Ongoing activity in peripheral nerve: Injury discharge

Wall, Patrick D.; Sg, Waxman; Basbaum, Allan I.

doi:10.1016/0014-4886(74)90163-0

Cited by 227 publications

(64 citation statements)

References 13 publications

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“…Previous studies that used the electrophysiological method have shown that inhibition of GT activity may not prolong significantly the single stimulus-induced excitatory postsynaptic glutamate-mediated currents, but it does so if the stimulus is repetitive and excessive (Overstreet et al, 1999), a condition that is encountered after peripheral nerve injury (Wall et al, 1974;Seltzer et al, 1991). In this regard, enhancing GT uptake activity by the positive GT activity regulator riluzole would be expected to reduce glutamate excitation regardless of changes in GT expression.…”

Section: Possible Mechanisms Of Gt Changes After CCImentioning

confidence: 99%

“…Both peripheral and central mechanisms have been proposed to explain clinical features of neuropathic pain. With regard to the peripheral mechanisms, abnormal expression or distribution of certain sodium channels and spontaneous ectopic discharges are some of the proposed mechanisms likely to be contributory to the development of neuropathic pain (Wall et al, 1974;Devor, 1983;Porreca et al, 1999;Waxman et al, 1999;Gold et al, 2003). For over a decade the central glutamatergic system has been a major focus of research interest on the central mechanisms of neuropathic pain.…”

Section: Contributions To the Central Mechanisms Of Neuropathic Painmentioning

confidence: 99%

“…Both peripheral and central mechanisms have been implicated in the pathogenesis of neuropathic pain (Wall et al, 1974;Devor, 1983;Woolf, 1983;Dubner, 1991;Mao et al, 1995;Woolf and Mannion, 1999), and dynamic interactions between peripheral and central mechanisms also have been indicated (Gracely et al, 1992;Mao et al, 1992b,c). An increase in neuronal excitability within the CNS may be initiated and maintained after excessive activation of central glutamate receptors by their endogenous ligands, namely glutamate and aspartate.…”

Section: Introductionmentioning

confidence: 99%

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Altered Expression and Uptake Activity of Spinal Glutamate Transporters after Nerve Injury Contribute to the Pathogenesis of Neuropathic Pain in Rats

2003

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The central glutamatergic system has been implicated in the pathogenesis of neuropathic pain, and a highly active central glutamate transporter (GT) system regulates the uptake of endogenous glutamate. Here we demonstrate that both the expression and uptake activity of spinal GTs changed after chronic constriction nerve injury (CCI) and contributed to neuropathic pain behaviors in rats. CCI induced an initial GT upregulation up to at least postoperative day 5 primarily within the ipsilateral spinal cord dorsal horn, which was followed by a GT downregulation when examined on postoperative days 7 and 14 by Western blot and immunohistochemistry. Intrathecal administration of the tyrosine kinase receptor inhibitor K252a and the mitogen-activated protein kinase inhibitor PD98059 for postoperative days 1-4 reduced and nearly abolished the initial GT upregulation in CCI rats, respectively. Prevention of the CCI-induced GT upregulation by PD98059 resulted in exacerbated thermal hyperalgesia and mechanical allodynia reversible by the noncompetitive NMDA receptor antagonist MK-801, indicating that the initial GT upregulation hampered the development of neuropathic pain behaviors. Moreover, CCI significantly reduced glutamate uptake activity of spinal GTs when examined on postoperative day 5, which was prevented by riluzole (a positive GT activity regulator) given intrathecally twice a day for postoperative days 1-4. Consistently, riluzole attenuated and gradually reversed neuropathic pain behaviors when the 4 d riluzole treatment was given for postoperative days 1-4 and 5-8, respectively. These results indicate that changes in the expression and glutamate uptake activity of spinal GTs may play a critical role in both the induction and maintenance of neuropathic pain after nerve injury via the regulation of regional glutamate homeostasis, a new mechanism relevant to the pathogenesis of neuropathic pain.

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Section: Possible Mechanisms Of Gt Changes After CCImentioning

confidence: 99%

Section: Contributions To the Central Mechanisms Of Neuropathic Painmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Altered Expression and Uptake Activity of Spinal Glutamate Transporters after Nerve Injury Contribute to the Pathogenesis of Neuropathic Pain in Rats

2003

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“…It was not considered, that an ectopic nerve potential spreads to both directions from the site of its origin [8] and thus a motor unit potential (MUP) or fasciculation potential should be recorded, not an EPS [9]. In addition, experimental studies do not support the hypothesis that irregular sustained action potentials like EPSs be activated by peripheral nerve injury or irritation [10][11][12]. To discuss the origin of EPSs, we have to look at the physiological properties of the muscle spindle.…”

Section: Muscle Pain Produced By a Needle During Needle Electromyographymentioning

confidence: 99%

Muscle Pain and Muscle Spindles

Partanen¹

2018

Anatomy, Posture, Prevalence, Pain, Treatment and Interventions of Musculoskeletal Disorders

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“…Goldschire establece que lo que produce el dolor es la sumación de estímulos y la convergencia de sensaciones que se presenta en el cuerno posterior de la médula. Weddel y Sinclair desarrollan en 1955 la forma más simple de la teoría de patrones, denominada teoría de patrón periféri-co (50)(51)(52). Ellos consideran que el dolor está provocado por un exceso de estimulación periférica que produce un patrón de impulsos nerviosos interpretados centralmente como dolor.…”

Section: Teoría De Patrones O De Codificación De La Actividad Neuronaunclassified

Ronald Melzack and Patrick Wall. La teoría de la compuerta: más allá del concepto científico dos universos científicos dedicados al entendimiento del dolor

González

2013

Rev. Soc. Esp. Dolor

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La teoría de la compuerta. Más allá del concepto cientí-fico dos universos científicos dedicados al entendimiento del dolor. Rev Soc Esp Dolor 2013; 20(4): 191-202. ABSTRACTThe quest to acquire knowledge and understanding of pain has had crucial moments in which the evolution of the process has been dramatically changed. These moments have been revelations that have opened the path to rethinking previously accepted knowledge and created new horizons of research, understanding and treatment. When Melzack and Wall first described what would come to be known as the "Gate Control theory" they were able not only to clarify basic aspects of pain development but to lead the way to further basic and clinical research studies. They psychological aspects, the clinical basis and the structural anatomical and physiological components created one of the most complete theories in medical sciences and the ground for the basic management of pain. It has been fifty years since the original article was published in Science magazine (Pain Mechanism: a new theory. A gate control system modulates sensory input from the skin before it evokes pain perception and response. Ronald Melzack and Patrick Wall. Science. November 19, 1965 volume 150, number 3699). It has been recognized even until today as the most cited reference in medical journals in the past 50 years. The paper was written during a very particular moment in scientific history and the context of two very different lives, which illustrates the incredible process that leads to scientific development. The analysis of what this paper has symbolized to pain science must be done not only from a purely scientific view point but from a human one as well. RESUMENLa evolución histórica para el conocimiento del dolor ha tenido momentos cruciales en los que el curso evolutivo se modificó. Esos momentos son situaciones relevantes que cambiaron los conceptos previamente aceptados y abrieron nuevos horizontes de investigación, de entendimiento y de tratamiento. Cuando Melzack y Wall desarrollaron la "Teoría de la Compuerta" lograron aclarar fenómenos básicos del entendimiento del dolor pero igualmente abrieron múltiples tópicos de futuras investigaciones básicas y clínicas. Dieron sustento, con su teoría, a múltiples tratamientos del dolor que son la base de procedimientos que en la actualidad realizamos. Los aspectos psicológicos, el componente clínico y la base estructural anatomofisiológica fueron poco a poco conformando una de las teorías más completas de la ciencia médica y por supuesto principio básico para el mejor tratamiento del dolor. Son 50 años que se cumplen de la publicación de aquel artí-culo en la revista Science (Pain Mechanism: a new theory. A gate control system modulates sensory input from the skin before it evoques pain perception and response. Ronald Melzack and Patrick Wall. Science. 19 november 1965, volumen 150, number 3699), el cual ha sido reconocido hasta la actualidad como la referencia bibliográfica más utilizada en la ciencia médica en los últimos 50 años....

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Ongoing activity in peripheral nerve: Injury discharge

Cited by 227 publications

References 13 publications

Altered Expression and Uptake Activity of Spinal Glutamate Transporters after Nerve Injury Contribute to the Pathogenesis of Neuropathic Pain in Rats

Altered Expression and Uptake Activity of Spinal Glutamate Transporters after Nerve Injury Contribute to the Pathogenesis of Neuropathic Pain in Rats

Muscle Pain and Muscle Spindles

Ronald Melzack and Patrick Wall. La teoría de la compuerta: más allá del concepto científico dos universos científicos dedicados al entendimiento del dolor

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