Journal ArticleDOI
Neurotrophins: Mediators and Modulators of Pain
Sophie Pezet,Stephen B. McMahon +1 more
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TLDR
The chapter reviews the evidence for these roles (and briefly the effects of other neurotrophins), the range of conditions under which they act, and their mechanism of action.Abstract:
The neurotrophin family of neurotrophic factors are well-known for their effects on neuronal survival and growth. Over the past decade, considerable evidence has accumulated from both humans and animals that one neurotrophin, nerve growth factor (NGF), is a peripheral pain mediator, particularly in inflammatory pain states. NGF is upregulated in a wide variety of inflammatory conditions, and NGFneutralizing molecules are effective analgesic agents in many models of persistent pain. Such molecules are now being evaluated in clinical trials. NGF regulates the expression of a second neurotrophin, brain-derived neurotrophic factor (BDNF), in nociceptors. BDNF is released when nociceptors are activated, and it acts as a central modulator of pain. The chapter reviews the evidence for these roles (and briefly the effects of other neurotrophins), the range of conditions under which they act, and their mechanism of action.read more
Citations
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Dissecting the human BDNF locus: Bidirectional transcription, complex splicing, and multiple promoters
TL;DR: It is shown that BDNF and antiBD NF transcripts form dsRNA duplexes in the brain in vivo, suggesting an important role for antiBDNF in regulating BDNF expression in human.
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Central mechanisms of pathological pain
TL;DR: This review focuses on the molecular determinants of network plasticity in the central nervous system (CNS) and discusses their relevance to the development of new therapeutic approaches.
Journal ArticleDOI
Clinical features and pathophysiology of complex regional pain syndrome
Johan Marinus,G. Lorimer Moseley,G. Lorimer Moseley,Frank Birklein,Ralf Baron,Christian Maihöfner,Wade S. Kingery,Jacobus J. van Hilten +7 more
TL;DR: The evidence points to CRPS being a multifactorial disorder that is associated with an aberrant host response to tissue injury, and variation in susceptibility to perturbed regulation of any of the underlying biological pathways probably accounts for the clinical heterogeneity of CRPS.
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Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions.
TL;DR: A psychophysiological systems view of pain in which physical injury, or wounding, generates a complex stress response that extends beyond the nervous system and contributes to the experience of pain is advanced.
Journal ArticleDOI
Pathophysiology of peripheral neuropathic pain : Immune cells and molecules
TL;DR: This review identifies the different immune cell types that contribute to neuropathic pain in the periphery and release factors that are crucial in this particular condition.
References
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Journal ArticleDOI
Neurotrophins and their receptors: a convergence point for many signalling pathways.
TL;DR: Recent findings that neurotrophins, in addition to promoting survival and differentiation, exert various effects through surprising interactions with other receptors and ion channels are reviewed.
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Induction of c-fos-like protein in spinal cord neurons following sensory stimulation.
TL;DR: Physiological stimulation of rat primary sensory neurons causes the expression of c-fos-protein-like immunoreactivity in nuclei of postsynaptic neurons of the dorsal horn of the spinal cord, suggesting that synaptic transmission may induce rapid changes in gene expression in certain post Synaptic neurons.
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Purification of a new neurotrophic factor from mammalian brain.
TL;DR: This factor is the first neurotrophic factor to be purified since NGF, from which it is clearly distinguished because it has different antigenic and functional properties.
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BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain
Jeffrey A. M. Coull,Simon Beggs,Dominic Boudreau,Dominick Boivin,Makoto Tsuda,Kazuhide Inoue,Claude Gravel,Michael W. Salter,Yves De Koninck +8 more
TL;DR: It is shown that ATP-stimulated microglia cause a depolarizing shift in the anion reversal potential (Eanion) in spinal lamina I neurons, and that BDNF is a crucial signalling molecule betweenmicroglia and neurons.
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Bradykinin and nerve growth factor release the capsaicin receptor from PtdIns(4,5)P2-mediated inhibition.
Huai-hu Chuang,Elizabeth D. Prescott,Haeyoung Kong,Shannon D. Shields,Sven-Eric Jordt,Allan I. Basbaum,Moses V. Chao,David Julius +7 more
TL;DR: It is shown that bradykinin- or NGF-mediated potentiation of thermal sensitivity in vivo requires expression of VR1, a heat-activated ion channel on sensory neurons, and biochemical studies suggest that VR1 associates with this complex.