ライフサイエンスコーパス: trigeminal

1 (K2P) channels, are clustered at NRs of rat trigeminal Abeta-afferent nerves with a density over 3,0

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

3 Orosensory thermal trigeminal afferent neurons respond to cool, warm, and n

4 nvestigate changes in response properties of trigeminal afferent neurons.

5 tes and reduced monocyte infiltration in the trigeminal afferent pathway.

6 e drugs, and activation and sensitisation of trigeminal afferents by meningeal inflammatory stimuli a

7 Stimulation of trigeminal afferents induced short-latency (SAI) but not

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

9 es innervated by functional rapidly adapting trigeminal afferents.

10 o tectal targets, just like the auditory and trigeminal AI zones project back to their respective sub

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

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

13 s and muscle afferents are segregated in the trigeminal and facial nerves, respectively.

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

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

16 projections of pruriceptive and nociceptive trigeminal and spinal neurons.

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

18 This study shows that the trigeminal- and vagus systems interconnect anatomically

19 l posterior clinoid processes and persistent trigeminal artery.

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

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

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

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

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

25 entrations had significantly lower perceived trigeminal burn intensity.

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

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

28 the concentration of carbonyl compounds and trigeminal burn.

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

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

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

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

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

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

35 Trigeminal denervation resulted in epithelial defects wi

36 fectious virus during acute infection in the trigeminal ganglia (TG) and brain stem compared to the c

37 s reduced by more than 93% in the cornea and trigeminal ganglia (TG) and by 99% in the liver of tamox

38 is a consequence of viral reactivations from trigeminal ganglia (TG) and occurs almost exclusively in

39 is study, reactivation was quantified in the trigeminal ganglia (TG) and the brain stem from the same

40 l, or nasal cavities, sensory neurons within trigeminal ganglia (TG) are an important site for latenc

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

42 ease in the number of viral genomes in mouse trigeminal ganglia (TG) infected with DeltaCTRL2, indica

43 from neurons in sensory ganglia such as the trigeminal ganglia (TG) is influenced by virus-specific

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

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

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

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

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

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

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

51 implex virus 1 (HSV-1) leads to infection of trigeminal ganglia (TG), typically followed by the estab

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

53 D8(+) T(RM) cells in both the cornea and the trigeminal ganglia (TG).

54 1 (BoHV-1) latency is sensory neurons within trigeminal ganglia (TG).

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

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

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

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

59 oding ORF63) in naturally VZV-infected human trigeminal ganglia (TG).

60 lifelong latent infections in neurons within trigeminal ganglia (TG); periodically, reactivation from

61 ration approaches and ganglion types [DRG vs trigeminal ganglia (TG)].

62 Replication in trigeminal ganglia and periocular tissue was promoted by

63 infectious virus was recovered from both the trigeminal ganglia and the brain stem of latently infect

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

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

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

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

68 ried out in vivo confocal calcium imaging of trigeminal ganglia in which neurons express GCaMP3 or GC

69 enes and cellular infiltrates in the eye and trigeminal ganglia of infected mice was less than that i

70 nes that contribute to the pain state in the trigeminal ganglia of injured mice.

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

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

73 protected ASYMP HLA transgenic rabbits, the trigeminal ganglia of non-protected SYMP HLA transgenic

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

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

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

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

78 and the frequency of virus reactivation from trigeminal ganglia were unaffected by US11 deletion, alt

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

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

81 Within trigeminal ganglia, afferents innervating craniofacial m

82 Virus was detected sequentially in the lip, trigeminal ganglia, and brain of infected animals.

83 ral proteins were detected in neurons of the trigeminal ganglia, but a cellular source of infectious

84 eactivation of herpes simplex virus 1 in the trigeminal ganglia, leading to dissemination of virus to

85 orneal scarring, latency-reactivation in the trigeminal ganglia, or T-cell exhaustion.

86 ral presence of latent viral genomes in both trigeminal ganglia, while for any given patient the dise

87 imary sensory neurons of the dorsal root and trigeminal ganglia.

88 mouse sensory neurons of the dorsal root and trigeminal ganglia.

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

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

91 genes in acutely and latently infected mouse trigeminal ganglia.

92 ression of inflammatory cytokines within the trigeminal ganglia.

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

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

95 of infectious virus were recovered from the trigeminal ganglia.

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

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

98 nal nerve (CN V) differentiation and altered trigeminal ganglion (CNgV) cellular composition prefigur

99 Nociceptors located in the trigeminal ganglion (TG) and DRG are the primary sensors

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

101 dding during reactivation from latency using trigeminal ganglion (TG) explants from Swiss Webster mic

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

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

104 r biology.SIGNIFICANCE STATEMENT The DRG and trigeminal ganglion (TG) provide sensory information fro

105 ts a specific transcriptome signature in the trigeminal ganglion (TG) that includes Rictor, the rapam

106 cornea, the virus enters latency within the trigeminal ganglion (TG), from which it can reactivate t

107 dental pulpal afferent (DPA) neurons of the trigeminal ganglion (TG).

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

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

110 deficient in Magel2, a PWS gene, within the trigeminal ganglion and regions that are anatomically re

111 The cornea is extensively innervated by trigeminal ganglion cold thermoreceptor neurons expressi

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

113 nt to feeding behavior and innervated by the trigeminal ganglion including the lateral periodontium,

114 ) to protect and regenerate isolated primary trigeminal ganglion neuronal cells (TGNC).

115 owever, the mechanoreceptive and nociceptive trigeminal ganglion neurons and the visual sensory retin

116 he periphery, where dorsal root ganglion and trigeminal ganglion neurons feed pain information into t

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

118 Recordings from primary sensory trigeminal ganglion neurons show that these neurons exhi

119 Here we recorded responses in mouse trigeminal ganglion neurons to investigate interactions

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

121 etected by polymodal and pure mechanosensory trigeminal ganglion neurons.

122 s, which in turn modulate gene expression in trigeminal ganglion neurons.

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

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

125 We established a co-culture system of trigeminal ganglion sensory neurons and vascular endothe

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

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

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

129 Here we show that the trigeminal ganglion, which provides sensory innervation

130 y, originating primarily from neurons in the trigeminal ganglion.

131 responses in hundreds of neurons across the trigeminal ganglion.

132 likely acquired from VZV reactivation in the trigeminal ganglion.

133 ker-sensitive primary sensory neurons in the trigeminal ganglion.

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

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

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

137 ed inhibition of the Vc, implying convergent trigeminal input contributed to such activity.

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

139 esting that the changes may ascend along the trigeminal lemniscus pathway.

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

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

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

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

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

145 eral, reciprocal connections between the two trigeminal motor nuclei and between the trigeminal senso

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

147 Prominent afferent input to the trigeminal motor nucleus originates from the nucleus lat

148 Neurotracer injections into the trigeminal motor nucleus revealed bilateral, reciprocal

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

150 about central pathways originating from the trigeminal motor nucleus.

151 dy focuses on the central connections of the trigeminal motor system to elucidate premotor centers co

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

153 Divergent trigeminal nerve (CN V) differentiation and altered trig

154 t prefigure disrupted differentiation of the trigeminal nerve (CN V), a cranial nerve essential for s

155 The trigeminal nerve (cranial nerve V), along with other cra

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

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

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

159 s of partial infraorbital transection of the trigeminal nerve at the cellular level.

160 uropeptides and their release from meningeal trigeminal nerve endings in the mechanism of migraine, b

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

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

163 Stimulation of trigeminal nerve induces pressor response and improves c

164 of this study showed that the stimulation of trigeminal nerve modulates both sympathetic and parasymp

165 erent regions of the brain via olfactory and trigeminal nerve pathways.

166 timulation of low threshold afferents in the trigeminal nerve produced a clear SAI (P < 0.05) when th

167 anscranial magnetic stimulation and external trigeminal nerve stimulation (all with regulatory cleara

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

169 Trigeminal nerve stimulation also decreased systemic inf

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

171 Trigeminal nerve stimulation elicited strong synergistic

172 Furthermore, trigeminal nerve stimulation generated sympathetically m

173 Trigeminal nerve stimulation is currently being evaluate

174 The effects of trigeminal nerve stimulation on survival rate, autonomic

175 t volume expansion with fluid resuscitation, trigeminal nerve stimulation significantly attenuated sy

176 Trigeminal nerve stimulation significantly increased the

177 The survival rate at 60 minutes was 90% in trigeminal nerve stimulation treatment group whereas 0%

178 omly assigned to either control, vehicle, or trigeminal nerve stimulation treatment groups.

179 Trigeminal nerve stimulation was explored as a novel res

180 arch examining the therapeutic mechanisms of trigeminal nerve stimulation.

181 that human OSCC tumors sensitize peripheral trigeminal nerve terminals, providing a unique opportuni

182 timulation of the infraorbital branch of the trigeminal nerve that enables future research examining

183 interface for the infraorbital branch of the trigeminal nerve utilizing a thin film (TF) nerve cuff c

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

185 driven orofacial pain, acute activity of the trigeminal nerve, or TMJ tissue degeneration and/or dama

186 ral and nasal papillae are innervated by the trigeminal nerve, the gill pore papillae are innervated

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

188 ajor organs, along with the nasal tissue and trigeminal nerve, were harvested to assess the biodistri

189 argets along extracellular components of the trigeminal nerve.

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

191 ntegral role for the neuropeptide-containing trigeminal nerve.

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

193 higher (80.0%) compared to the asymptomatic trigeminal nerves (56.9%).

194 cquisitions of the cisternal segments of the trigeminal nerves and vessels.

195 Trigeminal nerves collecting sensory information from th

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

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

198 of neurovascular contact on the symptomatic trigeminal nerves was higher (80.0%) compared to the asy

199 otal of 165 symptomatic and 153 asymptomatic trigeminal nerves were analysed.

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

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

202 lie in the trajectories of the olfactory and trigeminal nerves.

203 imaged its localization within the brain and trigeminal nerves.

204 TEMENT Prior data suggest that gustatory and trigeminal neural pathways intersect and overlap in the

205 arteriovenous malformations (1089 [22.2%]), trigeminal neuralgia (565 [11.5%]), pituitary adenomas (

206 in oral medicine and found it effective for trigeminal neuralgia (category A) and probably effective

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

208 l provide further insight into the causes of trigeminal neuralgia and its pathophysiology.

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

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

211 Trigeminal neuralgia is a very painful neurological cond

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

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

214 he past decade has offered new insights into trigeminal neuralgia symptomatology, pathophysiology, an

215 aetiological factor between SUNCT, SUNA and trigeminal neuralgia thereby further expanding the overl

216 radiosurgery for arteriovenous malformation, trigeminal neuralgia, or benign intracranial tumours, wh

217 lockers indicates a therapeutic overlap with trigeminal neuralgia, suggesting that sodium channels dy

218 simulations of Carbamazepine in treatment of Trigeminal Neuralgia.

219 Trigeminal neuron firing rate increases with airspeed, i

220 ed currents of different kinetics in corneal trigeminal neurons and contributes to transduction of me

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

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

223 caused PAR(2)-dependent hyperexcitability of trigeminal neurons from WT female mice.

224 cant but incomplete overlap between afferent trigeminal neurons that respond to oral thermal stimulat

225 dedicated population of about 50 specialized trigeminal neurons.

226 as bruxism, temporomandibular disorders, and trigeminal neuropathic pain.

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

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

229 to assess the prevalence and significance of trigeminal neurovascular contact in a large cohort of co

230 le aetiological and therapeutic relevance of trigeminal neurovascular contact in short lasting unilat

231 in gene-related peptide expression and basal trigeminal nociception.

232 l-established paradigm for functional MRI of trigeminal nociception.

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

234 ng extracellular adenosine generation in the trigeminal nociceptive pathway.

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

236 eurons can receive afferent projections from trigeminal nuclei and fire to oral nociceptive stimuli t

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

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

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

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

241 dal pressor area, and lamina I of the spinal trigeminal nucleus and all levels of the spinal cord.

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

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

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

245 afferents project to a wide area within the trigeminal nucleus complex, and central sensitization of

246 te activation of second-order neurons in the trigeminal nucleus complex, which leads to the maintenan

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

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

249 Stochasticity in the trigeminal nucleus pathway allows unpredictable turning

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

251 rents (nucleus of the solitary tract, spinal trigeminal nucleus, and dorsal horn [DH]).

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

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 s orofacial nociceptor afferents, the spinal trigeminal nucleus.

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

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

258 tectal related areas, sparing auditory, and trigeminal ones.

259 Many of these thermosensitive trigeminal orosensory afferent neurons also respond to c

260 th pulp inflammatory pain and other forms of trigeminal pain.

261 nts of boutons across premotor nuclei spinal trigeminal pars oralis (SpVO) and interpolaris rostralis

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

263 form parallel pathways to distinct pools of trigeminal premotor neurons that coordinate motor action

264 In trigeminal primary sensory neurons, we detected single-c

265 xpression of TRPM8 channels in these injured trigeminal primary sensory neurons.SIGNIFICANCE STATEMEN

266 We were further able to show that silencing trigeminal projections inhibited nociceptive activity in

267 piked to Vc pulse stimulation, implying that trigeminal projections reach PbN gustatory neurons.

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

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

270 contact and the point of contact around the trigeminal root were respectively proximal in 82.7% (67/

271 nly LY344864 induced neuroplastic changes in trigeminal sensory afferents, increasing calcitonin gene

272 two trigeminal motor nuclei and between the trigeminal sensory and motor nuclei by bilateral labelin

273 eives an important innervation from both the trigeminal sensory and motor systems.

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

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

276 her two-pore-domain K+ channels, to increase trigeminal sensory neuron excitability, leading to a mig

277 ring the transcriptomes of cancer-associated trigeminal sensory neurons with those of endogenous neur

278 ngs suggest that vascular compression of the trigeminal sensory root, may be a common aetiological fa

279 ges, neuroinflammation and activation of the trigeminal sensory system.

280 ted from the vagus trajectory and joined the trigeminal spinal nucleus (Sp5) and the sp5.

281 -images showed these striae to intersect the trigeminal spinal tract (sp5) in the lateral medulla.

282 ear SAI (P < 0.05) when the interval between trigeminal stimulation and transcranial magnetic stimula

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

284 As a response to painful trigeminal stimulation, activation of the hypothalamus w

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

286 f an oral somatosensory region of the spinal trigeminal subnucleus caudalis (Vc), which projects to t

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

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

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

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

291 involve somatosensory dysfunction beyond the trigeminal system.

292 ion is well established for the auditory and trigeminal systems, the arcopallial subdivision related

293 e connections between the electrosensory and trigeminal systems.

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

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

296 Capsaicin sensitizes warm trigeminal thermoreceptors and orosensory nociceptors; m

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

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

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

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

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

302 in between previously described auditory and trigeminal zones.