Search results for "Spinal Cord Dorsal Horn"

showing 4 items of 4 documents

Multiple mechanisms of secondary hyperalgesia

2000

Publisher Summary This chapter discusses the multiple mechanisms of secondary hyperalgesia. The chapter defines the minimal conditions of complexity that must be fulfilled by a model of plasticity of spinal nociceptive transmission in order to explain clinical and psychophysical observations in humans. Secondary hyperalgesia is characterized by a leftward shift of the stimulus-response function for noxious mechanical stimuli. In order to define the afferent pathways involved in inducing central sensitization and in mediating the hyperalgesia to noxious mechanical stimuli, several psychophysical experiments using selective nerve block techniques is performed. Secondary hyperalgesia is likely…

ChemistryNociceptionmedicine.anatomical_structurenervous systemSpinal Cord Dorsal HornNeuropathic painHyperalgesiamedicineNociceptive NeuronsIn patientNeuronmedicine.symptomNeuroscienceSensitization
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SETD7 mediates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury

2019

Abstract Gene transcription regulation is critical for the development of spinal microgliosis and neuropathic pain after peripheral nerve injury. Using a model of chronic constriction injury (CCI) of the sciatic nerve, this study characterized the role of SET domain containing lysine methyltransferase 7 (SETD7) which monomethylates histone H3 lysine 4 (H3K4me1), a marker for active gene transcription. SETD7 protein expression in the spinal dorsal horn ipsilateral to nerve lesion was increased from one day to 14 days after CCI, concomitantly with the expression of inflammatory genes, Ccl2, Il-6 and Il-1β. The CCI-induced SETD7 expression was predominantly localized to microglia, as demonstra…

Male0301 basic medicineSpinal Cord Dorsal HornPathologymedicine.medical_specialtyImmunologyCCL2MicrogliosisRats Sprague-Dawley03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinePeripheral Nerve InjuriesGanglia SpinalmedicineAnimalsGene knockdownMicrogliaEndocrine and Autonomic Systemsbusiness.industryHistone-Lysine N-MethyltransferaseNerve injurySciatic NerveSpineRats030104 developmental biologymedicine.anatomical_structureSpinal CordHyperalgesiaNeuropathic painPeripheral nerve injuryNeuralgiaFemaleMicrogliaSciatic nervemedicine.symptombusiness030217 neurology & neurosurgeryBrain, Behavior, and Immunity
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Oligodendrocyte ablation triggers central pain independently of innate or adaptive immune responses in mice.

2014

Mechanisms underlying central neuropathic pain are poorly understood. Although glial dysfunction has been functionally linked with neuropathic pain, very little is known about modulation of pain by oligodendrocytes. Here we report that genetic ablation of oligodendrocytes rapidly triggers a pattern of sensory changes that closely resemble central neuropathic pain, which are manifest before overt demyelination. Primary oligodendrocyte loss is not associated with autoreactive T- and B-cell infiltration in the spinal cord and neither activation of microglia nor reactive astrogliosis contribute functionally to central pain evoked by ablation of oligodendrocytes. Instead, light and electron micr…

NociceptionSpinothalamic tractSpinal Cord Dorsal HornSpinothalamic TractsT-LymphocytesGeneral Physics and AstronomyAdaptive ImmunityGeneral Biochemistry Genetics and Molecular BiologyArticleMicemedicineAnimalsOligodendrocyte; central painB-LymphocytesMultidisciplinaryMicrogliabusiness.industryGeneral Chemistrymedicine.diseaseSpinal cordOligodendrocyteAxonsImmunity InnateAstrogliosisMicroscopy ElectronOligodendrogliamedicine.anatomical_structureNociceptionSpinal CordAstrocytesNeuropathic painNeuralgiaNeuralgiaMicrogliabusinessNeuroscienceNature communications
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TAFA4 relieves injury-induced mechanical hypersensitivity through LDL receptors and modulation of spinal A-type K+ current

2021

Pain, whether acute or persistent, is a serious medical problem worldwide. However, its management remains unsatisfactory, and new analgesic molecules are required. We show here that TAFA4 reverses inflammatory, postoperative, and spared nerve injury (SNI)-induced mechanical hypersensitivity in male and female mice. TAFA4 requires functional low-density lipoprotein receptor-related proteins (LRPs) because their inhibition by RAP (receptor-associated protein) dose-dependently abolishes its antihypersensitive actions. SNI selectively decreases A-type K+ current (IA) in spinal lamina II outer excitatory interneurons (L-IIo ExINs) and induces a concomitant increase in IA and decrease in hyperpo…

Spinal Cord Dorsal HornSNiSpinal neuron[SDV]Life Sciences [q-bio]AnalgesicPainCHO CellsPharmacologyInhibitory postsynaptic potentialGeneral Biochemistry Genetics and Molecular BiologyTAFA4Mice03 medical and health sciencesCricetulus0302 clinical medicineAnimalsHumansMedicine030304 developmental biologyLDL-receptors0303 health sciencesbusiness.industryIA and IhNerve injury3. Good healthHEK293 CellsRAW 264.7 CellsReceptors LDLHyperalgesiainjury-induced mechanical painLDL receptorPotassiumExcitatory postsynaptic potentialCytokinesgating neuronsmedicine.symptomRAPbusiness030217 neurology & neurosurgeryLipoproteinCell Reports
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