ライフサイエンスコーパス: nociceptive

1 primary afferent neurons, many of which are nociceptive.

2 aracterized central projections of cutaneous nociceptive A and C fibers, selectively labeled with cho

3 cting afferents, at least in part, including nociceptive A-delta and C fibers in the dorsal horn.

4 t silencing trigeminal projections inhibited nociceptive activity in parabrachial bitter taste neuron

5 Further, nociceptive activity in PbN bitter taste neurons was sup

6 Here, high-speed videography during nociceptive Adelta fiber stimulation demonstrated engage

7 o compensate for the inhibitory influence of nociceptive afferent inputs on low-threshold motor units

8 These data support that cutaneous nociceptive afferent subtypes preferentially contribute

9 Nociceptive afferents in craniofacial muscles are predom

10 Central sprouting of nociceptive afferents in response to neural injury enhan

11 oxious irritants/pollutants activates airway nociceptive afferents resulting in reflex bradycardia in

12 extended the central termination profiles of nociceptive afferents with synaptoporin, an isoform of s

13 rdiovascular responses and the activation of nociceptive afferents, we analyzed BP and HR responses t

14 nic constriction injury bilaterally augments nociceptive amygdala (in the central nucleus of the amyg

15 d drug-taking to alleviate spontaneous pain, nociceptive and affective manifestations.

16 g/kg) produced a significant decrease in the nociceptive and inflammatory response to allyl isothiocy

17 damide and tested for changes in response to nociceptive and non-nociceptive stimuli.

18 revent innocuous stimuli from activating the nociceptive and pruritic transmission pathways.

19 homeostasis through anti-inflammatory, anti-nociceptive, and anti-secretory effects.

20 ion of metabolic, estrogen receptor-mediated nociceptive, and autoimmune signaling programs.

21 sensory experience during development alters nociceptive behavior and circuit physiology in Drosophil

22 Furthermore, while nociceptive behavior and cortical activity are normally

23 es from cancer cell line supernatant reduced nociceptive behavior in a paw withdrawal assay, supporti

24 eased tumor size was associated with greater nociceptive behavior in the mouse model and more pain ex

25 a significant reduction in formalin-induced nociceptive behavior was observed.

26 Here we have simultaneously measured nociceptive behavior, brain activity, and levels of phys

27 the heat-evoked action potential firing and nociceptive behavior.

28 ATP also induced robust biphasic spontaneous nociceptive behavior.

29 subtype of tongue cancer was associated with nociceptive behavior.

30 Our data demonstrate a role of for in larval nociceptive behavior.

31 erotonergic cells were dispensable for acute nociceptive behaviors and for aversion induced by therma

32 ent with A438079 abolished all BzATP-induced nociceptive behaviors, while ROS scavengers dose-depende

33 NaV 1.7(Nav1.8) mice showed normal nociceptive behaviours in response to intracolonic appli

34 hic pain is believed to arise from damage to nociceptive C fibres in diabetic neuropathy (DN).

35 te transient receptor potential ankyrin-1 on nociceptive C-fibers.

36 urified bacterial collagenase would initiate nociceptive cascades in the joint by degrading the capsu

37 tion, and instead appear to be driven by pro-nociceptive changes in the gut micro-environment.

38 athway-specific plasticity in the Drosophila nociceptive circuit is in part established through feedb

39 al hindpaw incision primes developing spinal nociceptive circuitry, resulting in enhanced hyperalgesi

40 ure projection neurons, and the "priming" of nociceptive circuits in the developing spinal cord, foll

41 ity due to inflammatory signaling within the nociceptive circuits of the spinal cord.

42 these aromatase neurons are poised to engage nociceptive circuits, whether it is through local estrog

43 utes to the onset and progression of adverse nociceptive conditions.

44 llary system), EEG event-related potentials (nociceptive cortical activity), and facial expression (b

45 Respiratory depression induced by an anti-nociceptive dose of morphine was significantly attenuate

46 sed as in vivo screening tool for novel anti-nociceptive drugs but requires careful evaluation of the

47 nM, E(Max) of 87.3%), and long lasting anti-nociceptive effects in mice when compared to DPDPE.

48 rodents, and the anti-inflammatory and anti-nociceptive effects of BAY-1797 were demonstrated in a m

49 The anti-nociceptive effects of sinusoidal rate modulation on EEG

50 These pro- and anti-nociceptive effects were blocked by co-injection of a TR

51 ifferent molecular weights produces opposing nociceptive effects.

52 hat endocannabinoids have both pro- and anti-nociceptive effects.

53 e recruitment of second-order neurons boosts nociceptive encodings at intermediate intensities.

54 GABAergic inhibition gates weak nociceptive encodings from being decoded, whereas escala

55 Silencing this nociceptive ensemble alleviated pain affective-motivatio

56 rve injury, innocuous stimuli activated this nociceptive ensemble to drive dysfunctional perceptual c

57 uropathic pain, although the role of HCN3 in nociceptive excitability and pain is less studied.

58 bstance P, a marker for a discrete subset of nociceptive, excitatory interneurons.

59 flammatory cytokine modulation of peripheral nociceptive fibres.

60 ells of the cochlea and are proposed to have nociceptive functions important for auditory function an

61 es not induce any transcriptional changes in nociceptive genes.

62 afferent neurons respond to cool, warm, and nociceptive hot temperatures with the majority activated

63 with orthotopic tumors significantly reduced nociceptive hypersensitivity and nerve fiber hypertrophy

64 both structural and functional mechanisms of nociceptive hypersensitivity in models of chronic pain i

65 rgeting spinal Wnt signaling for alleviating nociceptive hypersensitivity in vivo.

66 el with heightened anxiety-like behavior and nociceptive hypersensitivity.

67 leads to complete and persistent relief from nociceptive, inflammatory and neuropathic nociception an

68 tanding of the basic mechanisms that process nociceptive information and ultimately instantiate a sub

69 rge foramens; that central neurons receiving nociceptive information from the posterior dura are loca

70 circuits attribute this aversive quality to nociceptive information remains unknown.

71 tions of neurons produces representations of nociceptive information that are highly resilient to dis

72 The lateral parabrachial complex (PB) relays nociceptive information to brain circuits that are impor

73 l parabrachial complex (PB) conveys relevant nociceptive information to higher structures.

74 ajor spinoparabrachial pathway, relays acute nociceptive information, the ipsilateral PB is recruited

75 he processing and segregation of tactile and nociceptive information.

76 y that enables them to segregate tactile and nociceptive information.

77 esses contribute to pain beyond the level of nociceptive input and mediate psychological and behaviou

78 the dorsal horn synaptic network to amplify nociceptive input arising from muscle is predicted to fa

79 hrough neural entrainment to periodic thermo-nociceptive input as low as 0.1 Hz.

80 its (by noradrenergic action) the peripheral nociceptive input at the spinal cord level.

81 arget of spinal projection neurons conveying nociceptive input into supraspinal structures.

82 ral, but not ipsilateral, PB interfered with nociceptive input to RVM under basal conditions, as well

83 ogenous oxytocin release during inflammatory nociceptive input.

84 bcutaneous peripheral injection of formalin) nociceptive input.

85 inal pathways may modulate the processing of nociceptive inputs by SpVc, and regulate pain perception

86 ased more toward predictions and less toward nociceptive inputs in individuals who report less mindfu

87 in integrating, modulating, and interpreting nociceptive inputs in the TMJ, particularly in light of

88 e on the predicted threat than on changes in nociceptive inputs reported high pain catastrophizing an

89 ofound, immediate and precise integration of nociceptive inputs with ongoing motor activities leading

90 ific enhancement in the aversive response to nociceptive inputs.

91 o the neuropathology and treatments of these nociceptive, interoceptive and fatiguing illnesses.

92 al dorsal cutaneous nerves (DCNs) evokes the nociceptive intersegmental cutaneus trunci muscle (CTM)

93 potential ankyrin repeat 1 (TRPA1), a major nociceptive ion channel, but the underlying mechanisms a

94 predominantly through the activation of the nociceptive ion channel, transient receptor potential an

95 ntly reduced the ecto-AMPase activity in the nociceptive lamina in the brainstem.

96 ence of CD73 and ecto-AMPase activity in the nociceptive lamina of the trigeminal subnucleus caudalis

97 Our nociceptive lick-report detection assay will enable a ho

98 perfusion-affected muscle directly modulated nociceptive-like behaviors and increased exercise-mediat

99 ical profile of CSNs revealed an increase of nociceptive-like phenotype among neurons from CCI animal

100 ng neurons, with about two-thirds containing nociceptive markers.

101 ibuted nociceptive system, for understanding nociceptive mechanisms at a systems level by integrating

102 Yet, nociceptive mediators were increased in the periphery (s

103 to be enriched for expression and release of nociceptive mediators.

104 lter peripheral sensory neuron function in a nociceptive modality-specific manner.

105 entifies a novel role for Wnt5a signaling in nociceptive modulation at the spinal cord level.

106 e report a novel role for Wnt5a signaling in nociceptive modulation at the structural level.

107 he Mtb glycolipid sulfolipid-1 (SL-1) as the nociceptive molecule.

108 urons and their axonal fibers, including the nociceptive nerve fibers projecting into the brainstem.

109 r region of the heart and in pain-sensitive (nociceptive) nerve fibres.

110 Here we show that nociceptive nerves are required for enforced HSC mobiliz

111 Targeting the nociceptive nervous system could therefore represent a s

112 achial neurons, a major output of the spinal nociceptive network, which could contribute to the primi

113 of these sensory inputs to sensitize central nociceptive networks and thereby evoke persistent pain i

114 microglial activation selectively within the nociceptive neurocircuitry of the dorsal horn of the lum

115 PD-L1 also potently suppressed nociceptive neuron excitability in human DRGs.

116 multiple terminals; thus, the output of the nociceptive neuron is defined by the integration and com

117 m imaging show that tyra-2 expression in the nociceptive neuron, ASH, is necessary and sufficient to

118 specifically in the Class IV multidendritic nociceptive neuron, significantly attenuated ultraviolet

119 c protein expressing (GFAP(+)) glia modulate nociceptive neuronal activity in both the peripheral ner

120 trigger escape responses that are guided by nociceptive neuronal circuitry.

121 ive neurons were also immunopositive for the nociceptive neuronal markers IB4, TRPV1, CGRP, and subst

122 (Mtb)-specific lipid, SL-1, stimulates human nociceptive neurons and makes guinea pigs cough.

123 N2 modulates action potential firing rate in nociceptive neurons and plays a critical role in all mod

124 of ecto-5'-nucleotidase (CD73) in trigeminal nociceptive neurons and their axonal fibers, including t

125 show that the input-output properties of the nociceptive neurons depend on the length, the axial resi

126 Our findings help to predict how nociceptive neurons encode noxious stimuli and how this

127 Our data highlight that sensory nociceptive neurons exert a significant host protective

128 uncated rod-like unbranched cilia of the ASH nociceptive neurons in animals carrying a microtubule-de

129 ntaneous activities and hyperexcitability of nociceptive neurons in the adjacent uninjured L4 dorsal

130 ral responses, we chemogenetically activated nociceptive neurons in the amygdala, which further separ

131 late the HSC niche(3-6), the contribution of nociceptive neurons in the bone marrow remains unclear.

132 e show that an Mtb organic extract activates nociceptive neurons in vitro and identify the Mtb glycol

133 The cough reflex can be triggered by nociceptive neurons innervating the lungs, and some bact

134 lation of TRPV1 channels by noradrenaline in nociceptive neurons is a mechanism whereby noradrenaline

135 ain, crosstalk between the immune system and nociceptive neurons is central to inflammatory pain; the

136 n et al. report that activation of cutaneous nociceptive neurons leads to a nerve-reflex action that

137 is specifically expressed in small-diameter, nociceptive neurons of dorsal root ganglia (DRGs) and is

138 potential cation channel V1 expressed in the nociceptive neurons of dorsal root ganglion (DRG).

139 Selective ablation of nociceptive neurons significantly increased bacterial bu

140 The skin is densely innervated with nociceptive neurons specialized in detecting noxious and

141 ve response, and that multidendritic sensory nociceptive neurons synapse onto pr1 neurons in the VNC.

142 Sensory nociceptive neurons that can detect bacterial pathogens

143 b extract, but not SL-1, also stimulates non-nociceptive neurons that participate in the cough reflex

144 argets the OCTR-1 octopamine receptor on ASH nociceptive neurons to modulate an aversive olfactory re

145 actor (NGF) is a neurotrophin that activates nociceptive neurons to transmit pain signals from the pe

146 st time investigated TRESK function in human nociceptive neurons using induced pluripotent stem cell-

147 TRPV1, a PGE2-regulated channel in nociceptive neurons was also increased in the DRG.

148 Drosophila melanogaster larvae whose primary nociceptive neurons were reduced in levels of specific c

149 edge of the molecular composition of KARs in nociceptive neurons, a key piece in understanding the me

150 by changes in the excitability of peripheral nociceptive neurons, but the precise mechanisms controll

151 In small nociceptive neurons, genetic deletion of HCN2 abolished

152 nels regulate action potential generation in nociceptive neurons, identifying them as putative analge

153 or contributions to the hyperexcitability of nociceptive neurons, likely leading to altered sensory p

154 dependent spike initiation zone (Nav-SIZ) in nociceptive neurons, showing its plasticity under inflam

155 are detected by terminal endings of primary nociceptive neurons, which are organized into morphologi

156 put from the peripheral terminals of primary nociceptive neurons, which detect and encode the informa

157 i peppers that can trigger the activation of nociceptive neurons-significantly enhanced HSC mobilizat

158 ction mechanisms in this particular class of nociceptive neurons.

159 ptive terminal tree determines the output of nociceptive neurons.

160 ubtype predominantly expressed in peripheral nociceptive neurons.

161 brainstem to drive feedforward inhibition of nociceptive neurons.

162 between cranial sensory neurons and the PBL-nociceptive neurons.

163 cts the input-output relation of the primary nociceptive neurons.

164 In addition, GI pain can be nociceptive, neuropathic and associated with cancer, but

165 howed that such regulation was driven by the nociceptive neuropeptide calcitonin gene-related peptide

166 ion of a neuronal-specific gene set, notably nociceptive neuropeptides.

167 as been shown to decrease N/OFQ and increase nociceptive opioid peptide (NOP) receptors in the nucleu

168 ting mechanosensory input facilitate primary nociceptive output by releasing short neuropeptide F, th

169 n conveying key information about changes in nociceptive output in pathologic conditions, leading to

170 ividual terminals, thus leading to increased nociceptive output.

171 (-0.1 points [95% CI, -0.8 to 0.5 points]), nociceptive pain (-0.3 points [CI, -0.9 to 0.2 points]),

172 mine, gabapentin, clonidine, and lidocaine), nociceptive pain (ketoprofen, baclofen, cyclobenzaprine,

173 studies to establish specific mechanisms of nociceptive pain in chronic intervertebral disc degenera

174 ive central pain mechanisms and suggest that nociceptive pain processing may be similar across ethnic

175 validate the NPS as measuring a common core nociceptive pain system across pain types, and provide a

176 Neurologic Pain Signature (NPS), as a common nociceptive pain system across pain types.

177 ure, a neuromarker sensitive and specific to nociceptive pain, mediated painful heat effects on pain

178 or underlying mechanism (eg, painful cramps, nociceptive pain, or neuropathic pain).

179 Nociceptive (pain) behavior was measured with the dologn

180 A potential role in the transmission of nociceptive (pain) signals has remained controversial.

181 rity and increased myelination of the facial nociceptive pathway.

182 Although central nociceptive pathways contribute to OA pain, crosstalk be

183 se to neural injury enhances excitability of nociceptive pathways in the central nervous system, ofte

184 ng muscle appear more capable of sensitizing nociceptive pathways in the CNS compared with skin affer

185 avioral sensitivity, joint degeneration, and nociceptive pathways in the peripheral and central nervo

186 we determined whether a seizure can activate nociceptive pathways that carry pain signals from the me

187 ntial expression of genes (DEGs) involved in nociceptive pathways, including sensory neurons.

188 mmation or destruction of targets within the nociceptive pathways.

189 calcium influx, hyperalgesia and induced pro-nociceptive peptide release.

190 e to optogenetic activation of predominantly nociceptive peripheral afferent nerve fibers in head-res

191 ding protein eIF4E, attenuates many types of nociceptive plasticity induced by inflammatory mediators

192 e propose that p-S10H3 is a novel marker for nociceptive processing in SSDHN with high relevance to t

193 ce of this model to our understanding of the nociceptive processing which underlies the chronic pain

194 ue damage can result in long-term changes in nociceptive processing within the CNS.

195 nctions, such as tactile, proprioceptive and nociceptive processing, have been increasingly recognize

196 ure links altered sphingolipid metabolism to nociceptive processing.

197 s is central and peripheral sensitisation of nociceptive processing.

198 an underlying modular architecture in which nociceptive, pruritic, and innocuous stimuli are process

199 ry synaptic input from MrgA3/MrgD-expressing nociceptive/pruritoceptive afferents and C-low threshold

200 Data indicate the presence of a de novo nociceptive pulmonary-cardiac reflex triggering sympatho

201 pre-existing hypertension aberrantly shifts nociceptive pulmonary-cardiac reflexes towards sympathoe

202 pothesize that cardiovascular disease alters nociceptive pulmonary-cardiac reflexes.

203 Such data suggest distinct differences in nociceptive reflex pathways dependent on cardiovascular

204 nociceptive role for GPR55 in the control of nociceptive responding.

205 nanoparticles (NM0127) showed a strong anti-nociceptive response in multiple assays of evoked and on

206 gnified contribution of these neurons to the nociceptive response in the ACC.

207 entral nerve cord (VNC) are required for the nociceptive response, and that multidendritic sensory no

208 by quantifying palpebral opening and evoked nociceptive responses after corneal application of capsa

209 aling in sensory SGCs decreased heat-induced nociceptive responses and reversed inflammation-induced

210 In the absence of verbal report, these nociceptive responses are used as measures of pain sensa

211 imulation, which might modulate differential nociceptive responses in AD skin.

212 eceptors in the generalized sensitization of nociceptive responses in caterpillars.

213 Nociceptive responses to select noxious thermal and mech

214 sion in DRGs neurons and to evaluate whether nociceptive responses were affected in AS model mice (gl

215 in higher level cognitive processes or basic nociceptive responses.

216 op mechanical hyperalgesia, suggesting a pro-nociceptive role for GPR55 in the control of nociceptive

217 Using Drosophila larvae, we found that nociceptive rolling behavior was triggered at lower temp

218 n destabilized dendrite branches and reduced nociceptive sensitivity in Drosophila.

219 This suggests that nociceptive sensitivity in the first few hours of postna

220 the functional impact of peripheral Wnt3a on nociceptive sensitivity.

221 Our results suggest dual pathways for nociceptive sensitization after mTBI, direct 5-HT effect

222 for understanding cellular mechanisms behind nociceptive sensitization and perhaps their contribution

223 ently challenged by the observation [2] that nociceptive sensitization caused by a chronic pain-produ

224 e Receptor 2 (CXCR2) may support TBI-related nociceptive sensitization in a mouse model of mild TBI (

225 ent progress in mechanistic understanding of nociceptive sensitization in chronic pain with a focus o

226 at the chronic pain state and its associated nociceptive sensitization represented an adaptive functi

227 nucleotide-gated (HCN) channels play in this nociceptive sensitization using the inhibitors MK-801 an

228 manifestations of complex trauma, including nociceptive sensitization, bone fracture, muscle fibrosi

229 ration after TBI dose-dependently attenuated nociceptive sensitization.

230 enhance dendritic spine density, leading to nociceptive sensitization.

231 fers new approaches for reversing peripheral nociceptive sensitization.

232 hy, and it is an effective antagonist of the nociceptive sensor channel TRPA1.

233 l dorsal cutaneous nerves (DCNs) activates a nociceptive sensorimotor reflex and the same afferent st

234 To study of the role of nociceptive sensory afferents in freely behaving mice, w

235 We found that optogenetic inhibition of nociceptive sensory afferents reduced both ongoing pain

236 s and regulates sprouting and sensitivity of nociceptive sensory endings in mouse colon.

237 Downstream of the nociceptive sensory input, the neural signals trigger pr

238 nin gene-related peptide (CGRP), a marker of nociceptive sensory nerves.

239 ved in pain generation and modulation in the nociceptive sensory nervous system.

240 ociceptors, which are neuropeptide-producing nociceptive sensory neurons that express the ion channel

241 Organisms rely on nociceptive sensory neurons to detect and avoid potentia

242 ributes to the morphogenesis and function of nociceptive sensory neurons.

243 root ganglion neurons and is obligatory for nociceptive signal transmission.

244 rachial (PB) complex mediates both ascending nociceptive signaling and descending pain modulatory inf

245 ll surface with intact receptors and sustain nociceptive signaling by extracellular proteases.

246 tion in spinal cord yielded Ca(2+)-dependent nociceptive signaling induction in females that was supp

247 d sex differences in one of the oldest known nociceptive signaling molecule families, the prostagland

248 subfamily V, receptor 1 (TRPV1)-substance P nociceptive signaling pathway.

249 ed to study and manipulate somatosensory and nociceptive signaling pathways.

250 mission in the spinal cord dorsal horn gates nociceptive signaling, is essential in maintaining physi

251 ge-gated sodium (Na(V)) channels involved in nociceptive signaling.

252 Group III/IV muscle afferents transduce nociceptive signals and modulate exercise pressor reflex

253 erapeutic targets for pain treatment because nociceptive signals emanating from the periphery are cha

254 tial step in transforming transient afferent nociceptive signals into a stable pain perception.

255 ocal inflammatory responses and transmitting nociceptive signals.

256 sion of sensory, including trigeminovascular nociceptive, signals from thalamic nuclei to cortex and

257 3R mediated facilitation of both tactile and nociceptive spinal activity in the first three postnatal

258 e (isolation from the dam in infancy, versus nociceptive stimulation in adults).

259 ick reports to the detection of light-evoked nociceptive stimulation to the hind paw.

260 G and anandamide diminished sensitization to nociceptive stimuli although the effects of 2-AG were lo

261 h endocannabinoids enhanced responses to non-nociceptive stimuli and reduced responses to nociceptive

262 Physiological responses to nociceptive stimuli are initiated within tens of millise

263 model of fibromyalgia to innocuous and acute nociceptive stimuli by applying a step-wise graded elect

264 Activation to aversive nociceptive stimuli in gustatory cells was associated wi

265 behavioral responses to nociceptive vs. non-nociceptive stimuli in vivo.

266 ions from trigeminal nuclei and fire to oral nociceptive stimuli that excite somatosensory receptors

267 Sensitized responses to non-nociceptive stimuli were unaffected 2-AG or anandamide.

268 melanogaster larvae respond to a variety of nociceptive stimuli, including noxious touch and tempera

269 nociceptive stimuli and reduced responses to nociceptive stimuli.

270 r changes in response to nociceptive and non-nociceptive stimuli.

271 (CS(+)) and a 50% chance of an unconditioned nociceptive stimulus (US), and between CS(-) and the abs

272 Accepting reward coupled to a nociceptive stimulus resulted in decreased perceived int

273 ase when muscle pain is induced by injecting nociceptive substances into the muscle.

274 l mechanisms that feed back onto the primary nociceptive synapse and enhance the transfer of noxious

275 ge of the ability to selectively record from nociceptive synapses in this model organism.

276 ech), endocannabinoids were found to depress nociceptive synapses, but enhance non-nociceptive synaps

277 epress nociceptive synapses, but enhance non-nociceptive synapses.

278 understanding of how astrocytes can regulate nociceptive synaptic transmission via neuronal-glial and

279 ry in neonatal rodents primes the developing nociceptive system and enhances reinjury response in adu

280 ization and network hyperexcitability of the nociceptive system is a basic mechanism of neuropathic p

281 The distributed nociceptive system provides a foundation for understandi

282 Here, I provide a framework, the distributed nociceptive system, for understanding nociceptive mechan

283 ive behavior, but the evolutionary origin of nociceptive systems is not well understood.

284 planarians to humans, and imply that animal nociceptive systems may share a common ancestry, tracing

285 l stimulus changes revealing a mechanism for nociceptive temporal contrast enhancement (TCE).

286 The nociceptive terminal endings are morphologically complex

287 Here, we revealed that the structure of the nociceptive terminal tree determines the output of nocic

288 Here, we used a computational model of nociceptive terminal tree to study how the architecture

289 necessary for capsaicin-induced ablation of nociceptive terminals.

290 at jugular vagal sensory pathways input to a nociceptive thalamocortical circuit capable of regulatin

291 high-dose morphine (HDM, 3 mg/kg) increased nociceptive threshold (analgesia) and induced priming, n

292 Behavioural measures included mechanical nociceptive thresholds and distances run on exercise whe

293 neurin in regulating synaptic plasticity and nociceptive transmission and suggests new strategies for

294 the primary synapse, resulting in increased nociceptive transmission to higher brain centers.

295 f spinal DYN interneurons to limit ascending nociceptive transmission to the adult brain.

296 al neurons, which serve as a major source of nociceptive transmission to the brain.

297 However, the mechanoreceptive and nociceptive trigeminal ganglion neurons and the visual s

298 urons of murine dorsal root ganglia that pro-nociceptive TRPM3 channels, present in the peripheral pa

299 rectional effects on behavioral responses to nociceptive vs. non-nociceptive stimuli in vivo.

300 algesic mechanism within this early temporal nociceptive window.