Increases in the concentration of brain derived neurotrophic factor in the lumbar spinal dorsal horn are associated with pain behavior following chronic constriction injury in rats

Miletić, Gordana; Miletić, Vjekoslav

doi:10.1016/s0304-3940(01)02576-9

Cited by 86 publications

(75 citation statements)

References 20 publications

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“…Blocking the actions of IL-1ß and TNF-· attenuates mechanical allodynia in a gender-specific manner in an L 5 spinal nerve transsection rodent model of neuropathic pain [73]. Structural damage to peripheral axons in the rat chronic constriction injury model led to an inflammatory reaction at the site of injury, and subsequently to neuropathic pain [74]. In a rat model of peripheral neuritis, the sciatic nerve was exposed to carrageenan, an immune stimulant, which caused the infiltration of inflammatory cells such as macrophages, neutrophils, and CD4+ and CD8+ T cells to the site, accompanied by increases in the concentrations of cytokines and the development of endoneural neuropathic pain [75].…”

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confidence: 99%

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Lee¹,

Dantzer

Langley

et al. 2004

Neuroimmunomodulation

266

184

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While many of the multiple symptoms that cancer patients have are due to the disease, it is increasingly recognized that pain, fatigue, sleep disturbance, cognitive dysfunction and affective symptoms are treatment related, and may lead to treatment delays or premature treatment termination. This symptom burden, a subjective counterpart of tumor burden, causes significant distress. Progress in understanding the mechanisms that underlie these symptoms may lead to new therapies for symptom control. Recently, some of these symptoms have been related to the actions of certain cytokines that produce a constellation of symptoms and behavioral signs when given exogenously to both humans and animals. The cytokine-induced sickness behavior that occurs in animals after the administration of infectious or inflammatory agents or certain proinflammatory cytokines has much in common with the symptoms experienced by cancer patients. Accordingly, we propose that cancer-related symptom clusters share common cytokine-based neuroimmunologic mechanisms. In this review, we provide evidence from clinical and animal studies that correlate the altered cytokine profile with cancer-related symptoms. We also propose that the expression of coexisting symptoms is linked to the deregulated activity of nuclear factor-kappa B, the transcription factor responsible for the production of cytokines and mediators of the inflammatory responses due to cancer and/or cancer treatment. These concepts open exciting new avenues for translational research in the pathophysiology and treatment of cancer-related symptoms.

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mentioning

confidence: 99%

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Lee¹,

Dantzer

Langley

et al. 2004

Neuroimmunomodulation

266

184

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“…Os NGF, além de sensibilizarem diretamente os nociceptores na periferia, atuam em células do sistema inume e simpático 59 , enquanto o BDNF facilita a excitação dos neurônios do corno dorsal da medula espinal 60 . A expressão dessas substâncias aumenta, em modelos experimentais, na região relacionada com a lesão do nervo por constrição, assim como no gânglio da raiz dorsal correspondente 61 . Também, a injeção endoneural de fator neurotrófico provoca brotamentos de sinapses e sinais de hiperalgesia térmica, enquanto a administração perineural dessa substância determina o aparecimento de hiperalgesia mecânica.…”

Section: Neurotrofinasunclassified

“…Nerve growth factor besides causing direct sensitization of peripheral nociceptors affects immune and sympathetic cells 59 , while BDNF facilitates the excitation of dorsal horn neurons 60 . In experimental models, expression of those substances increases in the area related with the damaged nerve secondary to constriction as well as the corresponding dorsal root ganglion 61 . The endoneural injection of neurotrpphic factor causes budding of synapses and signs of thermic hyperalgesia, while the perineural administration of this substance determines the forthcoming of mechanical hyperalgesia.…”

Section: Neurotrophinsmentioning

confidence: 99%

Dor neuropática: aspectos neuroquímicos

Kraychete¹,

Gozzani²,

Kraychete³

2008

Rev. Bras. Anestesiol.

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Rev Bras AnestesiolARTIGO DE REVISÃO 2008; 58: 5: 492-505 REVIEW ARTICLE RESUMO Kraychete DC, Gozzani JL, Kraychete AC -Dor Neuropática -Aspectos Neuroquímicos. JUSTIFICATIVA E OBJETIVOS:A dor neuropática é causada por lesão ou inflamação do sistema nervoso. É síndrome complexa, com mecanismos biológicos pouco esclarecidos, envolvendo teorias inflamatórias e imunes. O objetivo desta revisão foi descrever os principais fatores biológicos relacionados com a dor neuropática, associando de forma lógica as hipóteses sugeridas pela literatura. CONTEÚDO:Foram descritos os principais neuromediadores, canais iônicos e células, incluindo as do sistema imune envolvidos na excitabilidade neuronal, assim como enfatizada possível seqüência de ativação ou interação desses agentes na alteração neuroplástica decorrente da agressão ao nervo.CONCLUSÕES: Do estudo, foi possível concluir que os avanços no conhecimento da fisiopatologia da dor neuropática podem determinar novos alvos para abordagem farmacológica dessa síndrome.Unitermos: DOR: neuropática; FISIOLOGIA: neurotransmissores. SUMMARYKraychete DC, Gozzani JL, Kraychete AC -Neuropathic PainNeurochemical Aspects. BACKGROUND AND OBJECTIVES:Neuropathic pain is caused by damage or inflammation of the nervous system. It is a complex syndrome and its biological mechanisms, involving inflammatory and immunologic theories, are not clear. The objective of this review was to describe the main biologic factors associated with neuropathic pain, making a logical association between hypotheses suggested in the literature. CONTENTS:The main neuromediators, ion channels, and cells, including cells in the nervous system involved in neuronal excitation are described, and the possible activation sequence or interaction among those agents in the neoplastic change secondary to nerve damage are emphasized. CONCLUSIONS:It was possible to conclude that the advances on the knowledge of the pathophysiology of neuropathic pain can determine new pharmacologic approaches for this syndrome.

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“…Nerve injury leads to multiple changes in spinal dorsal horn. Among them, increased release of neurotransmitter glutamate and neuromodulators such as brain-derived neurotrophic factor (BDNF) from primary afferent terminals in spinal dorsal horn is proved to be important for the initiation and maintenance of neuropathic pain (40). It has been shown that activation of G protein-coupled receptors can stimulate SFKs and PKC, leading to up-regulation of NMDA-receptor function (41).…”

Section: +mentioning

confidence: 99%

“…Increased release of glutamate stimulates group I mGluRs that enhance src kinases activity and tyrosine phosphorylation of NMDA receptors during pain hypersensitivity. The concentration of BDNF in lumbar spinal dorsal horn also markedly increases after nerve lesion, which occludes in the timeline with behavioral signs of neuropathic pain (40). SFKs play a key role in linking BDNF signaling with downstream NMDA receptors (43).…”

Section: +mentioning

confidence: 99%

Inhibition of Protein Tyrosine Kinases Attenuated Aβ-Fiber-Evoked Synaptic Transmission in Spinal Dorsal Horn of Rats With Sciatic Nerve Transection

Xin

et al. 2006

J Pharmacol Sci

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Abstract. Peripheral nerve injury leads to the establishment of a novel synaptic connection between afferent Aβ-fiber and lamina II neurons in spinal dorsal horn, which is hypothesized to underlie mechanical allodynia. However, how the novel synapses transmit nociceptive information is poorly understood. In the present study, the role of protein tyrosine kinases (PTKs) in Aβ-fiber-evoked excitatory postsynaptic currents (EPSCs) recorded in lamina II neurons in transverse spinal cord slices of rats was investigated using the whole-cell patch-clamp recording technique. In the slices from sciatic nerve transection (SNT) rats, genistein (50 µM), a broadspectrum PTKs inhibitor, or PP2 (20 µM), a selective Src family tyrosine kinase inhibitor, significantly reduced the amplitude of Aβ-fiber EPSCs. In sham-operated rats, however, Aβ-fiber EPSCs were insensitive to genistein and PP2. The N-methyl-D-aspartate (NMDA) receptor antagonist AP-V (50 µM) suppressed Aβ-fiber EPSCs in slices from SNT rats but not from sham-operated rats. Following nerve injury, the slow inward currents elicited by bath application of NMDA (100 µM) significantly increased at −70 mV. In SNT rats, genistein and PP2 reduced Aβ-fiber-evoked EPSCs mediated by NMDA receptor; however, genistein produced little effect on Aβ-fiber EPSCs mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor. These data suggested that PTKs, especially Src family members, participated in Aβ-fiber-evoked synaptic transmission following sciatic nerve injury via potentiation of NMDA receptor function.

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Increases in the concentration of brain derived neurotrophic factor in the lumbar spinal dorsal horn are associated with pain behavior following chronic constriction injury in rats

Cited by 86 publications

References 20 publications

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Dor neuropática: aspectos neuroquímicos

Inhibition of Protein Tyrosine Kinases Attenuated Aβ-Fiber-Evoked Synaptic Transmission in Spinal Dorsal Horn of Rats With Sciatic Nerve Transection

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