Inflammatory pain hypersensitivity mediated by phenotypic switch in myelinated primary sensory neurons

Nature ◽  
1996 ◽  
Vol 384 (6607) ◽  
pp. 360-364 ◽  
Author(s):  
Simona Neumann ◽  
Tim P. Doubell ◽  
Tabi Leslie ◽  
Clifford J. Woolf
Keyword(s):  
Sensory Neurons ◽  
Inflammatory Pain ◽  
Primary Sensory Neurons ◽  
Phenotypic Switch ◽  
Pain Hypersensitivity

scholarly journals Resolvin E1 Inhibits Substance P-Induced Potentiation of TRPV1 in Primary Sensory Neurons

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Youn Yi Jo ◽  
Ji Yeon Lee ◽  
Chul-Kyu Park
Keyword(s):  
Substance P ◽  
G Protein ◽  
Sensory Neurons ◽  
Inflammatory Pain ◽  
Dorsal Root Ganglion Neurons ◽  
Peripheral Inflammation ◽  
Transient Receptor Potential Vanilloid ◽  
Primary Sensory Neurons ◽  
Nociceptive Neurons ◽  
Ganglion Neurons

The neuropeptide substance P (SP) is expressed in primary sensory neurons and is commonly regarded as a “pain” neurotransmitter. Upon peripheral inflammation, SP activates the neurokinin-1 (NK-1) receptor and potentiates activity of transient receptor potential vanilloid subtype 1 (TRPV1), which is coexpressed by nociceptive neurons. Therefore, SP functions as an important neurotransmitter involved in the hypersensitization of inflammatory pain. Resolvin E1 (RvE1), derived from omega-3 polyunsaturated fatty acids, inhibits TRPV1 activity via activation of the chemerin 23 receptor (ChemR23)—an RvE1 receptor located in dorsal root ganglion neurons—and therefore exerts an inhibitory effect on inflammatory pain. We demonstrate here that RvE1 regulates the SP-induced potentiation of TRPV1 via G-protein coupled receptor (GPCR) on peripheral nociceptive neurons. SP-induced potentiation of TRPV1 inhibited by RvE1 was blocked by the Gαi-coupled GPCR inhibitor pertussis toxin and the G-protein inhibitor GDPβ-S. These results indicate that a low concentration of RvE1 strongly inhibits the potentiation of TRPV1, induced by the SP-mediated activation of NK-1, via a GPCR signaling pathway activated by ChemR23 in nociceptive neurons. RvE1 might represent a new therapeutic target for the treatment of inflammatory pain as a prospective endogenous inhibitor that strongly inhibits TRPV1 activity associated with peripheral inflammation.

scholarly journals Neuromedin B receptor stimulation of Cav3.2 T-type Ca2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity

Theranostics ◽  
2021 ◽  
Vol 11 (19) ◽  
pp. 9342-9357
Author(s):  
Yuan Zhang ◽  
Zhiyuan Qian ◽  
Dongsheng Jiang ◽  
Yufang Sun ◽  
Shangshang Gao ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Primary Sensory Neurons ◽  
Receptor Stimulation ◽  
Pain Hypersensitivity ◽  
Peripheral Pain ◽  
Neuromedin B ◽  
Ca2 Channels ◽  
Stimulation Of

scholarly journals Electrophysiological Identification of Tonic and Phasic Neurons in Sensory Dorsal Root Ganglion and Their Distinct Implications in Inflammatory Pain

2014 ◽  
pp. 793-799 ◽  
Author(s):  
Y.-Q. YU ◽  
X.-F. CHEN ◽  
Y. YANG ◽  
F. YANG ◽  
J. CHEN
Keyword(s):  
Sensory Neurons ◽  
Inflammatory Pain ◽  
Action Potentials ◽  
Dorsal Root ◽  
Dependent Manner ◽  
Primary Sensory Neurons ◽  
Drg Neurons ◽  
Fluorescent Tracer ◽  
Firing Patterns ◽  
Venom Toxin

In the mammalian autonomic nervous system, tonic and phasic neurons can be differentiated on firing patterns in response to long depolarizing current pulse. However, the similar firing patterns in the somatic primary sensory neurons and their functional significance are not well investigated. Here, we identified two types of neurons innervating somatic sensory in rat dorsal root ganglia (DRG). Tonic neurons fire action potentials (APs) in an intensity-dependent manner, whereas phasic neurons typically generate only one AP firing at the onset of stimulation regardless of intensity. Combining retrograde labeling of somatic DRG neurons with fluorescent tracer DiI, we further find that these neurons demonstrate distinct changes under inflammatory pain states induced by complete Freund’s adjuvant (CFA) or bee venom toxin melittin. In tonic neurons, CFA and melittin treatments significantly decrease rheobase and AP durations (depolarization and repolarization), enhance amplitudes of overshoot and afterhyperpolarization (AHP), and increase the number of evoked action potentials. In phasic neurons, however, the same inflammation treatments cause fewer changes in these electrophysiological parameters except for the increased overshoot and decreased AP durations. In the present study, we find that tonic neurons are more hyperexcitable than phasic neurons after peripheral noxious inflammatory stimulation. The results indicate the distinct contributions of two types of DRG neurons in inflammatory pain.

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