Afferent Neuron

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The Experts below are selected from a list of 159 Experts worldwide ranked by ideXlab platform

Carole A Williams - One of the best experts on this subject based on the ideXlab platform.

Xiaohui Ding - One of the best experts on this subject based on the ideXlab platform.

Jennifer J. Deberry - One of the best experts on this subject based on the ideXlab platform.

  • Urothelial bladder Afferent Neurons in the rat are anatomically and neurochemically distinct from non-urothelial Afferents.
    Brain Research, 2017
    Co-Authors: Buffie Clodfelder-miller, Hirosato Kanda, Jianguo G. Gu, Judy Creighton, Timothy J. Ness, Jennifer J. Deberry
    Abstract:

    Abstract There is mounting evidence underscoring a role for the urothelium in urinary bladder sensation. Previous functional studies have identified bladder primary Afferents with mechanosensitive properties suggesting urothelial innervation and/or communication. The current study identifies a group of urothelium-innervating Afferent Neurons in rat, and characterizes and compares the properties of these and non-urothelial Afferent Neuron populations. Lumbosacral (LS) primary Afferent Neurons were retrogradely labeled using intraparenchymal (IPar) microinjection or intravesical (IVes) infusion of tracer into the bladder. Using these techniques, separate populations of Neurons were differentiated by dorsal root ganglion (DRG) somata labeling and dye distribution within the bladder. IPar- and IVes-labeled Neurons accounted for 85.0% and 14.4% of labeled L6-S1 Neurons (P

Jianguo G. Gu - One of the best experts on this subject based on the ideXlab platform.

  • Urothelial bladder Afferent Neurons in the rat are anatomically and neurochemically distinct from non-urothelial Afferents.
    Brain Research, 2017
    Co-Authors: Buffie Clodfelder-miller, Hirosato Kanda, Jianguo G. Gu, Judy Creighton, Timothy J. Ness, Jennifer J. Deberry
    Abstract:

    Abstract There is mounting evidence underscoring a role for the urothelium in urinary bladder sensation. Previous functional studies have identified bladder primary Afferents with mechanosensitive properties suggesting urothelial innervation and/or communication. The current study identifies a group of urothelium-innervating Afferent Neurons in rat, and characterizes and compares the properties of these and non-urothelial Afferent Neuron populations. Lumbosacral (LS) primary Afferent Neurons were retrogradely labeled using intraparenchymal (IPar) microinjection or intravesical (IVes) infusion of tracer into the bladder. Using these techniques, separate populations of Neurons were differentiated by dorsal root ganglion (DRG) somata labeling and dye distribution within the bladder. IPar- and IVes-labeled Neurons accounted for 85.0% and 14.4% of labeled L6-S1 Neurons (P

  • Membrane Mechanics of Primary Afferent Neurons in the Dorsal Root Ganglia of Rats.
    Biophysical Journal, 2017
    Co-Authors: Hirosato Kanda, Jianguo G. Gu
    Abstract:

    Membrane mechanics is an important biological factor regulating many cellular functions including cell motility, intercellular and intracellular signaling, gene expression, and membrane ion channel activity. Primary Afferent Neurons transduce sensory information about temperature, touch, and pain. These sensory functions may be profoundly affected by the states of primary Afferent Neuron mechanics. However, membrane mechanics of primary Afferent Neurons is largely unknown. In this study, we established the optical trapping technique for determining membrane mechanics of cultured primary Afferent Neurons of the dorsal root ganglia (DRG). We further determined the roles of cytoskeleton and membrane lipids in DRG Neuron mechanics. We found that DRG Neurons had a plasma membrane tension of ∼54 pN/μm, and the tension was significantly decreased to ∼29 pN/μm by cytochalasin D treatment to disrupt actin cytoskeleton and increased to ∼79 pN/μm by methyl-β-cyclodextrin treatment to sequester membrane cholesterol. DRG Neuron membrane stiffness was not significantly affected by the cytoskeleton disruption but was significantly increased after cholesterol sequestration. Our findings elucidate membrane mechanical properties of primary Afferent Neurons, which provide, to our knowledge, a new perspective on their sensory functions.

Carlos Amilcar Parada - One of the best experts on this subject based on the ideXlab platform.

  • inflammatory pain in peripheral tissue depends on the activation of the tnf α type 1 receptor in the primary Afferent Neuron
    European Journal of Neuroscience, 2021
    Co-Authors: Silviane Fernandes De Magalhaes, Luis Paulo Manzo, Felipe Meira De Faria, Maria Claudia De Oliveirafusaro, Catarine Massucato Nishijima, Willians Fernando Vieira, Ivan Jose Magayewski Bonet, Gilson Goncalves Dos Santos, Claudia Herrera Tambeli, Carlos Amilcar Parada
    Abstract:

    The mechanism underlying the role of tumor necrosis factor alpha (TNF-α) in the development of inflammatory hyperalgesia has been extensively studied, mainly the role of TNF-α in the release of pro-inflammatory cytokines. The current concept relies in the fact that TNF-α stimulates the cascade release of other pro-inflammatory cytokines, such as IL-1β, IL-6, and IL-8 (CINC-1 in rats), triggering the release of the final inflammatory mediator prostaglandin E2 (PGE2 ) and sympathetic amines that directly sensitize the nociceptors. However, this may not be the sole mechanism involved as the blockade of TNF-α synthesis by thalidomide prevents hyperalgesia without interrupting the synthesis of IL-1β, IL-6, and CINC-1. Therefore, we hypothesized that activation of TNF-α receptor type 1 (TNFR1) by TNF-α increases nociceptors' susceptibility to the action of PGE2 and dopamine. We have found out that intrathecal administration of oligodeoxynucleotide-antisense (ODN-AS) against TNFR1 or thalidomide prevented carrageenan-induced hyperalgesia. The co-administration of TNF-α with a subthreshold dose of PGE2 or dopamine that does not induce hyperalgesia by itself in the hind paw of Wistar rats pretreated with dexamethasone (to prevent the endogenous release of cytokines) induced a robust hyperalgesia that was prevented by intrathecal treatment with ODN-AS against TNFR1. We consider that the activation of Neuronal TNFR1 by TNF-α decisively increases the susceptibility of the peripheral Afferent Neuron to the action of final inflammatory mediators - PGE2 and dopamine - that ultimately induce hyperalgesia. This mechanism may also underlie the analgesic action of thalidomide.

  • antihyperalgesic effect of cb1 receptor activation involves the modulation of p2x3 receptor in the primary Afferent Neuron
    European Journal of Pharmacology, 2017
    Co-Authors: Maria Claudia Goncalves Oliveirafusaro, Luis Paulo Manzo, Ivan Jose Magayewski Bonet, Gilson Goncalves Dos Santos, Claudia Herrera Tambeli, Cristiane I Zanoni, Dioneia Araldi, Elayne Vieira Dias, Carlos Amilcar Parada
    Abstract:

    Cannabinoid system is a potential target for pain control. Cannabinoid receptor 1 (CB1) activation play a role in the analgesic effect of cannabinoids once it is expressed in primary Afferent Neurons. This study investigates whether the anti-hyperalgesic effect of CB1 receptor activation involves P2X3 receptor in primary Afferent Neurons. Mechanical hyperalgesia was evaluated by electronic von Frey test. Cannabinoid effect was evaluated using anandamide or ACEA, a non-selective or a selective CB1 receptor agonists, respectively; AM251, a CB1 receptor antagonist, and antisense ODN for CB1 receptor. Calcium imaging assay was performed to evaluated α,β-meATP-responsive cultured DRG Neurons pretreated with ACEA. Anandamide or ACEA administered in peripheral tissue reduced the carrageenan-induced mechanical hyperalgesia. The reduction in the carrageenan-induced hyperalgesia induced by ACEA was completely reversed by administration of AM251 as well as by the intrathecal treatment with antisense ODN for CB1 receptor. Also, ACEA reduced the mechanical hyperalgesia induced by bradykinin and by α,β-meATP, a P2X3 receptor non-selective agonist, but not by tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and chemokine-induced chemoattractant-1 (CINC-1). Finally, CB1 receptors are co-localized with P2X3 receptors in DRG small-diameter Neurons and the treatment with ACEA reduced the number of α,β-meATP-responsive cultured DRG Neurons. Our data suggest that the analgesic effect of CB1 receptor activation is mediated by a negative modulation of the P2X3 receptor in the primary Afferent Neurons.