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At least 145 records · Page 8Linked to original sources
PubMed2000

Peripheral nerve regeneration across an 80-mm gap bridged by a polyglycolic acid (PGA)-collagen tube filled with laminin-coated collagen fibers: a histological and electrophysiological evaluation of regenerated nerves.

We evaluated peripheral nerve regeneration across an 80-mm gap using a novel artificial nerve conduit. The conduit was made of a polyglycolic acid (PGA)-collagen tube filled with laminin-coated collagen fibers. Twelve beagle dogs underwent implantation of the nerve conduit across an 80-mm gap in the left peroneal nerve. In four other dogs used as negative controls, the nerve was resected and left unconnected. Histological observation showed that numerous unmyelinated and myelinated nerve fibers, all smaller in diameter and with a thinner myelin sheath than normal nerve fibers, regrew through and beyond the gap 12 months after implantation. The distribution of the regenerated axonal diameters was different from that of the normal axonal diameters. Compound muscle action potentials, motor evoked potentials, and somatosensory evoked potentials were recorded in most animals 3 months after implantation. Peak amplitudes and latencies recovered gradually, which indicating the functional establishment of the nerve connection with the target organs. In addition to the ordinary electrophysiological recoveries, potentials with distinct latencies originating from Aalpha, Adelta and C fibers became distinguishable at the 6th lumbar vertebra following stimulation of the peroneal nerve distal to the gap 12 months after implantation. The pattern of walking without load was restored to almost normal 10-12 months after implantation. Neither electrophysiological nor histological restoration was obtained in the controls. Our nerve conduit can guide peripheral nerve elongation and lead to favorable functional recovery across a wider nerve gap than previously reported artificial nerve conduits.

Animals↗
PubMed2004

Pathologic classification of peripheral nerve tumors.

Peripheral nerve tumors show an interesting histologic variety despite being composed ofa limited array of cellular constituents. As we learn more about the interplay between the Schwann cells, perineurial cells, and ganglion cells that comprise these tumors, it is likely that we will better understand the biologic behavior of these important tumors. Key issues for the pathologist include distinguishing schwannomas from neurofibromas, ganglioneuromas from neurofibromas involving ganglia, and MPNSTs from cellular schwannomas or neurofibromas. The association of each of these tumors with genetic tumor disorders provides a unique window into discovering basic mechanisms of cell regulation and tumorigenesis that may ultimately shed light on the biology of a much wider array of human disease.

Ganglioneuroma↗
PubMed1999

Altered molecular architecture of peripheral nerves in mice lacking the peripheral myelin protein 22 or connexin32.

Peripheral nerves of mutant mice deficient for peripheral myelin protein 22 (PMP22) or connexin32 (Cx32) display similar pathologies as observed in hereditary human peripheral neuropathies. Mice lacking PMP22 develop focal hypermyelination followed by myelin degeneration and axonal atrophy. Cx32-deficient mice form normal myelin initially but develop demyelination and remyelination at older ages. We have examined the lack of PMP22 or Cx32 on the distribution of other components of the myelin sheath including myelin basic protein (MBP), E-cadherin, and myelin-associated glycoprotein (MAG), as well as the delayed rectifying potassium channel Kv1.1 as an intrinsic membrane protein of axons. In peripheral nerves of wild-type mice, Kv1.1 is present as a pair of juxtaparanodal clusters and a focal line extending longitudinally into the internode, branching parallel and adjacent to Schmidt-Lanterman incisures. Myelinated peripheral nerve fibers of 3-week-old PMP22(0/0) mice show tomacula and abnormally short internodes of variable lengths with minor effects on the localization of E-cadherin and Kv1.1. In older PMP22(0/0) mice, hypomyelinated fibers contain supernumerary Schwann cells and loose focally restricted E-cadherin and Kv1.1 expression. In contrast, remyelinated fibers in adult Cx32(0/0) mice exhibit a correct localization of these marker proteins, except that juxtaparanodal Kv1.1 clusters are aligned in abnormally short intervals of regular distances accompanied by an increased number of Schwann cells. Thus, different degrees of demyelination and remyelination in demyelinating mouse models have variable effects on the confinement of specific proteins to structural and functional internodal domains.

Animals↗
PubMed2005

The claw paw mutation reveals a role for Lgi4 in peripheral nerve development.

Peripheral nerve development results from multiple cellular interactions between axons, Schwann cells and the surrounding mesenchymal tissue. The delayed axonal sorting and hypomyelination throughout the peripheral nervous system of claw paw (clp) mutant mice suggest that the clp gene product is critical for these interactions. Here we identify the clp mutation as a 225-bp insertion in the Lgi4 gene. Lgi4 encodes a secreted and glycosylated leucine-rich repeat protein and is expressed in Schwann cells. The clp mutation affects Lgi4 mRNA splicing, resulting in a mutant protein that is retained in the cell. Additionally, siRNA-mediated downregulation of Lgi4 in wild-type neuron-Schwann cell cocultures inhibits myelination, whereas exogenous Lgi4 restores myelination in clp/clp cultures. Thus, the abnormalities observed in clp mice are attributable to the loss of Lgi4 function, and they identify Lgi4 as a new component of Schwann cell signaling pathway(s) that controls axon segregation and myelin formation.

Amino Acid Sequence↗
PubMed2006

Tumors of the peripheral nerves and plexuses.

Peripheral nerve tumors are a diverse group of lesions histologically and in their clinical behavior. The genetic disorders neurofibromatosis type 1 and 2 and schwannomatosis are significant risk factors for the development of peripheral nerve tumors. An understanding of these disorders is important in allowing appropriate management. Active treatment of peripheral nerve tumors is reserved for lesions that are malignant or causing neurologic dysfunction, pain, compressive symptomatology, or cosmetic concern. The mainstay of treatment is surgical intervention, the nature of which will vary with the type of tumor and anatomical location. In the case of malignant tumors, adjuvant chemotherapy and radiotherapy are commonly used. Developments in the understanding of the genetics and molecular biology of peripheral nerve tumors are opening up potentially exciting new avenues of treatment. The prognosis of benign peripheral nerve tumors is excellent, with a recurrence rate of just 5% or less after successful surgery. Malignant tumors have proven to be more challenging, with a much higher recurrence rate and a 5-year survival rate of 64%.

Journal Article↗
PubMed1990

Facilitated transport of L-phenylalanine across blood-nerve barrier of rat peripheral nerve.

L-Phenylalanine transport across the blood-nerve barrier was studied by perfusing Ringer solution containing trace amounts of L-[14C]phenylalanine and [3H]dextran (a vascular marker) through the hindlimb of an anesthetized rat. At the end of perfusion, a segment of sciatic nerve was removed, frozen, desheathed, and processed for radioactivity counting. The permeability-surface area product of the blood-nerve barrier (PABNB) to L-[14C]phenylalanine decreased from 58 +/- 9 X 10(-5) to 1.7 +/- 0.3 X 10(-5) (SE) ml.s-1.g wet wt-1, as the perfusate concentration of unlabeled L-phenylalanine was increased to 10 mM. D-Phenylalanine had less of an inhibitory effect on L-[14C]phenylalanine uptake than did L-phenylalanine. PABNB did not change in the presence of 50 mM alpha-(methylamino)isobutyric acid (MeAIB) in the perfusion medium, nor by replacing NaCl by Tris.HCl. However, addition of 50 mM 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid (BCH) reduced PABNB to 2.1 +/- 0.3 X 10(-5) ml.s-1.g wet wt-1 (n = 4). PA at epiperineurial barrier (PAper) of L-[14C]phenylalanine at the epiperineurial barrier, determined from in situ incubation, was 1.4 +/- 0.2 X 10(-5) ml.s-1.g wet wt-1 (n = 6) and was unaffected by 10 mM L-phenylalanine concentration in the incubation medium. The results demonstrate for the first time carrier-mediated transport system for L-phenylalanine at the blood-nerve barrier of the rat peripheral nerve.

Amino Acids↗
PubMed1997

Expression of fibroblast growth factor-2 and fibroblast growth factor receptor 1 messenger RNAs in spinal ganglia and sciatic nerve: regulation after peripheral nerve lesion.

In order to determine functional roles of basic fibroblast growth factor (FGF-2) in the peripheral nervous system we have analysed the expression of FGF-2 and FGF receptor 1 (FGFR1) in spinal ganglia and the sciatic nerve under normal conditions and after nerve crush using RNAse protection assay and in situ hybridization. In intact spinal ganglia, both FGF-2 and FGFR1 messenger RNAs are expressed, albeit at different levels. In situ hybridization identifies satellite cells as the source of FGF-2 and sensory neurons as the source of FGFR1 suggesting a paracrine mode of action of FGF-2 on sensory neurons. One day after crush lesion FGF-2 is significantly up-regulated in sensory ganglia L4-L6. Highest levels are found at day 7; control levels are approached after 28 days. FGFR1 messenger RNA, which is strongly expressed in intact spinal ganglia, displays no significant change after lesion. In the intact sciatic nerve, FGFR1 messenger RNA is detected at higher levels than FGF-2 messenger RNA. After injury, both transcripts display a time-dependent up-regulation in both the proximal and distal nerve stump. Schwann cells, as a putative source of the sciatic nerve-derived FGF-2, express both FGF-2 and FGFR1 messenger RNAs in vitro. The FGFR1 transcript level is increased in the presence of forskolin. FGF-2 does not affect expression of FGFR1 messenger RNA but stimulates its own expression. These results show that during peripheral nerve regeneration FGF-2 is up-regulated in both the crushed nerve and the respective spinal ganglia suggesting a possible physiological function of FGF-2 during the regeneration process.

Animals↗
PubMed2006

An objective assessment of nerve stimulators used for peripheral nerve blockade*.

Nerve stimulation is considered by many to be the current 'gold standard' for locating peripheral nerves. Thirteen nerve stimulators were subjected to a battery of tests performed by two independent observers under standardised conditions using a digital oscilloscope, a calibrated resistance and a novel scoring system. Individual scores were assigned for the signal waveform, current intensity, impulse duration, maximum load output and functionality of each nerve stimulator; the maximum score achievable was 20. A score of > or = 15/20 was achieved by six nerve stimulators: Stimuplex HNS 12 (B Braun); MultiStim Vario (Pajunk); Plexival (Medival, Vygon); MultiStim Sensor (Pajunk); Plexygon (Aryon, Vygon); Stimuplex HNS 11 (B Braun). Seven nerve stimulators scored < 15/20. Anaesthetists should be aware of the limitations of the nerve stimulator being used. Standardisation of features is desirable when manufacturing nerve stimulators.

Electric Stimulation↗
PubMed1999

Effects of Systemically Applied IGF-1 on Motor Nerve Recovery After Peripheral Nerve Transection and Repair in the Rat - A Functional Study.

The trophic effects of systemically applied Rh insulin-like growth factor-1 (rhIGF-1) on peripheral motor nerve regeneration following transection and epineural repair in rats median nerve have been examined. RhIGF-1 (0.5 mg/kg/rat) was administered subcutaneously to the neck region of the repaired side for 14 days post-operation. Motor recovery was tested with the grasping test that is an objective quantitative behavioural assessment of regeneration of the rats median nerve. Muscle twitch tension and muscle weight were measured in the flexor digitorum sublimus muscle. No significant differences between experimental and control animals regarding onset of muscle function, recovery of muscle power, and muscle weight were found. These results demonstrate that subcutaneously applied rhIGF-1 cannot improve functional motor recovery after nerve transection and repair in the rat as has been demonstrated after nerve crushing injury. This is regarded as a consequence of specificity failure during reinnervation, which occurs after nerve transection and repair, whereas after crushing injury specific reinnervation is a common feature.

Journal Article↗
PubMed2005

Differential pharmacological modulation of the spontaneous stimulus-independent activity in the rat spinal cord following peripheral nerve injury.

Peripheral nerve injury is a significant clinical problem that is often difficult to treat. The major clinical symptoms are numbness, tactile and cooling allodynia, hyperalgesias as well as ongoing pain. In animal models of neuropathy, abnormal responses to applied (or evoked) stimuli can be gauged, but spontaneous pain, a major clinical issue, has proved very difficult to assess. In neuropathic animals, spinal neuronal hyperexcitability indicative of peripheral and central changes with high levels of spontaneous neuronal firing has been reported. This latter stimulus-independent firing of sensory neurones may be a measure related to ongoing pain. Two weeks after L5/6 spinal nerve ligation, deep dorsal horn neurones were recorded in halothane-anesthetized rats. The majority of neurones in neuropathic rats showed increased levels of spontaneous firing with irregular firing patterns. We examined and compared the effects of 5 centrally acting pharmacological agents: morphine (i.t. or i.v.), gabapentin, ketamine, memantine and mepyramine on stimulus-independent neuronal firing. This ongoing activity showed high sensitivity to gabapentin (s.c.) and morphine (i.t.) administration, being significantly reduced in a dose-dependent manner. Morphine administered via the systemic route produced modest but non-significant reductions of spontaneous activity. The two NMDA receptor antagonists, ketamine and memantine, and the histamine H1 receptor antagonist, mepyramine, produced minor effects at doses known to be effective on stimulus evoked measures of deep dorsal horn neurones. This may form an electrophysiological basis for the efficacy of gabapentin and spinal morphine on ongoing pain in patients with peripheral neuropathy.

Action Potentials↗
PubMed1960

Electron microscope and x-ray diffraction studies of the effects of dehydrations on the structure of nerve myelin. I. Peripheral nerve.

The dehydration of frog sciatic nerve has been studied by allowing specimens to become partially or fully dried before fixation and preparation for electron microscopy. Low magnification electron micrographs of OsO(4)-fixed preparations showed marked tissue shrinkage which could be correlated quantitatively with the loss of water during the preliminary drying. KMnO(4)-fixation appeared to cause a rehydration of the dried tissue. Higher magnification electron micrographs of the OsO(4)-fixed preparations showed a sequence of modifications of the myelin layers which could be correlated with changes in the small-angle x-ray diffraction data which were recorded during drying. An intermediate stage of drying was characterised by a partial collapse of layers and a disappearance of the intraperiod dense line in some regions of the myelin sheath. Continuity between collapsed and non-collapsed layers was maintained throughout the sheath. The fully dried preparation showed two main modifications of the myelin layers. In many regions the layers (principal layers) resembled those of normal preparations, but showed an intensification and frequently a doubling of the intraperiod dense line. In addition, there was a very extensive system of fine (40 A periodicity) dense layers, some of which could be demonstrated to be continuous with the principal layers. In such cases it was observed that two of the fine layers were related to each principal layer. The correlation between diffraction data and electron microscope data is discussed, and some speculations are made concerning the molecular significance of the observations.

Animals↗
PubMed1996

Light induced EEG desynchronization and behavioral arousal in rats with restored retinocollicular projection by peripheral nerve graft.

Peripheral nerve (PN) was grafted to sectioned optic nerve and was bridged to the superior colliculus in adult rats. To test functional recovery of restored retinocollicular pathway, we examined cortical electroencephalogram (EEG) and behavioral arousal responses to light stimuli. In eight of 10 recording trials in PN grafted rats (n = 6) and in all of eight trials in normal rats (n = 5), cortical EEGs showed desynchronization to light stimuli. On the other hand, after bilateral sections of the optic nerve (n = 3) EEG desynchronization to light disappeared while it was induced by a white noise. Mean threshold duration of light for EEG desynchronization was significantly longer in the PN grafted rats (440 ms) than in normal rats (173 ms). In three of six trials in PN grafted rats (n = 4), and in four of eight trials in normal rats (n = 4), EEG desynchronization elicited by light stimulus was accompanied by behavioral arousal responses, whereas no behavioral arousal could be induced by light in blind rats (n = 3). These results strongly suggest that visual information processed through the restored retinocollicular pathway was further transmitted to the cerebral cortices and ultimately resulted in behavioral arousal of the PN grafted rats.

Animals↗
PubMed2004

Investigating mechanical behaviour at a core-sheath interface in peripheral nerve.

As peripheral nerves bend and stretch, internal elements need to move in relation to each other. However, the way in which intraneural components interact is poorly understood. Previous work identified a distinct core and sheath in the rat sciatic nerve and provides a useful model with which to investigate this interaction. Here we have focused on identifying the mechanical and anatomical characteristics of the interface between core and sheath. Nerve samples, 15 and 20 mm long, of rat sciatic nerves were harvested and placed in a purpose-built jig, and a tensile testing machine was used to pull core from sheath. Mechanical tests of specimens in which core had been previously pulled from sheath by 25% of its initial length achieved a mean pull-out force approximately six times smaller than that achieved using intact controls. These results are consistent with the proposal that core-sheath interactions involve physical connections rather than a viscous fluid interface. Anatomical features of this interface were characterised using transmission electron microscopy. It appeared that sheath was derived from epineurium and most of the perineurium, whilst core consisted of endoneurium and a small proportion of the perineurium: the plane of cleavage appeared to involve the innermost perineurial cell layer.

Animals↗