n-Hexane and benezene are organic compounds which have been widely used as industrial solvents. However, they are also increasingly recognized as important pollutants in working environment. The purpose of this study is to analyze neurotoxicity of benzene and n-Hexane. In this study, tibial nerve of Sprague-Dawley rats were observed after exposing them to two different concentrations of these compounds (6000 ppm of n-Hexane and 2000 ppm of benezene) which were known to be the levels to cause subacute toxicity for the three different periods; two weeks, four weeks, and sex weeks. The following results were obtained from the analysis of variance, Duncan's multiple comparison test, and regression analysis: 1) Myelin sheath thickness of nerve fiber for two n-Hexane exposed groups (four weeks and six weeks) were both reduced compared with the control group and the benezene exposed group. 2) There were positive relationships between nerve fiber diameter and myelin sheath thickness for both exposed and control groups. 3) There were significant difference in myelin sheath thickness from equal diameter nerve fibers between benzene exposed group and control group, but the greater number of thin myelin sheath were observed for n-Hexane exposed group compared with control group. Thus, it is concluded that n-Hexane tends to reduce the rate of growth of nerve fiber more than the benzene and control group. While these results shed light on understanding the effects of benzene and n-Hexane, the duration of exposure was not long enough to apply these results to real working environments. In addition, to further understand the mechanism of nerve degeneration caused by organic solvents, both epidemiological and biochemical studies should accompanied by this kind of study.
Animals ; Benzene* ; Myelin Sheath ; Nerve Degeneration ; Nerve Fibers ; Rats* ; Rats, Sprague-Dawley ; Solvents ; Tibial Nerve*

PURPOSE: Wallerian degeneration (WD) is an antegrade degenerative process distal to peripheral nerve injury. Numerous genes are differentially regulated in response to the process. However, the underlying mechanism is unclear, especially the early response. We aimed at investigating the effects of sciatic nerve injury on WD via CLDN 14/15 interactions in vivo and in vitro. METHODS: Using the methods of molecular biology and bioinformatics analysis, we investigated the molecular mechanism by which claudin 14/15 participate in WD. Our previous study showed that claudins 14 and 15 trigger the early signal flow and pathway in damaged sciatic nerves. Here, we report the effects of the interaction between claudin 14 and claudin 15 on nerve degeneration and regeneration during early WD. RESULTS: It was found that claudin 14/15 were upregulated in the sciatic nerve in WD. Claudin 14/15 promoted Schwann cell proliferation, migration and anti-apoptosis in vitro. PKCα, NT3, NF2, and bFGF were significantly upregulated in transfected Schwann cells. Moreover, the expression levels of the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK signaling pathways were also significantly altered. CONCLUSION Claudin 14/15 affect Schwann cell proliferation, migration, and anti-apoptosis via the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK pathways in vitro and in vivo. The results of this study may help elucidate the molecular mechanisms of the tight junction signaling pathway underlying peripheral nerve degeneration.
Animals ; Claudins ; Nerve Regeneration ; Peripheral Nerve Injuries ; Rats ; Schwann Cells/pathology* ; Sciatic Nerve ; Wallerian Degeneration/pathology*

A growing body of evidence suggests that glial cells play an important role in neural development, neural survival, nerve repair and regeneration, synaptic transmission and immune inflammation. As the highest number of cells in the central nervous system, the role of glial cells in Parkinson's disease (PD) has attracted more and more attention. It has been confirmed that nigral iron accumulation contributes to the death of dopamine (DA) neurons in PD. Until now, most researches on nigral iron deposition in PD are focusing on DA neurons, but in fact glial cells in the central nervous system also play an important role in the regulation of iron homeostasis. Therefore, this review describes the role of iron metabolism of glial cells in death of DA neurons in PD, which could provide evidence to reveal the mechanisms underlying nigral iron accumulation of DA neurons in PD and provide the basis for discovering new potential therapeutic targets for PD.
Dopaminergic Neurons ; Humans ; Iron ; Nerve Degeneration ; Neuroglia ; Parkinson Disease

This study was performed to investigate the changes of nerve after the injection of alcohol and glycerol at the infraorbital nerve in rats. Using the eighteen Sprague-Dawley rats, weighing 200-250g, 99% alcohol, pure glycerol, and sterile saline was injected to the epineurium of the infraorbital nerve. Glycerol injected rats were devided into 0.01ml, 0.03ml and 0.05ml groups. The alcohol and control group were injected 0.03ml at the left infraorbital nerve. The following results were obtained by histopathological examination after 1 week, 1 month, and 3 months. A few inflammatory cell infiltration and no signs of nerve degeneration were noted in control group. Total nerve degeneration was noted in the alcohol group and no regeneration was noted in 1month, and partial regeneration was noted at 3month. The nerve degeneration was noted at the periphery of nerve bundle in 0.01ml glycerol injection group. Total degeneration was noted in the 0.03ml and 0.05ml glycerol injection group and the degree was propotional to dose. These results suggest that injection of alcohol and glycerol are effective to nerve blockage by nerve degeneration, and nerve degeneration by glycerol injection is propotional to dose and nerve regeneration by glycerol injection is inversely propotional to dose.
Animals ; Glycerol* ; Nerve Degeneration ; Nerve Regeneration ; Peripheral Nerves ; Rats* ; Rats, Sprague-Dawley ; Regeneration

OBJECTIVE: To understand the neural generator of double-peak potentials and the change of latency and amplitude of double peaks with aging. METHOD: In 50 healthy subjects made up of groups of 10 people per decade from the age of 20 to 60, orthodromic sensory nerve conduction studies were performed on the median nerves using submaximal stimulation. Various stimulus durations and interstimulation distances were used to obtain each double peak in the different age groups. The latency and amplitude of the second peak were measured. Statistical analyses included one-way ANOVA and correlation tests. p-values<0.05 were considered significant. RESULTS: When the cathode moved in a proximal direction, the interpeak intervals increased. Second peak amplitudes decreased, and second peak latencies were delayed with aging (p<0.05). In some older people, second peaks were not obtained. CONCLUSION: Our experiments indicate that the double-peak response represented the two stimulation sites under the cathode and anode. The delayed latency and decreased amplitude of the second peak that occurs with aging represented peripheral nerve degeneration in aging, which starts at the distal nerve.
Aging ; Electrodes ; Humans ; Median Nerve ; Nerve Degeneration ; Neural Conduction ; Peripheral Nerves

The purposes of this study were therefore to characterize the degeneration and regeneration of nerves to the calf muscles after selective neurectomy, both macroscopically and microscopically, and to determine the incidence of such regeneration in a rabbit model. Seventy four New Zealand white rabbits were used. Selective neurectomy to the triceps surae muscles was performed, and the muscles were subsequently harvested and weighed 1-4 months postneurectomy. The gastrocnemius muscles were stained with Sihler's solution to enable the macroscopic observation of any nerve regeneration that may have occurred subsequent to neurectomy. The change in triceps surae muscle weight was measured along the time course of the experiment. After neurectomy, nerve degeneration was followed by regeneration in all cases. The weight of the triceps surae muscle decreased dramatically between completion of the neurectomy and 1 month postneurectomy, but increased thereafter. The nerve branches were weakly stained with Sihler's solution until 2 months postneurectomy, and then strongly stained after 3 months. The number of myelinated axons was decreased at 2 month after neurectomy compared to nonneurectomized controls, but then gradually increased thereafter. Although there are currently no reports on the incidence of recovery after calf reduction, it may be a very common occurrence in the clinical field based on our findings. The findings of this study provide fundamental anatomical and surgical information to aid planning and practice in calf-reduction surgery.
Axons ; Incidence ; Muscle, Skeletal ; Muscles ; Myelin Sheath ; Nerve Degeneration ; Nerve Regeneration* ; Rabbits ; Regeneration

OBJECTIVES: The retinal nerve fiber layer (RNFL) is a site of glaucomatous optic neuropathy whose early changes need to be detected because glaucoma is one of the most common causes of blindness. This paper proposes an automated RNFL detection method based on the texture feature by forming a co-occurrence matrix and a backpropagation neural network as the classifier. METHODS: We propose two texture features, namely, correlation and autocorrelation based on a co-occurrence matrix. Those features are selected by using a correlation feature selection method. Then the backpropagation neural network is applied as the classifier to implement RNFL detection in a retinal fundus image. RESULTS: We used 40 retinal fundus images as testing data and 160 sub-images (80 showing a normal RNFL and 80 showing RNFL loss) as training data to evaluate the performance of our proposed method. Overall, this work achieved an accuracy of 94.52%. CONCLUSIONS: Our results demonstrated that the proposed method achieved a high accuracy, which indicates good performance.
Blindness ; Glaucoma* ; Methods ; Nerve Fibers* ; Optic Nerve Diseases ; Retinal Degeneration ; Retinaldehyde*

A nerve block is an effective tool for diagnostic and therapeutic methods. If a diagnostic nerve block is successful for pain relief and the subsequent therapeutic nerve block is effective for only a limited duration, the next step that should be considered is a nerve ablation or modulation. The nerve ablation causes iatrogenic neural degeneration aiming only for sensory or sympathetic denervation without motor deficits. Nerve ablation produces the interruption of axonal continuity, degeneration of nerve fibers distal to the lesion (Wallerian degeneration), and the eventual death of axotomized neurons. The nerve ablation methods currently available for resection/removal of innervation are performed by either chemical or thermal ablation. Meanwhile, the nerve modulation method for interruption of innervation is performed using an electromagnetic field of pulsed radiofrequency. According to Sunderland's classification, it is first and foremost suggested that current neural ablations produce third degree peripheral nerve injury (PNI) to the myelin, axon, and endoneurium without any disruption of the fascicular arrangement, perineurium, and epineurium. The merit of Sunderland's third degree PNI is to produce a reversible injury. However, its shortcoming is the recurrence of pain and the necessity of repeated ablative procedures. The molecular mechanisms related to axonal regeneration after injury include cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules, and their receptors. It is essential to establish a safe, long-standing denervation method without any complications in future practices based on the mechanisms of nerve degeneration as well as following regeneration.
Axons ; Classification ; Denervation ; Electromagnetic Fields ; Extracellular Matrix ; Myelin Sheath ; Nerve Block ; Nerve Degeneration ; Nerve Fibers ; Nerve Growth Factors ; Nerve Regeneration ; Neuroglia ; Neurons ; Peripheral Nerve Injuries ; Peripheral Nerves ; Pulsed Radiofrequency Treatment ; Recurrence ; Regeneration* ; Sympathectomy ; Wallerian Degeneration

The human nervus terminalis (terminal nerve) and the nerves to the vomeronasal organ (VNON) are both associated with the olfactory nerves and are of major interest to embryologists. However, there is still limited knowledge on their topographical anatomy in the nasal septum and on the number and distribution of ganglion cells along and near the cribriform plate of the ethmoid bone. We observed serial or semiserial sections of 30 fetuses at 7–18 weeks (crown rump length [CRL], 25–160 mm). Calretinin and S100 protein staining demonstrated not only the terminal nerve along the anterior edge of the perpendicular lamina of the ethmoid, but also the VNON along the posterior edge of the lamina. The terminal nerve was composed of 1–2 nerve bundles that passed through the anterior end of the cribriform plate, whereas the VNON consisted of 2–3 bundles behind the olfactory nerves. The terminal nerve ran along and crossed the posterior side of the nasal branch of the anterior ethmoidal nerve. Multiple clusters of small ganglion cells were found on the lateral surfaces of the ethmoid's crista galli, which are likely the origin of both the terminal nerve and VNON. The ganglions along the crista galli were ball-like and 15–20 µm in diameter and, ranged from 40–153 in unilateral number according to our counting at 21-µm-interval except for one specimen (480 neurons; CRL, 137 mm). An effect of nerve degeneration with increasing age seemed to be masked by a remarkable individual difference.
Calbindin 2 ; Ethmoid Bone ; Fetus ; Ganglion Cysts ; Humans ; Individuality ; Masks ; Nasal Septum ; Nerve Degeneration ; Neurons ; Olfactory Nerve ; Vomeronasal Organ

In this study, the effects of Radio Electric Asymmetric Conveyer (REAC), a non-invasive physical treatment, on neuroinflammatory responses in a mouse model of parkinsonism induced by intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), were investigated in vivo. We found that the REAC tissue optimization treatment specific for neuro-regenerative purposes (REAC TO-RGN-N) attenuated the inflammatory picture evoked by MPTP-induced nigro-striatal damage in mice, decreasing the levels of pro-inflammatory molecules and increasing anti-inflammatory mediators. Besides, there was a significant reduction of both astrocyte and microglial activation in MPTP-treated mice exposed to REAC TO-RGN-N. These results indicated that REAC TO-RGN-N treatment modulates the pro-inflammatory responses and reduces neuronal damage in MPTP-induced parkinsonism.
Animals ; Corpus Striatum ; pathology ; Electric Stimulation ; methods ; Inflammation ; pathology ; Male ; Mice ; Nerve Degeneration ; pathology ; Nerve Regeneration ; physiology ; Parkinsonian Disorders ; pathology