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At least 451 records · Page 25Linked to original sources
PubMed2000

Neurotrophins from dorsal root ganglia trigger allodynia after spinal nerve injury in rats.

Injury to peripheral nerves often results in chronic pain which is difficult to relieve. The mechanism underlying the pain syndrome remains largely unknown. In previous studies we showed that neurotrophins are up-regulated in satellite cells around sensory neurons following sciatic nerve lesion. In the present study, we have examined whether the neurotrophins in the dorsal root ganglia play any role in allodynia after nerve injury. Antibodies to different neurotrophins, directly delivered to injured dorsal root ganglia, significantly reduced (with different time sequences) the percentage of foot withdrawal responses evoked by von Frey hairs. The antibodies to nerve growth factor acted during the early phase but antibodies to neurotrophin-3 and brain-derived neurotrophic factor were effective during the later phase. Exogenous nerve growth factor or brain-derived neurotrophic factor, but not neurotrophin-3, directly delivered to intact dorsal root ganglia, trigger a persistent mechanical allodynia. Our results showed that neurotrophins within the dorsal root ganglia after peripheral nerve lesion are involved in the generation of allodynia at different stages. These studies provide the first evidence that ganglia-derived neurotrophins are a source of nociceptive stimuli for neuropathic pain after peripheral nerve injury.

Animals↗
PubMed1989

Developmental competency in spinal nerve fiber extension on a reconstituted basement-membrane-like matrix.

Nerve fibers readily extend from larval frog spinal cord explants when cultured on a commercially available reconstituted basement-membrane-like matrix derived from the EHS mouse sarcoma. This superior, naturally derived substratum enables the in vitro development of complex neuritic arrays with long survival times in a defined medium, thus permitting the detailed analysis of spontaneous and target-mediated neuritogenesis.

Animals↗
PubMed1987

Recording of single unit potentials in human spinal nerve roots: a new diagnostic tool.

Single unit potentials can be recorded directly with wire electrodes during an operation in man. Since averaging is not necessary this recording method is a fast neuromonitoring tool. Using 2 pairs of platinum electrodes it was possible to record extracellular single unit potentials at 2 sites in nerve root filaments in the spinal canal and to determine conduction velocities. Afferent and efferent single unit potentials could be distinguished from each other by a reversed conduction time and a reversed potential change making a differentiation between dorsal and ventral root parts possible. An activity increase due to touching the skin could be recorded. Therefore dermatomes of nerve root filaments and root filaments of dermatomes can be identified during the operation.

Action Potentials↗
PubMed1996

Virally mediated misexpression of Hoxc-6 in the cervical mesoderm results in spinal nerve truncations.

Members of the Hox gene family appear to regulate anterior-posterior (A-P) regionalization in embryos. Genetic manipulation of numerous Hox genes in the developing trunk region of vertebrates results in changes in the morphology of individual vertebrae. We have used virally mediated, targeted misexpression to ectopically express the Hoxc-6 protein in chick embryos. Hoxc-6 has an anterior border of expression at the cervical-thoracic transition in tetrapods. Misexpression of this gene in the cervical mesoderm of chick embryos results in dramatic truncations of the ventral rami of cervical spinal nerves in the infected region. These data point to a role for Hoxc-6 in axon guidance, and suggest that in addition to regulating proliferative rates, Hox gene expression provides positional information utilized in producing domain-specific extracellular signals.

Animals↗
PubMed1999

Neuronal nitric oxide synthase mRNA upregulation in rat sensory neurons after spinal nerve ligation: lack of a role in allodynia development.

Pharmacological evidence suggests a functional role for spinal nitric oxide (NO) in the modulation of thermal and/or inflammatory hyperalgesia. To assess the role of NO in nerve injury-induced tactile allodynia, we examined neuronal NO synthase (nNOS) expression in the spinal cord and dorsal root ganglia (DRG) of rats with tactile allodynia because of either tight ligation of the left fifth and sixth lumbar spinal nerves or streptozotocin-induced diabetic neuropathy. RNase protection assays indicated that nNOS mRNA (1) was upregulated in DRG, but not spinal cord, neurons on the injury side beginning 1 d after nerve ligation, (2) peaked (approximately 10-fold increase) at 2 d, and (3) remained elevated for at least 13 weeks. A corresponding increase in DRG nNOS protein was also observed and localized principally to small and occasionally medium-size sensory neurons. In rats with diabetic neuropathy, there was no significant change in DRG nNOS mRNA. However, similar increases in DRG nNOS mRNA were observed in rats that did not develop allodynia after nerve ligation and in rats fully recovered from allodynia 3 months after the nerve ligation. Systemic treatment with a specific pharmacological inhibitor of nNOS failed to prevent or reverse allodynia in nerve-injured rats. Thus, regulation of nNOS may contribute to the development of neuronal plasticity after specific types of peripheral nerve injury. However, upregulation of nNOS is not responsible for the development and/or maintenance of allodynia after nerve injury.

Animals↗
PubMed1996

The afferent pathways of discogenic low-back pain. Evaluation of L2 spinal nerve infiltration.

The afferent pathways of discogenic low-back pain have not been fully investigated. We hypothesised that this pain was transmitted mainly by sympathetic afferent fibres in the L2 nerve root, and in 33 patients we used selective local anaesthesia of this nerve. Low-back pain disappeared or significantly decreased in all patients after the injection. Needle insertion provoked pain which radiated to the low back in 23 patients and the area of skin hypoalgesia produced included the area of pre-existing pain in all but one. None of the nine patients with related sciatica had relief of that component of their symptoms. Our findings show that the main afferent pathways of pain from the lower intervertebral discs are through the L2 spinal nerve root, presumably via sympathetic afferents from the sinuvertebral nerves. Discogenic low-back pain should be regarded as a visceral pain in respect of its neural pathways. Infiltration of the L2 nerve is a useful diagnostic test and also has some therapeutic value.

Adolescent↗
PubMed2001

Electrophysiologic evidence for increased endogenous gabaergic but not glycinergic inhibitory tone in the rat spinal nerve ligation model of neuropathy.

BACKGROUND: Changes in the inhibitory activity mediated by gamma-aminobutyric acid (GABA) and glycine, acting at spinal GABAA receptors and strychnine-sensitive glycine receptors, are of interest in the development of neuropathic pain. There is anatomic evidence for changes in these transmitter systems after nerve injuries, and blocking either GABAA or glycine receptors has been shown to produce allodynia-like behavior in awake normal animals. METHODS: In this study, the possible changes in GABAergic and glycinergic inhibitory activity in the spinal nerve ligation model of neuropathic pain were studied by comparing the effects of the GABAA-receptor antagonist bicuculline and the glycine-receptor antagonist strychnine in neuropathic rats to their effects in sham-operated and nonoperated control rats. RESULTS: Bicuculline produced a dose-related facilitation of the Adelta-fiber-evoked activity in all study groups and increased C-fiber-mediated activity in the spinal nerve ligation group but not in either of the control groups. There were no differences in the effect of bicuculline on low threshold responses between the study groups. The glycine receptor antagonist strychnine did not have a statistically significant effect on any of the parameters studied in any of the control groups. CONCLUSIONS: These results support the idea of an increased GABAergic inhibitory tone in the spinal cord of neuropathic rats, possibly as compensation for increased excitability after nerve injury.

Animals↗
PubMed2003

Peripheral and central sites of action for A-85380 in the spinal nerve ligation model of neuropathic pain.

Neuronal nicotinic receptor (NNR) agonists such as ABT 594 have been shown to be effective in a wide range of preclinical models of acute and neuropathic pain. The present study, using the NNR agonist A-85380, sought to determine if NNR agonists are acting via similar or differing mechanisms to induce anti-nociception and anti-allodynia. A systemic administration of the quaternary NNR antagonist chlorisondamine (0.4 micromol/kg, intraperitoneal (i.p.)) did not alter A-85380-induced (0.75 micromol/kg, i.p.) anti-nociception in the rat paw withdrawal model of acute thermal pain. In contrast, previous studies have demonstrated that blockade of central NNRs by prior administration of chlorisondamine (10 microg i.c.v.) prevents A-85380 induced anti-nociception indicating a predominantly central site of action of NNR agonists in relieving acute pain. In the rat spinal nerve ligation model of neuropathic pain, A-85380 induced a dose-dependent anti-allodynia (0.5-1.0 micromol/kg) that was blocked by pretreatment with mecamylamine (1 micromol/kg). Interestingly, unlike acute pain, both systemic and central administration of chlorisondamine blocked A-85380-induced anti-allodynia, an effect that was determined not to be due to a non-specific effect of chlorisondamine or to chlorisondamine crossing the blood-brain barrier. The peripheral site of action was shown not to be the primary receptive field, since A-85380 had equally potent anti-allodynic effects when it was injected into either the affected or unaffected paw. In contrast, infusion of A-85380 directly onto the L5 dorsal root ganglion on the affected side resulted in a dose-dependent and marked anti-allodynia (10-20 microg) at doses that had no effect when injected systemically. This effect was blocked by pretreatment with chlorisondamine. Together these data further support the idea that different mechanisms underlie different pain states and suggest that the effects of NNR agonists in neuropathic pain may be due in part to peripheral actions of the compounds.

Animals↗
PubMed1998

Systemic morphine in the prevention of allodynia in the rat spinal nerve ligation model of neuropathic pain.

Peripheral nerve injury may lead to neuropathic pain that has been considered unresponsive to opioids. In animal models of neuropathic pain, there are previous data of both increased and decreased effect of opioids, but only limited information of the long-term effects of opioid treatment on the development of the symptoms of neuropathy. The possibility of preventing the development of signs of neuropathy with either a single pre-injury injection or chronic postinjury administration of morphine was studied in rats with unilateral peripheral neuropathy due to tight ligation of the L5 and L6 spinal nerves. These rats developed both mechanical and cold allodynia, but no thermal hyperalgesia. Neither subcutaneous morphine given as single injection (10 mg/kg) before the nerve injury nor chronic administration starting immediately after surgery using slow-release pellets (one, two or five pellets containing 75 mg of morphine, resulting in a total dose of 75, 150 or 375 mg) prevented the development of either mechanical or cold allodynia. No autotomy, signs of distress, altered social behaviour or morphine withdrawal was seen in any of the rats. The fact that neuropathic pain-like symptoms were not attenuated by any of the treatments studied could indicate that neither premedication nor postoperative pain management with systemic morphine is effective in preventing postoperative neuropathic pain. Copyright 1998 European Federation of Chapters of the International Association for the Study of Pain.

Journal Article↗
PubMed2000

Mediation of spinal nerve injury induced tactile allodynia by descending facilitatory pathways in the dorsolateral funiculus in rats.

Evidence exists to indicate that tactile allodynia arising from peripheral nerve injury is integrated predominately at supraspinal, rather than spinal, sites. In the present experiments, the possibility that disruption of descending pathways through the dorsolateral funiculus (DLF) might alter expression of nerve-injury induced tactile allodynia was explored. Male, Sprague-Dawley rats received L(5)/L(6) spinal nerve ligation (SNL). Lesions to the DLF were made ipsilateral or contralateral to SNL. Tactile allodynia was determined by measuring withdrawal thresholds to probing with von Frey filaments. Rats with DLF lesions presented no apparent motor deficits and did not alter sensory threshold in sham-SNL operated rats. DLF lesions made ipsilateral to SNL completely blocked tactile allodynia in SNL rats. Contralateral DLF lesions and sham surgery did not have any effect on SNL-induced allodynia. These results indicate that tactile allodynia after peripheral nerve injury is dependent upon tonic activation of net descending facilitation from supraspinal sites and support the hypothesis of tonic activation of descending facilitation as a basis for chronic pain.

Animals↗
PubMed1987

Nodal and paranodal structure during Wallerian degeneration in frog spinal nerve.

The nodal and paranodal regions of myelinated peripheral nerve fibers in frogs were examined at sequential times (1-24 days) during Wallerian degeneration. In the region up to 3 mm distal to the transection, paranodal demyelination and axoplasmic degeneration became apparent on day 4 and progressed to involve most of the nodes by day 8. The E-fracture face of the axolemma showed a patchy distribution of nodal particles and some paranodal demyelination on days 4 and 6. On day 8, nodal particles were evenly distributed at low concentration and the adjacent demyelinated paranodal regions showed a corresponding increase in particle density, suggesting redistribution of the nodal particles. The sequence of changes seen in comparable to that in Wallerian degeneration of central nervous system (CNS) fibers but progressed more rapidly in the peripheral nervous system (PNS). In addition a higher proportion of PNS fibers shows pathological changes at corresponding time periods.

Animals↗