely damaged facial nerve remains an important issue. The authors report a patient who was had a good recovery after a facial nerve reconstruction using fibrin glue-coated collagen fleece for a totally transected facial nerve during VS surgery. And, we verifed the anatomical preservation and functional outcome of the facial nerve with postoperative diffusion tensor (DT) imaging facial nerve tractography, electroneurography (ENoG) and House-Brackmann (HB) grade. DT imaging tractography at the 3rd postoperative day revealed preservation of facial nerve. And facial nerve degeneration ratio was 94.1% at 7th postoperative day ENoG. At postoperative 3 months and 1 year follow-up examination with DT imaging facial nerve tractography and ENoG, good results for facial nerve function were observed.     

Possible neural basis for age-dependent resistance to neurologic disease from herpes simplex virus

Twenty-week-old mice are known to be resistant to HSV induced neurologic disease, while 5-week-old mice are susceptible. Although age-dependent resistance to disease has been attributed to immunologic maturation, most immunologic development is complete by about 3 weeks of age. We, therefore, postulated that differences in neural spread were involved and we compared the pathogenesis of viral spread in 5-week- and 20-week-old mice. Following footpad infection with 10(5.3) PFU HSV-1, virus was detected in homogenates of sciatic nerve and spinal cord 3-4 days sooner in 5-week-old versus 20-week-old mice. Virus titers in footpad homogenates were 10(5.2) to 10(6.0) in both groups, thus differences in virus replication or immunologic restriction at the initial site of infection could not account for the difference in neural spread. The rate of virus spread to the dorsal root ganglia (DRG) was assessed by ganglia explant/co-cultivation to detect virus presence at various times after footpad infection and by measuring sciatic nerve length. In 5- and 20-week-old mice the rate of virus spread to DRG was 28 mm/day and 4-12 mm/day respectively. We conclude that neural uptake and/or transport of virus may contribute to the difference in susceptibility to neurologic disease.     

Myokymic discharges and enhanced facial nerve reflex responses after recovery from idiopathic facial palsy.

A functional disorder of facial muscle activity commonly occurs in patients after recovery from Bell's palsy with axonal degeneration. The postparalytic facial dysfunction is probably related to the aberrant growing of regenerating axons, although other theories such as ephaptic transmission, spontaneous generation of impulses, and enhancement of motoneuron excitability should also be considered. In this work, we have carried out a comparative electrophysiological study of both sides of the face in 23 patients who had recovered from a unilateral Bell's palsy with axonal degeneration. At rest, spontaneous firing of motor units was observed in muscles of the previously paralyzed side. Direct motor responses to facial nerve stimulation were smaller in the muscles of the previously paralyzed side, but reflex responses obtained in the same muscles by stimulation of either the facial or trigeminal nerve were larger when compared with those of the contralateral side. These data indicate that patients with "postparalytic facial dysfunction" may have an increased background muscle activity, as well as an enhanced recruitment of facial motoneurons to reflex activation in the side of the previous paralysis. These findings are compatible with an enhanced level of motoneuron excitability in the facial nucleus.     

面肌痉挛显微血管减压术中的面神经根解剖变异

目地 探讨小脑脑桥角面神经根解剖变异与原发性面肌痉挛的关系及手术治疗.方法 采用显微血管减压术治疗的1221例面肌痉挛病例中,10例(0.82%)术中探查发现面神经根存在解剖变异,面神经根出脑干区距离听神经根进脑干区均大于10mm.均采用显微血管减压术治疗,其中4例术中采用责任动脉悬吊法.结果 9例患者术后面肌痉挛立即消失,1例患者术后痉挛减轻但未消失,随访5个月时完全消失.所有患者随访2-96个月,平均26.8个月,复发1例,治愈率90%.术后并发症包括:中度面瘫2例,1例随访期间恢复正常,1例轻度恢复;展神经麻痹致复视3例,2例随访期间恢复正常,1例仅随访3个月,有好转;患侧听力丧失1例,随访21个月未恢复.结论 小脑脑桥角面神经出脑干区异位至距离听神经进脑干区大于10mm者罕见,动脉性血管压迫仍然是此类患者原发性面肌痉挛的主要病因,采用显微血管减压术治疗可获良效,但术后发生面瘫、展神经麻痹、听力障碍的概率升高.应用责任动脉悬吊法有利于提高疗效、减少并发症.     

Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination

Apolipoprotein E (apo E) is synthesized and released in greatly increased amounts by peripheral nerve following Wallerian degeneration; it has been suggested that this protein may function in the transport of degenerated myelin lipid. The purpose of this study was to determine if the amount of apo E released by rat peripheral nerve is increased following selective demyelination, in the absence of significant axonopathy. Using an immunoturbidimetric assay, release of apo E from excised sciatic nerve segments was measured during the phases of acute demyelination and remyelination caused by tellurium (Te) toxicity, during segmental demyelination in chronic lead (Pb) poisoning, and during Wallerian degeneration following nerve crush. Morphologic changes were examined in contralateral sciatic nerves by nerve-fiber teasing or by light and electron microscopy of transverse sections. As in previous studies, the amount of apo E released from the nerves was greatly increased following Wallerian degeneration due to nerve crush. In Te neuropathy, increased release of apo E was first detected on the fourth day of Te exposure, corresponding temporally to the acute onset of paralysis and segmental demyelination. Apolipoprotein E release rose steeply to a maximum of ten times the control values by day 9 and then gradually waned during the next five weeks, corresponding to a period of active remyelination and resolution of the neuropathy. In the demyelinating neuropathy of chronic lead poisoning, apo E release was increased four times over control animals after seven weeks of exposure, with less than 10% of teased fibers showing early paranodal demyelination and no evidence of remyelination.(ABSTRACT TRUNCATED AT 250 WORDS)     

The central projections of the trigeminal,facial and anterior lateral line nerves in the carp (Cyprinus carpio L.)

The central projections of the trigeminal, facial and anterior lateral line nerves were studied in the carp (Cyprinus carpio) by the Nauta and Fink-Heimer silver techniques following rhizotomy. Degenerating trigeminal fibers were found projecting on the nucleus of the descending trigeminal root and on the medial funicular nucleus. The former can be subdivided in five portions lying dorsal to the various cranial motor nuclei. The afferent facial fibers could be traced into the facial, glossopharyngeal and vagal lobes, while the anterior lateral line nerve projects on rostral, medial and caudal parts of the medial nucleus and on the eminetia granularis. The anterior lateral line nerve can be divided into a dorsal and a ventral root, each following the same course. The role trigeminal and facial nerves play in proprioception of respiratory muscles is discussed.     

Change in gene expression in facial nerve nuclei and the effect of superoxide dismutase in a rat model of ischemic facial paralysis

Peripheral nerve injury induces changes in gene expressions of a variety of neuroactive substances in cell somata, which may have roles in the adaptive response to the injury, neuronal survival, growth and regeneration. In this study, we designed a rat model of ischemic peripheral facial paralysis with a selective embolization technique, and observed mRNA expression of calcitonin gene-related peptide (CGRP), c-jun, and growth associated protein (GAP)-43 in facial nerve nuclei using in situ hybridization histochemistry. The rats were demonstrated to have a transient facial paralysis consistently, and thus this method was regarded as a model of minor peripheral nerve injury. The mRNA of CGRP, c-jun and GAP-43 showed a distinct pattern of induction and time course of increase after the ischemic nerve injury. The results suggest that the small injury to the peripheral nerve was able to induce changes in mRNA expression in the cell body of motoneurons. We also investigated the protective effect of superoxide dismutase (SOD), which is a free radical-scavenging enzyme involved in cellular antioxidant defenses. The SOD treatment clearly alleviated the behavioral impairment and decreased the CGRP mRNA expression at 3rd day after injury. These data suggest that a free radical generated by the ischemia may be partially responsible for ischemic nerve damage and the change in gene expression in motoneurons.     

Central distribution of afferent and efferent components of the chorda tympani in the cat as revealed by the horseradish peroxidase method

Central distribution of afferent and efferent components of the chorda tympani (CT) in the cat was examined by using the anterograde and retrograde tracing techniques of horseradish peroxidase (HRP). HRP was applied to the CT in the tympanic cavity. HRP-labeled CT fibers were traced to the brain stem along the ventral surface of the vestibular nerve. The afferent CT fibers were divided into ascending and descending components. The rostrally directed ascending fibers ended within and around the dorsomedial portions of the principal sensory trigeminal nucleus. The descending fibers entered the solitary tract to run caudally as far as the levels slightly rostral to the obex, giving terminals to the solitary nucleus. A cluster of HRP-labeled neurons were seen ipsilaterally in the lateral reticular formation medial to the spinal trigeminal nucleus; it was observed from the caudalmost levels of the exiting root of the facial nerve to the caudal levels of the facial nucleus. HRP-labeled axons arising from the HRP-labeled neurons firstly ran dorsomedially and then medially under the genu of the facial nerve to form a small genu at the region medial to the genu of the facial nerve. Subsequently the labeled axons ran laterally and ventrolaterally to join other CT fibers at the dorsomedial aspect of the spinal trigeminal tract.     

大鼠面神经切断和切断修复后面神经核内鞘脂激活蛋白原的变化

BACKGROUND： Studies have demonstrated that damaged facial nerves synthesize prosaposin to promote repair of facial neurons. OBJECTIVE： To observe time-course changes of prosaposin expression in the facial nerve nucleus of Sprague Dawley rats following facial nerve transection and repair. DESIGN, TIME AND SETTING： A randomized control neuropathological animal experiment was performed in Chongqing Medical University between March 2007 and September 2008. MATERIALS： A total of 48 adult, male, Sprague Dawley rats were selected and randomly divided into transection and transection ＋ end-to-end anastomosis groups （n =24）. Rabbit anti-rat prosaposin antibody, instant SABC immunohistochemical kit, and antibody dilution solution were purchased from Wuhan Uscn Science Co., Ltd., China. METHODS： In the transection group, the nerve trunk of the distal retroauricular branch of the left facial nerves was ligated in Sprague Dawley rats, and a 5-mm nerve trunk at the distal end of the ligation site was removed. In the transection ＋ end-to-end anastomosis group, epineurial anastomosis was performed immediately following transection of the left facial nerves. The right facial nerves in the two groups served as the normal control group. MAIN OUTCOME MEASURES： The number of prosaposin-positive neurons, as welt as intensity of immunostaining in facial nerve nucleus, following transection and end-to-end anastomosis were determined by immunohistochemistry at 1, 3, 7, 14, 21, and 35 days after injury. RESULTS： Transection group： transection of facial nerves resulted in increased number of prosaposin-positive neurons and immunoreactivity intensity in the facial nucleus on day 1. These values significantly increased by day 3. Expression was greater than in the control side. The peak of the reduction was reached at 7 days post-surgery. Transection ＋ end-to-end anastomosis group： the number of prosaposin-positive neurons and immunoreactivity intensity was reduced in the facial nerve nucleus following immediate end-to-end anastomosis on day 7 post-surgery. These values began to gradually increase by day 14 post-anastomosis. By day 35 post-anastomosis, the number of prosaposin-positive neurons in the operated side recovered to normal levels. The number of prosaposin-positive neurons, as well as immunoreactivity intensity, was significantly greater in the facial nerve nucleus, compared with the transection group on days 14, 21, and 35 post-surgery （P 〈 0.05）. The rhythmic whisking of vibrissa recovered, and recovery time was consistent with increased numbers of prosaposin-positive neurons. CONCLUSION： Within 7 days after injury, prosaposin expression in the facial nerve nucleus exhibited an initial increase, followed by a decrease, and was not affected by facial nerve repair. Following facial nerve damage, neural anastomosis was shown to increase prosaposin expression in the facial nerve nucleus after 14 days. Recovery of prosaposin occurred simultaneously with reinnervation.