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Nociceptive Neurons (nociceptive + neuron)
Selected AbstractsTranslating nociceptor sensitivity: the role of axonal protein synthesis in nociceptor physiologyEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2009Theodore J. Price Abstract The increased sensitivity of peripheral pain-sensing neurons, or nociceptors, is a major cause of the sensation of pain that follows injury. This plasticity is thought to contribute to the maintenance of chronic pain states. Although we have a broad knowledge of the factors that stimulate changes in nociceptor sensitivity, the cellular mechanisms that underlie this plasticity are still poorly understood; however, they are likely to involve changes in gene expression required for the phenotypic and functional changes seen in nociceptive neurons after injury. While the regulation of gene expression at the transcriptional level has been studied extensively, the regulation of protein synthesis, which is also a tightly controlled process, has only recently received more attention. Despite the established role of protein synthesis in the plasticity of neuronal cell bodies and dendrites, little attention has been paid to the role of translation control in mature undamaged axons. In this regard, several recent studies have demonstrated that the control of protein synthesis within the axonal compartment is crucial for the normal function and regulation of sensitivity of nociceptors. Pathways and proteins regulating this process, such as the mammalian target of rapamycin signaling cascade and the fragile X mental retardation protein, have recently been identified. We review here recent evidence for the regulation of protein synthesis within a nociceptor's axonal compartment and its contribution to this neuron's plasticity. We believe that an increased understanding of this process will lead to the identification of novel targets for the treatment of chronic pain. [source] The medullary dorsal reticular nucleus enhances the responsiveness of spinal nociceptive neurons to peripheral stimulation in the ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003Christophe Dugast Abstract Single-unit spinal recordings combined with application of glutamate into the medullary dorsal reticular nucleus were used to assess the action of this nucleus upon deep dorsal horn neurons in rats. Injection of high glutamate concentrations (10 and 100 mm) induced a dramatic and long-lasting increase of the responses of wide-dynamic range neurons to electrical stimulation of the sciatic nerve in the noxious range, without affecting ongoing discharges. Post-stimulus time histograms revealed that this increase concerned the post-discharge, but not A- or C-fibre-mediated responses, which remained unchanged independently of the stimulation frequency applied. The onset of the glutamate-induced response enhancement occurred with a concentration-dependent time delay and developed slowly until its maximum. These data indicate that the medullary dorsal reticular nucleus exerts a facilitating action upon deep dorsal horn wide-dynamic range neurons by enhancing their capacity to respond to peripheral stimulation through prolongation of their discharge. This action is accompanied by the strengthening of wind-up of deep dorsal horn wide-dynamic range neurons, hence providing a plausible substrate for chronic pain states. These results are in agreement with previous behavioural studies suggesting a pronociceptive role for the dorsal reticular nucleus [Almeida et al. (1996) Brain Res. Bull., 39, 7,15; Almeida et al. (1999) Eur. J. Neurosci., 11, 110,122], and support the involvement of a reverberating circuit, previously described in morphological studies [Almeida et al. (1993) Neuroscience, 55, 1093,1106; Almeida et al. (2000) Eur. J. Pain, 4, 373,387], which probably operates only at a certain threshold of activation. [source] Migraine Pain and Nociceptor Activation,Where Do We Stand?HEADACHE, Issue 5 2010Dan Levy PhD The mechanisms underlying the genesis of migraine pain remain enigmatic largely because of the absence of any identifiable cephalic pathology. Based on numerous indirect lines of evidence, 2 nonmutually exclusive hypotheses have been put forward. The first theorizes that migraine pain originates in the periphery and requires the activation of primary afferent nociceptive neurons that innervate cephalic tissues, primarily the cranial meninges and their related blood vessels. The second maintains that nociceptor activation may not be required and that the headache is promoted primarily as a result of abnormal processing of sensory signals in the central nervous system. This paper reviews the evidence leading to these disparate theories while siding with the primacy of nociceptor activation in the genesis migraine headache. The paper further examines the potential future use of established human models of migraine for addressing the origin of migraine headache. [source] Intervertebral disc, sensory nerves and neurotrophins: who is who in discogenic pain?JOURNAL OF ANATOMY, Issue 1 2010José García-Cosamalón Abstract The normal intervertebral disc (IVD) is a poorly innervated organ supplied only by sensory (mainly nociceptive) and postganglionic sympathetic (vasomotor efferents) nerve fibers. Interestingly, upon degeneration, the IVD becomes densely innervated even in regions that in normal conditions lack innervation. This increased innervation has been associated with pain of IVD origin. The mechanisms responsible for nerve growth and hyperinnervation of pathological IVDs have not been fully elucidated. Among the molecules that are presumably involved in this process are some members of the family of neurotrophins (NTs), which are known to have both neurotrophic and neurotropic properties and regulate the density and distribution of nerve fibers in peripheral tissues. NTs and their receptors are expressed in healthy IVDs but much higher levels have been observed in pathological IVDs, thus suggesting a correlation between levels of expression of NTs and density of innervation in IVDs. In addition, NTs also play a role in inflammatory responses and pain transmission by increasing the expression of pain-related peptides and modulating synapses of nociceptive neurons at the spinal cord. This article reviews current knowledge about the innervation of IVDs, NTs and NT receptors, expression of NTs and their receptors in IVDs as well as in the sensory neurons innervating the IVDs, the proinflammatory role of NTs, NTs as nociception regulators, and the potential network of discogenic pain involving NTs. [source] Conduction velocity is regulated by sodium channel inactivation in unmyelinated axons innervating the rat cranial meningesTHE JOURNAL OF PHYSIOLOGY, Issue 4 2008Roberto De Col Axonal conduction velocity varies according to the level of preceding impulse activity. In unmyelinated axons this typically results in a slowing of conduction velocity and a parallel increase in threshold. It is currently held that Na+,K+ -ATPase-dependent axonal hyperpolarization is responsible for this slowing but this has long been equivocal. We therefore examined conduction velocity changes during repetitive activation of single unmyelinated axons innervating the rat cranial meninges. In direct contradiction to the currently accepted postulate, Na+,K+ -ATPase blockade actually enhanced activity-induced conduction velocity slowing, while the degree of velocity slowing was curtailed in the presence of lidocaine (10,300 ,m) and carbamazepine (30,500 ,m) but not tetrodotoxin (TTX, 10,80 nm). This suggests that a change in the number of available sodium channels is the most prominent factor responsible for activity-induced changes in conduction velocity in unmyelinated axons. At moderate stimulus frequencies, axonal conduction velocity is determined by an interaction between residual sodium channel inactivation following each impulse and the retrieval of channels from inactivation by a concomitant Na+,K+ -ATPase-mediated hyperpolarization. Since the process is primarily dependent upon sodium channel availability, tracking conduction velocity provides a means of accessing relative changes in the excitability of nociceptive neurons. [source] | ||||||||||