ライフサイエンスコーパス: trigeminal ganglia

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

2 stablishes latency in sensory neurons within trigeminal ganglia.

3 s lifelong latency in sensory neurons within trigeminal ganglia.

4 of infectious virus were recovered from the trigeminal ganglia.

5 ocalize with the capsaicin receptor TRPV1 in trigeminal ganglia.

6 expression of VEGF and VEGF receptors in the trigeminal ganglia.

7 at two inflammatory sites, namely cornea and trigeminal ganglia.

8 s performed with immunohistochemistry on rat trigeminal ganglia.

9 of reactivation from latently infected mouse trigeminal ganglia.

10 educed in the double mutant Brn3a-/-;Klf7-/- trigeminal ganglia.

11 rkA enhancer is inactive in Brn3a-/-;Klf7-/- trigeminal ganglia.

12 Trk(+) neurons are lost in Brn3a-/-;Klf7-/- trigeminal ganglia.

13 ation in the eye and explant reactivation in trigeminal ganglia.

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

15 ed by nociceptive neurons in dorsal root and trigeminal ganglia.

16 y in the mouse corneal epithelium and to the trigeminal ganglia.

17 s that were overexpressed in dorsal root and trigeminal ganglia.

18 and viral genome loads in rabbit corneas and trigeminal ganglia.

19 infected the olfactory bulbs, brain, and the trigeminal ganglia.

20 latently infected versus mock-infected mouse trigeminal ganglia.

21 s, olfactory placode, eye primordia, and the trigeminal ganglia.

22 g latent infection in sensory neurons of the trigeminal ganglia.

23 neurons of the dorsal root ganglia (DRG) and trigeminal ganglia.

24 s equivalent to wild-type replication in the trigeminal ganglia.

25 ithin the retina, inner ear, dorsal root and trigeminal ganglia.

26 lifelong latent infection in neurons of the trigeminal ganglia.

27 s of sensory ganglia, including those of the trigeminal ganglia.

28 from the membrane fractions of adult DRG and trigeminal ganglia.

29 se specifically in neuronal cells within the trigeminal ganglia.

30 ter neurons of dorsal root ganglia (DRG) and trigeminal ganglia.

31 and KOSV2R from explanted latently infected trigeminal ganglia.

32 SV-1) and type 2 (HSV-2) genomes in 15 human trigeminal ganglia.

33 was enhanced by up to 1,000-fold in eyes and trigeminal ganglia.

34 in the HSV-1-infected neurons in ipsilateral trigeminal ganglia.

35 r sensory neurons of dorsal root ganglia and trigeminal ganglia.

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

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

38 genes in acutely and latently infected mouse trigeminal ganglia.

39 ression of inflammatory cytokines within the trigeminal ganglia.

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

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

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

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

44 the spinal cord and sensory (dorsal root and trigeminal) ganglia.

45 re being present in 17- than 17 N/H-infected trigeminal ganglia (6.22% versus 3.5%) and a decrease in

46 termine whether neurons in latently infected trigeminal ganglia activated the ICP4 promoter.

47 Within trigeminal ganglia, afferents innervating craniofacial m

48 cumulation of HSV-2-specific CD8+ T cells in trigeminal ganglia after challenge with wild-type virus.

49 e viruses reactivated from latently infected trigeminal ganglia, albeit inefficiently, and most virus

50 n nociceptive neurons of the dorsal root and trigeminal ganglia allowed us to test this concept.

51 NA was readily detectable in the three human trigeminal ganglia analyzed, we failed to detect any VZV

52 etween stages 8 and 9 resulted in diminished trigeminal ganglia and absence of corneal innervation.

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

54 1 (Cavalpha2delta1) protein dysregulation in trigeminal ganglia and associated spinal subnucleus caud

55 Virus titers were elevated in the trigeminal ganglia and brain stem with virus disseminati

56 ral replication in the eye and spread to the trigeminal ganglia and brain.

57 P release was inhibited by 50% (p < 0.05) in trigeminal ganglia and by 26% (p < 0.05) in dental pulp

58 beta-galactosidase-labeled cells in trigeminal ganglia and cerebral cortex of ICP0 and ICP27

59 tivity of capsaicin-sensitive nociceptors in trigeminal ganglia and dental pulp.

60 ty of capsaicin-sensitive nociceptors in the trigeminal ganglia and dental pulp.

61 mportantly, Cdk5 activity was reduced in the trigeminal ganglia and DRG of 14-day-old TGF-beta1 knock

62 F-beta signaling is significantly reduced in trigeminal ganglia and DRG.

63 d staining for VEGF and its receptors in the trigeminal ganglia and for VEGFR1, VEGFR2, and neuropili

64 KOSV2R in cell culture, murine corneas, and trigeminal ganglia and had a reactivation frequency simi

65 mitters within the orofacial division of the trigeminal ganglia and in development of cutaneous allod

66 f VEGF and its receptors was examined in the trigeminal ganglia and in the cornea by RT-PCR, immunohi

67 sory neurons in retina, dorsal root ganglia, trigeminal ganglia and inner ear.

68 le TrkA expression is unaffected in Brn3a-/- trigeminal ganglia and only slightly decreased in Klf7-/

69 Replication in trigeminal ganglia and periocular tissue was promoted by

70 ific CD8(+) T cells in DLN, conjunctiva, and trigeminal ganglia and reduced HSV-1 replication in tear

71 3.1, p2rx3.2 and p2rx8 were expressed in the trigeminal ganglia and subsets of Rohon-Beard neurons.

72 t VEGF and VEGF receptors are present in the trigeminal ganglia and that abrogation of VEGF signaling

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

74 l sensory neurons of dorsal root ganglia and trigeminal ganglia and the nonmyelinated axons that aris

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

76 d the titers of HSV-IL-2 in the tears, eyes, trigeminal ganglia, and brains of infected mice, so that

77 cant decrease in replication in the corneas, trigeminal ganglia, and brains, as well as a significant

78 igeminal pathway including the whisker pads, trigeminal ganglia, and brainstem were cultured in serum

79 These splicing events occur exclusively in trigeminal ganglia, and not in dorsal root ganglia, ther

80 e expression within the dorsal root ganglia, trigeminal ganglia, and olfactory epithelium, and less i

81 nduces higher levels of apoptotic neurons in trigeminal ganglia, and ORF2 interferes with apoptosis.

82 utation enhanced virus growth in the cornea, trigeminal ganglia, and periocular skin following cornea

83 te gene expression with replication in eyes, trigeminal ganglia, and periocular tissue.

84 cranial ganglia, including epibranchial and trigeminal ganglia, and sensory structures, the ear, nos

85 in ngn1 domains of the midbrain, hindbrain, trigeminal ganglia, and ventral-neural tube appear redun

86 he basal and KCl-evoked release of SP within trigeminal ganglia are greatly increased on the inflamed

87 ssion in neuronal cell bodies located in the trigeminal ganglia, as well as in their proximal and dis

88 opulation that include subsequent defects in trigeminal ganglia assembly.

89 Reporter activity rose in the trigeminal ganglia at 60 h and peaked at 72 h, concomita

90 crest-derived neurons in the dorsal root and trigeminal ganglia at any stage, suggesting either that

91 ed in ciliary ganglia at E6, subsequently in trigeminal ganglia at E9, and in vestibular ganglia at E

92 ugh 240 postinoculation in latently infected trigeminal ganglia before and at 22 h after hyperthermic

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

94 eurons of the dorsal root ganglia (DRGs) and trigeminal ganglia, but its roles in cold and mechanotra

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

96 vitro, VEGF promoted the growth of explanted trigeminal ganglia by 91%.

97 FACS analysis revealed CD8+ T cells in the trigeminal ganglia by day 7, with more being present in

98 tified the latent viral loads in dissociated trigeminal ganglia by real-time PCR, the numbers of infi

99 k HSV-1 reactivation from latency in ex vivo trigeminal ganglia cultures through production of IFN-ga

100 The trigeminal ganglia differentiate in part from specialize

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

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

103 (LR) RNA, which is alternatively spliced in trigeminal ganglia during acute infection.

104 viral protein 16) and viral load in eyes and trigeminal ganglia during acute infection.

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

106 is and leukocyte infiltration in corneas and trigeminal ganglia during primary HSV-1 infection of mic

107 s have observed a lack of apoptosis in HSV-1 trigeminal ganglia even in the presence of cytotoxic imm

108 VEGF-mediated nerve growth was measured in a trigeminal ganglia explant assay.

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

110 In rabbit trigeminal ganglia, extensive apoptosis occurred with LA

111 that occur in cellular mRNA levels in mouse trigeminal ganglia following explantation, a stimulus th

112 y techniques that SP is also released within trigeminal ganglia following intraganglionic application

113 nnot establish detectable infection in mouse trigeminal ganglia following intranasal and ocular inocu

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

115 on of these viruses was examined in eyes and trigeminal ganglia for 1-7 d after corneal inoculation i

116 Analysis of latently infected human trigeminal ganglia for 66-pk expression by reverse trans

117 Here, using real-time PCR, we analyzed 28 trigeminal ganglia from 14 humans for RNA corresponding

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

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

120 ead, which was seen in the eye (from day 1), trigeminal ganglia (from day 2), and brain (from day 3)

121 CD8+ T cells in both 17- and 17 N/H-infected trigeminal ganglia had undergone apoptosis.

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

123 In murine trigeminal ganglia harvested during HSV latency, 25% of

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

125 brain, and virtually complete destruction of trigeminal ganglia in mice that may ultimately succumb t

126 wing axons of the ophthalmic branch from the trigeminal ganglia in p75 -/- embryos.

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

128 d caspase-3 activation in sciatic nerves and trigeminal ganglia indicates that Schwann cell hyperplas

129 Our findings demonstrate that the trigeminal ganglia innervating the star are enriched in

130 nglia and only slightly decreased in Klf7-/- trigeminal ganglia, it is severely reduced in the double

131 essed 8.4-kb LAT was not detected in porcine trigeminal ganglia latently infected with this novel rec

132 Deep sequencing of human trigeminal ganglia latently infected with two pathogenic

133 ex RT-PCR analysis to mRNA extracted from 26 trigeminal ganglia latently infected with VZV and one co

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

135 ied a fifth HSV-1 miRNA in latently infected trigeminal ganglia, miR-H6, which derives from a previou

136 hus, adenoviral gene transfer can be used in trigeminal ganglia neurons for studying the mechanisms o

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

138 le agonists and capsaicin-evoked currents in trigeminal ganglia neurons under normal and phosphorylat

139 ime-dependent up-regulation of TRPA1 mRNA in trigeminal ganglia neurons, as detected by real-time RT-

140 GRP release, was localized in cell bodies of trigeminal ganglia neurons.

141 ists (butaprost and sulprostone) in cultured trigeminal ganglia neurons.

142 mustard oil (MO)-evoked TRPA1 activation in trigeminal ganglia neurons.

143 in the functional up-regulation of TRPA1 in trigeminal ganglia neurons.

144 promoter activity in primary cultures of rat trigeminal ganglia neurons.

145 In trigeminal ganglia, neurons expressing trkB receptor wer

146 ulations of neurons and satellite cells from trigeminal ganglia of 18 humans who had previously had a

147 s-induced apoptosis both in vitro and in the trigeminal ganglia of acutely infected rabbits.

148 At the RNA level, trigeminal ganglia of artemin overexpresser mice (ART-OE

149 at lower levels of viral DNA were present in trigeminal ganglia of calves infected with the LR mutant

150 ion, BHV-1-positive neurons were detected in trigeminal ganglia of calves infected with the wt but no

151 Sensory neurons in the dorsal root and trigeminal ganglia of Hmx1dm/dm mouse embryos have no de

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

153 T cells resulted in decreased latency in the trigeminal ganglia of infected mice.

154 903 induces increased levels of apoptosis in trigeminal ganglia of infected rabbits compared to LAT+

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

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

157 In trigeminal ganglia of latently infected calves, an sncRN

158 herpesvirus 1 is abundantly expressed in the trigeminal ganglia of latently infected calves.

159 encoded within the LR gene are expressed in trigeminal ganglia of latently infected calves.

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

161 In trigeminal ganglia of mice acutely infected with the wil

162 ble to replicate efficiently in the eyes and trigeminal ganglia of mice during acute infection, to ef

163 fied 85 genes with changed expression in the trigeminal ganglia of mice lacking Brn3a, a transcriptio

164 of infected mice nor can it reactivate from trigeminal ganglia of mice latently infected by CJ83193

165 ed that both LAT sRNAs were expressed in the trigeminal ganglia of mice latently infected with an HSV

166 (RT-PCR) in homogenates of latently infected trigeminal ganglia of mice.

167 f the neuropeptide neuromedin B (NMB) in the trigeminal ganglia of mice.

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

169 ribution of such antibody in the corneas and trigeminal ganglia of the mice was then investigated by

170 expression patterns of each Trk receptor in trigeminal ganglia of wild type and NT-3 mutants between

171 results from reactivation of latent virus in trigeminal ganglia, often following immunosuppression or

172 the yields of challenge HSV in the eyes and trigeminal ganglia on days 3, 5, and 7 postchallenge.

173 eplicates transiently but barely invades the trigeminal ganglia or brain, which is a difference from

174 le or no detectable activity was observed in trigeminal ganglia or periocular tissue.

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

176 dergone apoptosis in 17- and 17 N/H-infected trigeminal ganglia, respectively.

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

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

179 ever, reactivated efficiently from explanted trigeminal ganglia, showing that vhs is dispensable for

180 -beta RNA expression was readily detected in trigeminal ganglia (TG) 4 days after infection.

181 V type 1 specifically establishes latency in trigeminal ganglia (TG) after corneal infection of mice.

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

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

184 DNA, was significantly reduced in both mouse trigeminal ganglia (TG) and guinea pig DRG latently infe

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

186 mice expressed abundant 2.2-kb major LATs in trigeminal ganglia (TG) and other tissues.

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

188 CD8(+) effector T cells in acutely infected trigeminal ganglia (TG) and the CD8(+) memory T cells in

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

190 Sensory neurons within trigeminal ganglia (TG) are the primary site for bovine

191 Although sensory neurons in the trigeminal ganglia (TG) are the primary site of BHV-1 la

192 on day 30 postinfection, infiltration of the trigeminal ganglia (TG) by CD4, CD8, programmed death 1

193 IFN-beta transgene treatment protects mouse trigeminal ganglia (TG) cells from acute HSV-1 infection

194 the ability of mutant Sy2 to reactivate from trigeminal ganglia (TG) derived from latently infected m

195 ss, viral titers were analyzed in cornea and trigeminal ganglia (TG) during acute ocular HSV-1 infect

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

197 ed to lower virus replication in the eye and trigeminal ganglia (TG) during the early period of infec

198 titers were below the level of detection in trigeminal ganglia (TG) during the first 9 days postinfe

199 lly retained in the ophthalmic branch of the trigeminal ganglia (TG) even at the time when replicatin

200 mine the viral DNA copy number in individual trigeminal ganglia (TG) from 17 subjects.

201 ency of RNA expression for nine VZV genes in trigeminal ganglia (TG) from 35 human subjects, includin

202 Trigeminal ganglia (TG) from rabbits latently infected w

203 eron (IFN-gamma) are persistently present in trigeminal ganglia (TG) harboring latent HSV-1.

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

205 We separated human trigeminal ganglia (TG) into neuronal and nonneuronal fr

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

207 Infection of the mouse trigeminal ganglia (TG) is the most commonly used model

208 Careful studies of mouse trigeminal ganglia (TG) latently infected with herpes si

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

210 ingle cells recovered from sections of human trigeminal ganglia (TG) obtained at autopsy.

211 iability of the HSV-1 TK gene pool in paired trigeminal ganglia (TG) of 5 immunocompetent individuals

212 d to compare cellular gene expression in the trigeminal ganglia (TG) of calves latently infected with

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

214 e eye and on the establishment of latency in trigeminal ganglia (TG) of immunized and ocularly infect

215 ntaining ORF-E was consistently expressed in trigeminal ganglia (TG) of latently infected calves, pro

216 ion of dysfunctional T cell responses in the trigeminal ganglia (TG) of latently infected mice is not

217 HSV-1 latency-associated transcript (LAT) in trigeminal ganglia (TG) of latently infected mice.

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

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

220 r estradiol alters gene transcription in the trigeminal ganglia (TG) of ovariectomized rats (OVX).

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

222 f replication at the body surface and within trigeminal ganglia (TG) on the establishment of latent i

223 e delta-opioid receptor (DOR) for inhibiting trigeminal ganglia (TG) sensory neurons.

224 t anterogradely from neuronal cell bodies in trigeminal ganglia (TG) to nerve ending in the noses and

225 atterns of latent and butyrate-treated mouse trigeminal ganglia (TG) via chromatin immunoprecipitatio

226 Sixty days after ocular infection, trigeminal ganglia (TG) were removed from the latently i

227 Fifty CG and 47 trigeminal ganglia (TG) were resected from 63 formalin-f

228 es simplex virus type 1 (HSV-1) DNA in human trigeminal ganglia (TG) with respect to age, gender, and

229 d, selectively retained in latently infected trigeminal ganglia (TG), and appear to decrease HSV-1 re

230 ontrast, titers of DoriL-I(LR) in tear film, trigeminal ganglia (TG), and hindbrain were reduced and

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

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

233 es, including the dorsal root ganglia (DRG), trigeminal ganglia (TG), brain, skin, liver, and kidney.

234 It is known to persist in trigeminal ganglia (TG), but how it reaches this site ha

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

236 ntly from explanted, latently infected mouse trigeminal ganglia (TG), indicating that ICP0 is not ess

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

238 Virus replication in the eye and trigeminal ganglia (TG), survival, CS, and relative amou

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

240 In the trigeminal ganglia (TG), we demonstrated that GFP is exc

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

242 memory population in HSV-1 latently infected trigeminal ganglia (TG), whereas non-HSV-specific CD8(+)

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

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

245 ly infected cells and 4 in latently infected trigeminal ganglia (TG).

246 ral gene expression in the latently infected trigeminal ganglia (TG).

247 ivation and CD8(+) T cell function in murine trigeminal ganglia (TG).

248 type 1 (HSV-1) reactivation from latency in trigeminal ganglia (TG).

249 1 establishes latency in sensory neurons of trigeminal ganglia (TG).

250 1 (BoHV-1) latency is sensory neurons within trigeminal ganglia (TG).

251 for BHV-1 latency is sensory neurons in the trigeminal ganglia (TG).

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

253 d by viral genome loads in latently infected trigeminal ganglia (TG).

254 nt cocultivation of latently infected murine trigeminal ganglia (TG).

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

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

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

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

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

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

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

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

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

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

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

266 ) and in vivo (in infected mouse corneas and trigeminal ganglia [TG] of BALB/c and C57BL/6 mice).

267 cell types (including sensory neurons of the trigeminal ganglia [TG]) in vitro and in vivo, as indica

268 eal infection, CD8(+) T cells infiltrate the trigeminal ganglia (TGs) of mice, and are retained in la

269 cells (DCs) on the level of HSV-1 latency in trigeminal ganglia (TGs) of ocularly infected BALB/c and

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

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

272 Our results show that (i) in the corneas and trigeminal ganglia, the maximum amount of virus present

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

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

275 Microdialysis probes inserted into trigeminal ganglia (TRGs) of anesthetized guinea pigs we

276 o significantly lower titers in the corneas, trigeminal ganglia, vaginas, dorsal root ganglia, spinal

277 rimary afferent and sensory ganglia neurons--trigeminal ganglia (Vg), and dorsal root ganglia (DRG):

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

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

280 ication of HSV-IL-4 in tissue culture and in trigeminal ganglia was similar to that of wild-type viru

281 , the persistence of infectious virus in the trigeminal ganglia was the same for all strains infected

282 of protein and transcript of TRPV1 in mouse trigeminal ganglia, we demonstrate that dentinal applica

283 5, 11, 23, and 37 days postinfection (dpi), trigeminal ganglia were examined for beta-galactosidase-

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

285 In isoflurane-anesthetized male rats, trigeminal ganglia were explored extracellularly in vivo

286 ctivation from latency, Notch3 RNA levels in trigeminal ganglia were higher than those during latency

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

288 cells induced in DLNs, conjunctiva, and the trigeminal ganglia were inversely proportional with corn

289 th fixative, and the left and right IANs and trigeminal ganglia were processed using indirect immunof

290 Titers of Phos 1 and 2 trigeminal ganglia were reduced as much as 16- and 20-fo

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

292 ctivate glial cells, primary cultures of rat trigeminal ganglia were utilized to study the effects of

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

294 ctivation was particularly pronounced in the trigeminal ganglia, where MOR-1 gene expression was firs

295 anisms that specify neuronal identity in the trigeminal ganglia, which relays sensory information fro

296 reactivates more efficiently than HSV-2 from trigeminal ganglia while HSV-2 reactivates more efficien

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

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

299 Upon infection of murine trigeminal ganglia with herpes simplex virus type 1 (HSV

300 wing explanation and cocultivation of murine trigeminal ganglia with Vero cells at a frequency simila