ライフサイエンスコーパス: trigeminal

1 spinal trigeminal nucleus (DMSp5), but this trigeminal activation is not associated with the presenc

2 ration of the respiratory rate indicative of trigeminal activation.

3 inal mesencephalic root, some Schnauzenorgan trigeminal afferents terminated in the trigeminal motor

4 aneous end organs in the bill, innervated by trigeminal afferents.

5 es innervated by functional rapidly adapting trigeminal afferents.

6 vascular smooth muscle cells, and neurons in trigeminal and dorsal root ganglia, as detected by light

7 bundant in a subpopulation of neurons in the trigeminal and dorsal root ganglia, but was absent in sy

8 ve beta2-antagonist in BE(2)-C cells, and in trigeminal and dorsal root ganglia.

9 Nevertheless, the movement of trigeminal and facial BM somata is stalled, and their pe

10 eneral mucosal innervation is carried by the trigeminal and glossopharyngeal nerves.

11 relevance of microglial signaling in chronic trigeminal and orofacial pain.

12 was reduced and conduction velocities of the trigeminal and sciatic nerves were decreased.

13 projections of pruriceptive and nociceptive trigeminal and spinal neurons.

14 tors to cortex, which includes the principal trigeminal and ventral-posterior-medial thalamic nuclei,

15 expression, whereas those in the oculomotor, trigeminal, and facial nuclei are spared.

16 PolySias promote fasciculation of trigeminal axons in vivo and in vitro, whereas, in contr

17 ivering an air puff to one eye to invoke the trigeminal blink reflex as monkeys performed this visual

18 al perturbation of ongoing fixation with the trigeminal blink reflex in monkeys (Macaca mulatta) alte

19 inhibition on the saccadic system using the trigeminal blink reflex, triggering saccades at earlier-

20 In the mouse vibrissa system, trigeminal brainstem circuits are thought to mediate the

21 ts from the oropharynx terminate in both the trigeminal brainstem complex and the rostral part of the

22 Our finding that different trigeminal brainstem maps can exaggerate different parts

23 id-induced c-Fos activity in the dorsomedial trigeminal brainstem nucleus situated laterally adjacent

24 We identified a novel region of trigeminal brainstem, spinal trigeminal nucleus pars mur

25 ositions of the terminal fields of the three trigeminal branches move from medial to lateral in the d

26 entrations had significantly lower perceived trigeminal burn intensity.

27 The influence of carbonyl species on the trigeminal burn of distilled spirit model systems was in

28 hat addition of carbonyl compounds increased trigeminal burn perception in model systems; confirming

29 ciceptors such as TRPV1 and TRPA1 and elicit trigeminal burn.

30 the concentration of carbonyl compounds and trigeminal burn.

31 o encode for stimulus modality (olfactory vs trigeminal) by differential patterns of firing.

32 evealed expression of CGRP, CLR and RAMP1 in trigeminal cells.

33 The trigeminal circuit relays somatosensory input from the f

34 ecture and immunohistochemistry, the sensory trigeminal column can be subdivided from caudal to rostr

35 hisker-related excitatory afferents from the trigeminal complex and barrel cortex, inhibitory afferen

36 Rather, the neuronal activation in the trigeminal complex likely is attributable to direct depo

37 describe the cytoarchitecture of the sensory trigeminal complex, the patterns of calbindin-like and s

38 rganization of afferent input to the sensory trigeminal complex, which includes both the PrV and the

39 ery large and contain both motor and sensory trigeminal components as well as an electrosensory pathw

40 Trigeminal denervation resulted in epithelial defects wi

41 Chemical ablation of peptidergic trigeminal fibers prevented the SCC-induced nasal inflam

42 Trigeminal fibers terminate within the facial mucosa and

43 subsequently transmit signals to neighboring trigeminal fibers.

44 on in the eye, the level of viral DNA in the trigeminal ganglia (TG) during latency, and the amount o

45 etected ecto-AMPase activity in dental pulp, trigeminal ganglia (TG) neurons, and their nerve fibers.

46 We report that trigeminal ganglia (TG) of domestic and wild tactile-for

47 both in vitro and in vivo, as well as in the trigeminal ganglia (TG) of latently infected mice.

48 osed that CD8(+) T cells maintain latency in trigeminal ganglia (TG) of mice latently infected with h

49 umbar 4/5 dorsal root ganglia (DRG), and the trigeminal ganglia (TG) of streptozotocin-diabetic and h

50 Virus replication in the eye, latency in trigeminal ganglia (TG), and markers of T cell exhaustio

51 stablishes latency within sensory neurons of trigeminal ganglia (TG), and TG-resident CD8(+) T cells

52 blishes lifelong infection in the neurons of trigeminal ganglia (TG), cycling between productive infe

53 transduction of dorsal root ganglia (DRG) or trigeminal ganglia (TG), respectively.

54 the number of T cells expressing PD-1 in the trigeminal ganglia (TG), whereas depletion of DCs in mic

55 ent infections in the sensory neurons of the trigeminal ganglia (TG), wherein it retains the capacity

56 ed protein 2 (SFRP2), were induced in bovine trigeminal ganglia (TG), which correlated with reduced b

57 in HSV-1 latently infected human and rabbit trigeminal ganglia (TG).

58 tory epithelial cells and then colonizes the trigeminal ganglia (TG).

59 es latency within the sensory neurons of the trigeminal ganglia (TG).

60 ategy on the establishment of latency in the trigeminal ganglia (TG).

61 nohistochemistry on paraffin sections of the trigeminal ganglia (TG).

62 SV type 1 (HSV-1) in a latent state in their trigeminal ganglia (TG).

63 le for nitric oxide (NO) in neurons from the trigeminal ganglia (TG).

64 d vasoactive intestinal peptide (vip) in the trigeminal ganglia (TG).

65 impacts the placode cell contribution to the trigeminal ganglia and also changes neural crest cell Ca

66 1 (Cavalpha2delta1) protein dysregulation in trigeminal ganglia and associated spinal subnucleus caud

67 opulation that include subsequent defects in trigeminal ganglia assembly.

68 results show that resistance to HSV-1 in the trigeminal ganglia during acute infection is conferred i

69 terms of infectious virus production in the trigeminal ganglia during acute infection, mouse mortali

70 gher levels of ICP0 and lytic transcripts in trigeminal ganglia during establishment of latency, and

71 est cells that will give rise to the cranial trigeminal ganglia express alphaN-catenin and Cadherin-7

72 nd CD8(+) TRM cells within latently infected trigeminal ganglia following virus reactivation.

73 Cultures of trigeminal ganglia from 5-day-old mice were treated with

74 Transcriptome analysis of trigeminal ganglia from latently HSV-1-infected, glutami

75 ll establishment of latency, the fraction of trigeminal ganglia harboring detectable lytic transcript

76 ed extensive neurite growth and branching in trigeminal ganglia neurons in a manner that required sel

77 etected in significantly more neurons in the trigeminal ganglia of latently infected calves than in t

78 nversely, augmenting the amount of CXCL10 in trigeminal ganglia of latently infected CXCL10-deficient

79 pressed in a subset of dorsal root (DRG) and trigeminal ganglia sensory neurons.

80 range of mechano-activated currents in duck trigeminal ganglia than in mouse trigeminal ganglia.

81 periocular disease and increased corneal and trigeminal ganglia titers, although there was no differe

82 d molecular analyses of palisade endings and trigeminal ganglia to determine whether cat palisade end

83 hich HSV-1 reactivation in latently infected trigeminal ganglia was induced by UV-B light, we demonst

84 When explant cocultivation of trigeminal ganglia was performed, the virus was recovere

85 At 62 days postinfection, trigeminal ganglia were excised and profiled by deep seq

86 embryonic day (E)5-14 chick eyefronts and E9 trigeminal ganglia were identified using Western blottin

87 establishes latency primarily in neurons of trigeminal ganglia when only the transcription of the la

88 In trigeminal ganglia with genetically encoded Ca(2+) indic

89 stablishes latency in sensory neurons within trigeminal ganglia, but stress can induce reactivation f

90 neuronal subtypes (A5+ and KH10+) in murine trigeminal ganglia, results which correlate with restric

91 idic protein by glial satellite cells in the trigeminal ganglia, the location of the neuronal cell bo

92 nts in duck trigeminal ganglia than in mouse trigeminal ganglia.

93 ral progenitor cells, in comparison with the trigeminal ganglia.

94 n levels are essential to achieve latency in trigeminal ganglia.

95 ed in sensory neurons of the dorsal root and trigeminal ganglia.

96 ng sensory neurons, primarily located in the trigeminal ganglia.

97 n migratory neural crest cells that form the trigeminal ganglia.

98 genes in acutely and latently infected mouse trigeminal ganglia.

99 ression of inflammatory cytokines within the trigeminal ganglia.

100 R111 readily established latent infection in trigeminal ganglia; however, although the amounts of vir

101 SP release from HNECs, MNECs, and trigeminal ganglial neurons was quantified with EIA.

102 epithelial cells (MNECs) and isolated murine trigeminal ganglial neurons.

103 Both sensory trigeminal ganglion (TG) and sympathetic superior cervic

104 thy1-YFP mouse and determine if they promote trigeminal ganglion (TG) cell neurite growth.

105 Axonal branches of the trigeminal ganglion (TG) display characteristic growth a

106 virus 1 (HSV-1) infection in the tree shrew trigeminal ganglion (TG) following ocular inoculation.

107 KLF15 were frequently expressed in the same trigeminal ganglion (TG) neuron during reactivation and

108 solated mouse dorsal root ganglion (DRG) and trigeminal ganglion (TG) neurons expressing the cold-sen

109 CD8(+) T cells provide immunosurveillance of trigeminal ganglion (TG) neurons that harbor latent HSV-

110 in nonneuronal cells (MRC5) and adult murine trigeminal ganglion (TG) neurons using the Illumina plat

111 The ability to genetically manipulate trigeminal ganglion (TG) neurons would be useful in the

112 nt TRESK subunits in HEK293T cells and mouse trigeminal ganglion (TG) neurons.

113 demonstrate receptor binding sites in rhesus trigeminal ganglion (TG).

114 information, primary sensory neurons in the trigeminal ganglion (Vg) have often been described as en

115 on of calcitonin gene-related peptide in the trigeminal ganglion and c-Fos in the trigeminal nucleus

116 Thus, somatotopy of trigeminal ganglion and nerve organization is only parti

117 sumption that primary sensory neurons of the trigeminal ganglion are sensitive to various combination

118 We hypothesized that the trigeminal ganglion could be one possible site.

119 iability of the labeled DPANs in dissociated trigeminal ganglion cultures using calcium microfluorome

120 ex vivo neurite outgrowth and myelination of trigeminal ganglion explants.

121 Furthermore, we examined if the trigeminal ganglion is protected by the blood-brain barr

122 o2 expression occurs in approximately 26% of trigeminal ganglion neurons and 30% of corneal afferent

123 elated with Cavalpha2delta1 up-regulation in trigeminal ganglion neurons and Vc/C2.

124 VEGF enhanced neurite elongation in isolated trigeminal ganglion neurons in a dose-dependent manner.

125 (HMGA1), was readily detected in a subset of trigeminal ganglion neurons in latently infected calves

126 motes export of endogenous deltaR in primary trigeminal ganglion neurons.

127 Neither the trigeminal ganglion nor the ophthalmic branch of the tri

128 ial dura, using single-unit recording in the trigeminal ganglion of anesthetized male rats.

129 Single-unit recordings made in the trigeminal ganglion of rats were used to test changes in

130 el of chronic orofacial pain; in this model, trigeminal ganglion Panx1 expression and function are ma

131 A 3-dimensional reconstruction of an entire trigeminal ganglion with 2-photon laser scanning fluores

132 ed and uninjured nerves in the skin, soma in trigeminal ganglion, and central terminals in the spinal

133 which resides in the sensory neurons of the trigeminal ganglion, could be stress reactivated to prod

134 resents VZV reactivation, most likely in the trigeminal ganglion, in the absence of clinical herpes z

135 e transport from the application site to the trigeminal ganglion, the numbers of stained DPANs, and t

136 somatosensory neurons of the dorsal root and trigeminal ganglion, the transient receptor potential me

137 likely acquired from VZV reactivation in the trigeminal ganglion.

138 xpression of CGRP and its receptor in rhesus trigeminal ganglion.

139 t precocious neuronal differentiation of the trigeminal ganglion.

140 responses in hundreds of neurons across the trigeminal ganglion.

141 ay, was frequently detected in ORF2-positive trigeminal ganglionic neurons of latently infected, but

142 tion factors are induced by dexamethasone in trigeminal ganglionic neurons within 1.5 h after dexamet

143 r for polymodal nociceptors, suggesting that trigeminal general mucosal innervation carries informati

144 Sensory trigeminal growth cones innervate the cornea in a coordi

145 (Panx1) in various types of pain, including trigeminal hypersensitivity, neuropathic pain and migrai

146 sents a sight-threatening complication after trigeminal impairment.

147 rophysiological evidence for the encoding of trigeminal information at this level of processing is un

148 To our knowledge, the duration for which trigeminal injury may affect corneal structures and func

149 ) strongly projects to the brain stem spinal trigeminal interpolaris nucleus, which contains whisker

150 l pathway, which includes the rostral spinal trigeminal interpolaris, posteromedial thalamic, and ven

151 novel compounds attenuate pain behavior in a trigeminal irritant pain model that is known to rely on

152 e we described the normal development of the trigeminal lemniscal pathway in the mouse.

153 ockout mice have impaired development of the trigeminal-lemniscal pathway.

154 rons could be identified in the brain as the trigeminal mesencephalic root, some Schnauzenorgan trige

155 Neurons in the trigeminal (Mo5), facial (Mo7), ambiguus (Amb), and hypo

156 examined the excitability of ALS-vulnerable trigeminal motoneurons (TMNs) controlling jaw musculatur

157 ive both excitatory and inhibitory inputs to trigeminal motoneurons when optogenetically activated in

158 cting to both the left and right jaw-closing trigeminal motoneurons.

159 or command system, or the electrosensory and trigeminal motor command.

160 ound throughout the ventral main body of the trigeminal motor nucleus but not among the population of

161 organ trigeminal afferents terminated in the trigeminal motor nucleus, suggesting a monosynaptic, pos

162 The present study focuses on the trigeminal motor pathway that controls Schnauzenorgan mo

163 d motor nuclei (e.g., oculomotor, trochlear, trigeminal motor, abducens, and vagal motor nuclei) cont

164 ipsilateral principal sensory nucleus of the trigeminal nerve (PrV) correspond to the whiskers.

165 The principal sensory nucleus of the trigeminal nerve (PrV) relays the facial sensations to t

166 nnervation of the nasal mucosa by monitoring trigeminal nerve activity in patients with IR and health

167 Disordered sensory input from trigeminal nerve afferents, such as aberrant feedback fr

168 thalmic and maxillary divisions of the right trigeminal nerve and cervical spinal nerve afferents.

169 of afferents from the three branches of the trigeminal nerve and from the lingual branch of the hypo

170 Two patients with unilateral trigeminal nerve anesthesia-one following basal skull fr

171 e, the ophthalmic, maxillary, and mandibular trigeminal nerve branches maintain a somatotopic segrega

172 ists of a thin membrane, innervated by three trigeminal nerve branches that project to a specific nuc

173 al tracers to identified pit-organ-supplying trigeminal nerve branches.

174 al ganglion nor the ophthalmic branch of the trigeminal nerve contained cholinergic elements.

175 cleus also showed substantial innervation by trigeminal nerve fibers immunoreactive for calcitonin ge

176 outlier, with more than twice the number of trigeminal nerve fibers than any other species.

177 e to direct depolarization of acid-sensitive trigeminal nerve fibers, for example, polymodal nocicept

178 Effects of polySia removal on trigeminal nerve growth behavior were determined in vivo

179 the emerging fibers of the motor root of the trigeminal nerve in the mouse, which we have called the

180 Stimulation of trigeminal nerve induces pressor response and improves c

181 investigate a potential mechanism underlying trigeminal nerve injury-induced orofacial hypersensitivi

182 Trigeminal nerve lesions at differing levels can result

183 Trigeminal nerve number was by far the largest and also

184 ble of increasing cerebral perfusion, making trigeminal nerve stimulation (TNS) a promising strategy

185 s such as deep brain stimulation, vagus, and trigeminal nerve stimulation are effective only in a fra

186 f injury to the maxillary branch (V2) of the trigeminal nerve to produce constant and long-lasting pr

187 enhancement of the cauda equina nerve roots, trigeminal nerve, and pachymeninges.

188 ity properties in the root entry zone of the trigeminal nerve, the spinal trigeminal tract, or the ve

189 tion, to ablate the ophthalmic branch of the trigeminal nerve.

190 essure, as induced by occlusal loads, on the trigeminal nerve.

191 alization of DPANs in all 3 divisions of the trigeminal nerve.

192 rovascular canals, that include parts of the trigeminal nerve; many branches of this complex terminat

193 Trigeminal nerves collecting sensory information from th

194 Injury to the trigeminal nerves may cause maladaptive changes in synap

195 nt stress, local constriction, and injury in trigeminal nerves may contribute to the pathogenesis of

196 es between the peripheral electrosensory and trigeminal nerves, but these senses remain separate in t

197 y to the infraorbital nerve, a branch of the trigeminal nerves, led to synaptic ultrastructural chang

198 However little is known about how trigeminal neuralgia (TN), a condition in which trigemin

199 e attacks with autonomic symptoms (SUNA) and trigeminal neuralgia are considered different disorders,

200 therapeutic overlap between SUNCT, SUNA, and trigeminal neuralgia has challenged this traditional vie

201 ety and efficacy of BIIB074 in patients with trigeminal neuralgia in a phase 2a study.

202 ed investigation of BIIB074 in patients with trigeminal neuralgia in future clinical trials.

203 Trigeminal Neuralgia is a disorder that is characterized

204 Current standard of care for trigeminal neuralgia is treatment with the sodium channe

205 ble patients aged 18-80 years with confirmed trigeminal neuralgia received open-label, BIIB074 150 mg

206 ological evidence on whether SUNCT, SUNA and trigeminal neuralgia should be considered separate entit

207 simulations of Carbamazepine in treatment of Trigeminal Neuralgia.

208 dromes have shown striking similarities with trigeminal neuralgia.

209 ader nosological concept of SUNCT, SUNA, and trigeminal neuralgia.

210 hophysiological basis between SUNCT/SUNA and trigeminal neuralgia.

211 the adverse events such as xerophthalmia and trigeminal neuralgia.

212 a substrates in vitro inhibited outgrowth of trigeminal neurites and promoted their fasciculation.

213 Removal of polySia on trigeminal neurites inhibited neurite outgrowth and caus

214 trast, proNGF does not promote the growth of trigeminal neurites.

215 ns in vivo but surprisingly fail to activate trigeminal neuron monocultures.

216 visually foraging bird, the majority of duck trigeminal neurons are mechanoreceptors that express the

217 Knockdown of Piezo2 in duck trigeminal neurons attenuates mechano current with inter

218 Trigeminal neurons innervating gingivomucosa were identi

219 dy aims to morphometrically characterize rat trigeminal neurons, which express TLR4, and to investiga

220 odontitis upregulates TLR4 expression in the trigeminal neurons.

221 between human HaCaT keratinocytes and mouse trigeminal neurons.

222 ensory neuron-specific GCaMP3 imaging with a trigeminal neuropathic pain model, we detected robust ne

223 In 22 subjects with painful trigeminal neuropathy and 44 pain-free controls, voxel-b

224 ventral trigeminothalamic tracts in painful trigeminal neuropathy subjects compared with controls.

225 expression of ecto-5'-nucleotidase (CD73) in trigeminal nociceptive neurons and their axonal fibers,

226 y, but not exclusively, expressed in smaller trigeminal nociceptive neurons in the rat.

227 ng extracellular adenosine generation in the trigeminal nociceptive pathway.

228 unctional specialization of DPANs within the trigeminal nociceptive system and 2) to recognize exclus

229 thogenesis of periodontitis by activation of trigeminal nociceptors through TLR4 should be explored.

230 gic neurotransmission to trigger peptidergic trigeminal nociceptors, which link SCCs to the neurogeni

231 the face project to multiple regions of the trigeminal nuclear complex in the brainstem.

232 ry information, and the spinal and principal trigeminal nuclei, which integrate somatosensory informa

233 chlear nucleus, but not in the vestibular or trigeminal nuclei.

234 in the laterally adjacent mediodorsal spinal trigeminal nucleus (DMSp5), but this trigeminal activati

235 se, which we have called the interfascicular trigeminal nucleus (IF5).

236 has been largely restricted to the principal trigeminal nucleus (PrV) and its ascending projections t

237 The region encompassing the spinal trigeminal nucleus also displayed increased regional hom

238 he spinal cord dorsal horn and caudal spinal trigeminal nucleus and in the nucleus of the solitary tr

239 et neurons in the spinal cord and the spinal trigeminal nucleus caudalis (SpVc).

240 d the contribution of 5-HT3 receptors in the trigeminal nucleus caudalis (Vc), the homolog of the spi

241 in the trigeminal ganglion and c-Fos in the trigeminal nucleus caudalis.

242 natomical changes were present in the spinal trigeminal nucleus in subjects with chronic orofacial ne

243 ized trigeminovascular neurons in the spinal trigeminal nucleus of anesthetized male and female rats.

244 rom wide dynamic range neurons in the spinal trigeminal nucleus of anesthetized rats.

245 novel region of trigeminal brainstem, spinal trigeminal nucleus pars muralis, which contains a class

246 Stochasticity in the trigeminal nucleus pathway allows unpredictable turning

247 reticulospinal neurons are excited through a trigeminal nucleus pathway and swimming starts first on

248 to 'win' because excitation from a shorter, trigeminal nucleus pathway becomes reliable and can init

249 sized there were star patterns in the spinal trigeminal nucleus subnuclei interpolaris and caudalis.

250 neurons in the caudal division of the spinal trigeminal nucleus that project to the principal nucleus

251 ntine raphe nucleus, gracile nucleus, spinal trigeminal nucleus, and spinal cord.

252 und in many other regions such as the spinal trigeminal nucleus, cerebellum and basal ganglia.

253 ng pain pathway, including within the spinal trigeminal nucleus, somatosensory thalamus, thalamic ret

254 mean diffusivity decreases within the spinal trigeminal nucleus, specifically the subnucleus oralis.

255 icroscopic immunochemistry in the rat spinal trigeminal nucleus, we show that PKCgamma-immunoreactivi

256 anglion, and central terminals in the spinal trigeminal nucleus.

257 s orofacial nociceptor afferents, the spinal trigeminal nucleus.

258 and a lateral band of the principal sensory trigeminal nucleus.

259 inferior olive, abducens nucleus, and motor trigeminal nucleus; protein coexpression of CLR and RAMP

260 Direct chemical excitation of trigeminal pain fibers by capsaicin evokes neurogenic in

261 results indicate that the input stage of the trigeminal pathway has extraordinary spike-timing precis

262 asal thalamus, suggesting that the ascending trigeminal pathways in birds and mammals are more simila

263 Schnauzenorgan trigeminal primary afferent projections extend throughou

264 We found that spike-timing precision of trigeminal primary afferents in rats and mice is limited

265 ether cat palisade endings are a cholinergic trigeminal projection.

266 sive array of whiskers is matched by a large trigeminal representation in the brainstem with well-def

267 The strongest potentiators of the trigeminal response were carbonyl compounds octanal, non

268 Trigeminal sensations can arise from the direct stimulat

269 ncentrations of most odors typically provoke trigeminal sensations in vivo but surprisingly fail to a

270 rect interconnections were found between the trigeminal sensory and electromotor command system, or t

271 TTD and the afferents from the syrinx to the trigeminal sensory column.

272 eurons located in the oralis division of the trigeminal sensory complex.

273 controls Schnauzenorgan movement and on its trigeminal sensory innervation and central representatio

274 Intranasal trigeminal sensory input, often perceived as a burning,

275 localized within developing eyefronts and on trigeminal sensory nerves.

276 projections extend throughout the descending trigeminal sensory nuclei, and a few fibers enter the fa

277 The next group of mice underwent either trigeminal stereotactic electrolysis (TSE), or sham oper

278 geminal neuralgia (TN), a condition in which trigeminal stimulation triggers paroxysmal facial pain,

279 r information rapidly even in the absence of trigeminal stimulation.

280 l imaging data suggest that the influence of trigeminal stimuli on odor information processing may oc

281 se activity in the nociceptive lamina of the trigeminal subnucleus caudalis (TSNC) in the brainstem.

282 al medullary and spinal dorsal horn from the trigeminal subnucleus caudalis to C2.

283 issae, the principal sensory nucleus, spinal trigeminal subnucleus interpolaris, and subnucleus cauda

284 istics that differentiate nociception in the trigeminal system from that in the somatic system.

285 Our knowledge of the avian sensory trigeminal system has been largely restricted to the pri

286 chemosensors linking the environment and the trigeminal system via ATP signaling.

287 us contains third-order relay neurons of the trigeminal system, and animal models as well as prelimin

288 y the classical feedforward model of the rat trigeminal system.

289 involve somatosensory dysfunction beyond the trigeminal system.

290 numerous receptors expressed on terminals of trigeminal (TG) nociceptive afferent neurons.

291 tic GABAAreceptor-mediated inhibition in the trigeminal thalamocortical pathway of mice lacking activ

292 brain, the nucleus of the lateral descending trigeminal tract (LTTD).

293 er, the role of the nuclei of the descending trigeminal tract (nTTD) in this scenario is unclear, par

294 oth the PrV and the nuclei of the descending trigeminal tract (nTTD), have only been performed in pig

295 ganglion neuron rostrocaudal segregation and trigeminal tract somatotopy are similar to mouse.

296 he interpolaris subnucleus of the descending trigeminal tract, a caudolateral region of the nucleus t

297 try zone of the trigeminal nerve, the spinal trigeminal tract, or the ventral trigeminothalamic tract

298 sce into a nucleus adjacent to the ascending trigeminal tract.

299 e postherpetic itch, brachioradial pruritus, trigeminal trophic syndrome, and ischaemic stroke-relate

300 land, and the remarkable abilities of their trigeminal whisker system.