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PubMed2004

Enhancement of stimulation-induced ERK activation in the spinal dorsal horn and gracile nucleus neurons in rats with peripheral nerve injury.

It has been suggested that low-threshold sensory pathways have an important role in the formation and maintenance of sensory abnormalities which are observed after peripheral nerve injury. In the present study, we examined the involvement of these pathways in the development of hyperexcitability after sciatic nerve injury (SNI) by detecting the intracellular signal molecule. The rats that received a transection of the sciatic nerve 7 days before were electrically stimulated at 0.1 mA and 3 mA in the proximal region of the nerve injury site. We found a small number of phosphorylated extracellular signal-regulated kinase (pERK)-labelled neurons in laminae I-II and III-IV of the spinal dorsal horn in the control rats after 0.1 mA stimulation. By contrast, there was a marked increased of pERK-labelled neurons both in the superficial laminae and laminae III-IV after the same stimulation in the SNI rats. Enhancement of ERK activation induced by 3 mA stimulation was also observed. Immunoreactivity of pERK in gracile nucleus neurons was also dramatically increased after 0.1 mA stimulation to the injured nerve. These data suggest that the rats with peripheral nerve injury had an increased responsiveness to the low- or high-threshold peripheral stimuli in I-II, III-IV and gracile nucleus neurons. Furthermore, SNI rats that received neonatal capsaicin treatment showed a decreased number of pERK neurons after 0.1 mA stimulation in the dorsal horn and gracile nucleus neurons compared to the control rats. Thus, C-fibres may contribute to the enhanced excitability of the low-threshold sensory neurons after peripheral nerve injury.

Animals↗
PubMed1977

[Surgery of therapy-resistant pain due to peripheral nerve injury].

1. The forms of peripherally triggered or localized pains are differentiated: Local pain of a neuromatous character, propagated pain, sympathalgia, phantom pain, causalgia, and combined forms. 2. Surgical operations are performed locally, to the spinal cord, brain, and sympathicus, as well as by neurostimulation on all levels. 3. The areas of indication differ according to the localization of pain and its probable cause. 4. Serving the prevention of pain after peripheral nerve injuries are the particular topical treatment of a fresh injury, psychic guidance, specific aftercare and physiotherapy, elimination of pension payment problems, and optimum reintegration into normal working life]

Cordotomy↗
PubMed1996

The epidemiology and management of upper limb peripheral nerve injuries in modern practice.

This paper reports an epidemiological and clinical study of 813 patients with 1,111 peripheral nerve injuries who were treated for upper limb trauma, which included nerve injury, at two plastic surgery units in south-east England, predominantly between the years 1982 and 1991. The frequency distributions of the levels of nerve injury, and the causes of nerve injury in the sample, are presented, together with the surgical management and timing of nerve repair in these patients. 1,018 clinically suspected nerve injuries in 730 patients (91.6% of nerves, 89.8% of patients) were treated by primary nerve repair, elective delayed nerve repair or primary surgical exploration alone. Divisions of 93 nerves in 83 patients (8.3% of nerves, 10.2% of patients) were treated other than by primary repair or elective delayed repair, due to delayed referral from accident and emergency departments, resulting from missed or uncertain diagnosis at presentation or otherwise unaccounted delay in the initial referral.

Adolescent↗
PubMed1993

A quantitative analysis of the microglial cell reaction in central primary sensory projection territories following peripheral nerve injury in the adult rat.

The time course of the microglial cell reaction in central nervous system primary sensory projection territories has been examined following peripheral nerve injury in the adult rat using qualitative and quantitative analysis of immunoreactivity with the monoclonal antibody OX-42, which recognises the complement receptor CR3. The regions examined included the gracile nucleus, the column of Clarke and the spinal cord dorsal horn (superficial and deep laminae separately) after unilateral sciatic nerve transection, and the spinal trigeminal nucleus following unilateral infraorbital nerve transection. In all territories examined a qualitative increase in OX-42 immunoreactivity was observed 24 h postlesion. Further, quantitative analysis revealed an exponential development of the OX-42 immunoreactivity, with a peak at one week postlesion, thereafter showing a slow exponential decline. Our results show that the signal (or signals) that induces the microglial cell response in primary sensory projection territories is rapid in comparison to previously described central degenerative changes following peripheral nerve lesions (transganglionic degeneration). These findings are compatible with the hypothesis that activated microglia play a pathogenetic role in the development of transganglionic degeneration.

Afferent Pathways↗
PubMed2003

The pattern of norepinephrine release in the hypothalamic paraventricular nucleus in response to repeated peripheral nerve injury differs in the acute and chronic stage in conscious rats.

We investigated the change in norepinephrine (NE) release in the hypothalamic paraventricular nucleus (PVN) in response to ligature of the median and ulnar nerves using a brain microdialysis technique in conscious rats. Primary ligature was performed of the right median and ulnar nerves, and then repeated injury was performed on the left nerves 6 h or 3 weeks after the primary ligature. Primary ligature of the nerves produced a significant increase that peaked at a mean 330% above basal NE release in the first 20 min. The NE release after reinjury 6 h later was significantly higher (a peak of 650%) than after primary nerve injury, although that at 3 weeks was significantly lower (a peak of 280%). The present study demonstrated that peripheral nerve injury induces an elevated response of the PVN, which is an integral center of the autonomic nervous system. NE release after reinjury differed in the acute and chronic stages.

Acute Disease↗
PubMed2002

Dynamic pattern of reg-2 expression in rat sensory neurons after peripheral nerve injury.

The 16 kDa pancreatitis-associated protein Reg-2 has recently been shown to facilitate the regeneration of motor and sensory neurons after peripheral nerve injury in the adult rat. Reg-2 has also been shown to be a neurotrophic factor that is an essential intermediate in the pathways through which CNTF supports the survival of motor neurons during development. Here we report the dynamic expression of Reg-2 in rat sensory neurons after peripheral nerve injury. Reg-2 is normally not expressed by dorsal root ganglion (DRG) cells, but we show, using immunocytochemistry, that Reg-2 is rapidly upregulated in DRG cells after sciatic nerve transection and after 24 hr recovery is expressed almost exclusively in small-diameter neurons that bind the lectin Griffonia simplicifolia IB4 and express the purinoceptor P2X3. However, by 7 d after axotomy, Reg-2 is expressed in medium to large neurons and coexists partly with the neuropeptides galanin and neuropeptide Y, which are also upregulated after peripheral nerve transection. At this time point, Reg-2 is no longer expressed in small neurons, and there is no colocalization with IB4 binding neurons, demonstrating a shift in Reg-2 expression from one subset of DRG neurons to another. We also show by double labeling for activating transcription factor 3, a transcription factor that is upregulated after nerve injury, that Reg-2 expression occurs predominantly in axotomized DRG cells but that a small percentage of uninjured DRG cells also upregulate Reg-2. The selective expression within IB4/P2X3 cells, and the dynamic shift from small to large cells, is unique among DRG peptides and suggests that Reg-2 has a distinctive role in the injury response.

Activating Transcription Factor 3↗
PubMed2004

T lymphocytes play a role in neuropathic pain following peripheral nerve injury in rats.

A catastrophic consequence of peripheral nerve injury is the development of abnormal, chronic neuropathic pain. The inflammatory response at the injury site is believed to contribute to the generation and maintenance of such persistent pain. However, the physiological significance and potential contribution of T cells to neuropathic pain remains unclear. Here we show that T cells infiltrate injured sciatic nerves following chronic constriction injury (CCI), but not uninjured nerves. Congenitally athymic nude rats, which lack mature T cells, developed a significantly reduced mechanical allodynia and thermal hyperalgesia following CCI, compared with their heterozygous littermates. To understand further the role played by different T-cell subsets, we generated polarized populations of type 1 and type 2 T cells, with different cytokine secretion profiles, from spleens of sciatic nerve-injured heterozygous rats. Passive transfer of type 1 T cells, which produce proinflammatory cytokines, into nude rats enhanced the recipients' pain hypersensitivity to a level similar to that of heterozygous donor rats. In contrast, passive transfer of polarized type 2 T cells, which produce anti-inflammatory cytokines, into heterozygous rats modestly though significantly attenuated their pain hypersensitivity. Thus, injection of type 1 and type 2 T-cell subsets produces opposing effects on neuropathic pain. These findings suggest the modulation of the T-cell immune response as a potential target for the treatment of neuropathic pain.

Animals↗
PubMed2006

The low-density lipoprotein receptor-related protein is a pro-survival receptor in Schwann cells: possible implications in peripheral nerve injury.

Schwann cells undergo phenotypic modulation in peripheral nerve injury. In the adult rodent, Schwann cells are resistant to death-promoting challenges. The responsible receptors and signaling pathways are incompletely understood. In this study, we demonstrate that low-density lipoprotein receptor-related protein-1 (LRP-1) is expressed in adult sciatic nerve. After crush injury, LRP-1 is lost from the axoplasm and substantially upregulated in Schwann cells. Increased LRP-1 mRNA expression was observed locally at the injury site in multiple forms of sciatic nerve injury, including crush injury, chronic constriction injury, and axotomy. Endogenously produced tumor necrosis factor-alpha (TNF-alpha) was mostly responsible for the increase in LRP-1 expression; this activity was reproduced by direct injection of TNF-alpha into injured nerves in the TNF-alpha gene knock-out mouse. TNF receptor II was primarily involved. TNF-alpha also increased LRP-1 mRNA in Schwann cells in primary culture. Silencing of Schwann cell LRP-1 with siRNA decreased phosphorylated Akt and increased activated caspase-3. Equivalent changes in cell signaling were observed in LRP-1-deficient murine embryonic fibroblasts. Schwann cell death was induced in vitro by serum withdrawal or TNF-alpha, to a greater extent when LRP-1 was silenced. Schwann cell death was induced in vivo by injecting the LRP-1 antagonist, receptor-associated protein, into axotomy sites in adult rats. These results support a model in which LRP-1 functions as a pro-survival receptor in Schwann cells.

Animals↗
PubMed2005

[Advances of functional electrical stimulation in treatment of peripheral nerve injuries].

OBJECTIVE: To review the advances of functional electrical stimulation (FES) in treatment of peripheral nerve injuries. METHODS: By index of recent literature, the measures of stimulation, the mechanisms of FES and unsolved problems were evaluated and analyzed. RESULTS: Great advances have been made in the treatment of peripheral nerve injuries. It can not only enhance the regeneration of injured peripheral nerve, but also prevent muscular atrophy. CONCLUSION: FES is an effective treatment for peripheral nerve injuries.

Electric Stimulation↗
PubMed2005

Peripheral nerve injury induces cannabinoid receptor 2 protein expression in rat sensory neurons.

We have localized cannabinoid receptor 2 protein in rat and mouse somatic sensory nervous system, using an antibody that recognizes mouse cannabinoid receptor 2. Little or no cannabinoid receptor 2 immunoreactivity was found in sections of naive rat or mouse dorsal root ganglia or spinal cord. This was in accord with the lack of detectable cannabinoid receptor 2 mRNA in (dorsal root ganglion) neurons by in situ hybridization experiments described in the literature. However, we could detect cannabinoid receptor 2 immunoreactivity following unilateral nerve damage-either by sciatic nerve section, or by spinal nerve ligation. It was localized to the superficial laminae of the dorsal horn of the spinal cord, ipsilateral to the nerve damage, coincident with the area of termination of damaged afferents which was marked by loss of isolectin B4 binding. This upregulation was not seen in cannabinoid receptor 2 null mice. The cannabinoid receptor 2 protein in spinal cord appeared to be expressed on sensory neuron afferent terminals as it colocalized with two markers of damaged afferents, namely growth associated protein-43 and the neuropeptide galanin. Moreover, it did not colocalize with markers of activated microglial cells (OX-42) or astroglial cells (glial fibrillary acidic protein) in rat spinal cord. In the peripheral nerve, accumulation of cannabinoid receptor 2 immunoreactivity was seen in nerve sections proximal, but not distal, to the ligation site, suggesting transport down the nerve from the cell bodies. Although convincing cannabinoid receptor 2 immunoreactivity was seen in neither uninjured nor injured dorsal root ganglion neuron cell bodies in tissue sections, expression was detectable in isolated, cultured neurons that had received a prior axotomy in vivo. This clear demonstration of CB(2) receptors on sensory neurons suggests an additional cellular target for CB(2) agonist induced analgesia, at least in neuropathic models.

Animals↗
PubMed2006

Possible involvement of increase in spinal fibronectin following peripheral nerve injury in upregulation of microglial P2X4, a key molecule for mechanical allodynia.

We have recently demonstrated that the P2X4 receptor, an ATP-gated cation channel, in spinal microglia is a key molecule that mediates the mechanical allodynia induced by peripheral nerve injury. Although microglial P2X4 receptor expression is increased after peripheral nerve injury, the molecular mechanism(s) underlying its upregulation remains largely unknown. Fibronectin is a member of the extracellular matrix molecules and is actively produced in response to injury and diseases in the CNS. Here, we describe the influence of fibronectin on P2X4 receptor expression in microglia and the upregulation of fibronectin after peripheral nerve injury. Microglia that were cultured on fibronectin-coated dishes showed a marked increase in P2X4 receptor expression, both at the mRNA and protein levels, as compared to those cultured on control dishes. Fibronectin also enhanced the microglial Ca2+ responses mediated by P2X4 receptors. Moreover, Western blot examination of the spinal cord from a rat with spinal nerve injury indicated that fibronectin was upregulated on the ipsilateral side. Interestingly, intrathecal injection of ATP-stimulated microglia to the rat lumber spinal cord revealed that microglia cultured on fibronectin-coated dishes was more effective in the induction of allodynia than microglia cultured on control dishes. Taken together, our results suggest that spinal fibronectin is elevated after the peripheral nerve injury and it may be involved in the upregulation of the P2X4 receptor in microglia, which leads to the induction of neuropathic pain.

Adenosine Triphosphate↗
PubMed1992

Effect of systemic lidocaine on dorsal horn neuron hyperactivity following chronic peripheral nerve injury in rats.

Systemic lidocaine (3-4 mg/kg) was tested for its effect on identified spinal cord wide-dynamic-range (WDR) neurons in rats with a unilateral chronic neuropathy induced by two different peripheral nerve injuries (section or compression by ligatures). In both cases, neurons on the side ipsilateral to the injuries showed a spontaneous firing frequency higher than that of the opposite intact side (23.5 +/- 3.4 vs 4.2 +/- 1.5 spikes/sec). The hyperactivity was not affected by a sensory block of the peripheral receptive field. It was consistently found that lidocaine suppressed or reduced the spontaneous neuronal hyperactivity on the ipsilateral side, whereas it had no effect on the normal spontaneous activity of the neurons on the intact side. In all recordings, the hyperactivity returned to the prelidocaine injection rates within 20 min. These results indicate a preferential action of subanesthetic doses of lidocaine on the hyperactive WDR neurons. Such preferential action is related to a susceptibility acquired by WDR neurons of the peripherally injured side and is not simply attributable to the increased frequency of firing.

Animals↗
PubMed1995

Modulation of NMDA receptor expression in the rat spinal cord by peripheral nerve injury and adrenal medullary grafting.

Excessive activation of N-methyl-D-aspartate (NMDA) receptors in the spinal cord consequent to peripheral injury has been implicated in the initiation of neuropathologic events leading to a state of chronic hyperexcitability and persistence of exaggerated sensory processing. In other CNS disease or injury states, NMDA-mediated neurotoxic damage is associated with a loss of NMDA receptors, and outcome may be improved by agents reducing NMDA activation. Previous findings in our laboratory have demonstrated that the transplantation of adrenal medullary tissue into the spinal subarachnoid space can alleviate sensory abnormalities and reduce the induction of a putative nitric oxide synthase consequent to peripheral nerve injury. In order to determine changes in NMDA receptor expression in the spinal cord following peripheral nerve injury and adrenal medullary grafting, NMDA receptor binding using a high-affinity competitive NMDA receptor antagonist, CGP-39653, and NMDAR1 subunit distribution using immunocytochemistry were investigated. Two weeks following peripheral nerve injury by loose ligation of the right sciatic nerve, either adrenal medullary or striated muscle (control) tissue pieces were implanted in the spinal subarachnoid space. Binding studies revealed a marked reduction in [3H]CGP-39653 binding at L4-L5 levels ipsilateral to peripheral nerve injury in control transplanted animals. In contrast, NMDA binding was normalized in adrenal medullary grafted animals. In addition, NMDAR1 immunoreactivity was reduced in both the dorsal horn neuropil and motor neurons of the ventral horn in animals with peripheral nerve injury, while levels in adrenal medullary grafted animals appeared similar to intact controls. These results suggest that adrenal medullary transplants reduce abnormal sensory processing resulting from peripheral injury by intervening in the spinal NMDA-excitotoxicity cascade.

2-Amino-5-phosphonovalerate↗
PubMed1987

Peripheral nerve injury associated with fracture or fracture-dislocation of the pelvis in dogs and cats: 34 cases (1978-1982).

Peripheral nerve injury was associated with fracture or fracture-dislocation of the pelvis in 23 dogs and 11 cats. In most cases, peripheral nerve injury resulted from ilial fracture with craniomedial displacement of bone fragments, or from sacroiliac fracture-dislocation with cranial displacement of the ilium. Sciatic nerve injury was associated with fracture of the acetabulum in 2 dogs. A combination of sensory, voluntary motor, and reflex abnormalities were observed in the ipsilateral extremity of affected animals. Signs of severe pain were noticed in 4 of the dogs and in 1 cat. Eight of the animals died or were euthanatized for reasons not directly related to the severity of peripheral nerve injury. Of the remaining 26 animals, 21 (81%) had good or excellent limb function 16 weeks after peripheral nerve injury was sustained. Limb function was lost or self-mutilation occurred in 4 (15%) of the animals.

Animals↗