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Cord Dorsal Horn (cord + dorsal_horn)
Kinds of Cord Dorsal Horn Selected AbstractsUltrastructural evidence for a pre- and postsynaptic localization of full-length trkB receptors in substantia gelatinosa (lamina II) of rat and mouse spinal cordEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2005Chiara Salio Abstract Brain-derived neurotrophic factor (BDNF) exerts its trophic effects by acting on the high-affinity specific receptor trkB. BDNF also modulates synaptic transmission in several areas of the CNS, including the spinal cord dorsal horn, where it acts as a pain modulator by yet incompletely understood mechanisms. Spinal neurons are the main source of trkB in lamina II (substantia gelatinosa). Expression of this receptor in dorsal root ganglion (DRG) cells has been a matter of debate, whereas a subpopulation of DRG neurons bears trkA receptors and contains BDNF. By the use of two different trkB antibodies we observed that 7.7% and 10.8% of DRG neurons co-expressed BDNF + trkB but not trkA, respectively, in rat and mouse. Ultrastructurally, full-length trkB (fl-trkB) receptors were present at somato-dendritic membranes of lamina II neurons (rat: 66.8%; mouse: 73.8%) and at axon terminals (rat: 33.2%; mouse: 26.2%). In both species, about 90% of these terminals were identified as primary afferent fibres (PAFs) considering their morphology and/or neuropeptide content. All fl-trkB-immunopositive C boutons in type Ib glomeruli were immunoreactive for BDNF and, at individual glomeruli and axo-dendritic synapses, fl-trkB receptors were located in a mutually exclusive fashion at pre- or postsynaptic membranes. Thus, only a small fraction of fl-trkB-immunoreactive dendrites were postsynaptic to BDNF-immunopositive PAFs. This is the first ultrastructural description of fl-trkB localization at synapses between first- and second-order sensory neurons in lamina II, and suggests that BDNF may be released by fl-trkB-immunopositive PAFs to modulate nociceptive input in this lamina of dorsal horn. [source] Galanin knockout mice reveal nociceptive deficits following peripheral nerve injuryEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2000Bradley J. Kerr Abstract The neuropeptide galanin has been identified as a potential neurotransmitter/neuromodulator within the central nervous system. In the present study, the role of endogenous galanin in nociceptive processing in the nervous system has been analysed by using mice carrying a targeted mutation in the galanin gene. Supporting this, the effect of chronic administration of exogenous galanin on nociceptive sensory inputs has been assayed in adult rats. In the absence of peripheral nerve injury, the sensitivity to threshold noxious stimuli is significantly higher in galanin mutant mice than wild-type controls. Following peripheral nerve injury, in conditions under which endogenous galanin levels are elevated, spontaneous and evoked neuropathic pain behaviours are compromised in mutant mice. Conversely, chronic intrathecal delivery of exogenous galanin to nerve-intact adult rats is associated with persistent behavioural hypersensitivity, a significant increase in c-fos expression and an increase in PKC, immunoreactivity within the spinal cord dorsal horn. The present results demonstrate that a relationship exists between the degree of nerve injury-induced galanin expression and the degree of behavioural hypersensitivity, and show that galanin may play a role in nociceptive processing in the spinal cord, with interrelated inhibitory and excitatory effects. [source] A novel transverse push,pull microprobe: in vitro characterization and in vivo demonstration of the enzymatic production of adenosine in the spinal cord dorsal hornJOURNAL OF NEUROCHEMISTRY, Issue 1 2001Shawnna L. Patterson Adenosine produces analgesia in the spinal cord and can be formed extracellularly through enzymatic conversion of adenine nucleotides. A transverse push,pull microprobe was developed and characterized to sample extracellular adenosine concentrations of the dorsal horn of the rat spinal cord. Samples collected via this sampling technique reveal that AMP is converted to adenosine in the dorsal horn. This conversion is decreased by the ecto-5,-nucleotidase inhibitor, ,,,-methylene ADP. Related behavioral studies demonstrate that AMP administered directly to the spinal cord can reverse the secondary mechanical hyperalgesia characteristic of the intradermal capsaicin model of inflammatory pain. The specific adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT) inhibits the antihyperalgesia produced by AMP. This research introduces a novel microprobe that can be used as an adjunct sampling technique to microdialysis and push,pull cannulas. Furthermore, we conclude that AMP is converted to adenosine in the dorsal horn of the spinal cord by ecto-5,-nucleotidase and subsequently may be one source of adenosine, acting through adenosine A1 receptors in the dorsal horn of the spinal cord, which produce antihyperalgesia. [source] Effects of Intrathecal Injection of Nicotine on the Analgesic Effects of Isoflurane in a Model of Inflammatory PainBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2009Wei Cheng After having established the mice model of analgesia by intraperitoneally injecting (i.p.) appropriate doses of isoflurane, nicotine, a neuronal nicotinic acetylcholine receptor agonist was intrathecally injected. The effects of isoflurane and nicotine on paw licking times and formalin-induced c-fos expression in the spinal cord dorsal horn were examined. Our correlative studies have shown that isoflurane can decrease the paw licking times and simultaneously suppress c-fos expression after injection of formalin in the mice. Nicotine can partially antagonize the effects induced by isoflurane above. Spinal neuronal nicotinic acetylcholine receptors may be important targets for the analgesic effects of isoflurane in formalin pain. [source] | ||||||||||