ライフサイエンスコーパス: trigeminal ganglia

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

2 ocalize with the capsaicin receptor TRPV1 in trigeminal ganglia.

3 genes in acutely and latently infected mouse trigeminal ganglia.

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

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

6 s performed with immunohistochemistry on rat trigeminal ganglia.

7 of reactivation from latently infected mouse trigeminal ganglia.

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

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

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

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

12 ression of inflammatory cytokines within the trigeminal ganglia.

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

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

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

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

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

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

19 latently infected versus mock-infected mouse trigeminal ganglia.

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

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

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

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

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

25 lifelong latent infection in neurons of the trigeminal ganglia.

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

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

28 se specifically in neuronal cells within the trigeminal ganglia.

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

30 and KOSV2R from explanted latently infected trigeminal ganglia.

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

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

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

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

35 neurons within dorsal root ganglia (DRG) and trigeminal ganglia.

36 but is critical for productive growth in the trigeminal ganglia.

37 the predominant site of latent VZV in human trigeminal ganglia.

38 rneas of mice and be transported back to the trigeminal ganglia.

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

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

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

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

43 stablishes latency in sensory neurons within trigeminal ganglia.

44 s lifelong latency in sensory neurons within trigeminal ganglia.

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

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

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

48 mal murine trigeminal ganglia, and in murine trigeminal ganglia acutely infected with McKrae strain h

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

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

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

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

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

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

55 DNA and RNA were isolated from corneas and trigeminal ganglia and amplified by PCR using gene-speci

56 1 (Cavalpha2delta1) protein dysregulation in trigeminal ganglia and associated spinal subnucleus caud

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 3.1, p2rx3.2 and p2rx8 were expressed in the trigeminal ganglia and subsets of Rohon-Beard neurons.

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

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

75 he preferential expression of NaN in DRG and trigeminal ganglia and the reduction of NaN mRNA levels

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 factor (TNF) receptor mRNA in normal murine trigeminal ganglia, and in murine trigeminal ganglia acu

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

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

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

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

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

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

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

87 sed signal for TNFR mRNA in acutely infected trigeminal ganglia appears to reflect infiltration by re

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

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

90 opulation that include subsequent defects in trigeminal ganglia assembly.

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

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

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

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

95 DeltaSER did not grow in the trigeminal ganglia but did express low levels of several

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

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

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

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

100 othesize that (i) poly(A)+ LRT is spliced in trigeminal ganglia by neuron-specific factors, (ii) vira

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

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

103 The trigeminal ganglia differentiate in part from specialize

104 Neuron number in trigeminal ganglia, DRG, and SCG were unchanged, althoug

105 ecific viral nucleic acid sequences in mouse trigeminal ganglia during acute ganglionic infection by

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

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

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

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

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

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

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

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

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

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

116 In rabbit trigeminal ganglia, extensive apoptosis occurred with LA

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

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

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

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

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

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

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

124 s controversy we examined fixed wax-embedded trigeminal ganglia from 30 individuals obtained at autop

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

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

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

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

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

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

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

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

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

134 background reactivated from latency in mouse trigeminal ganglia, in contrast to similar mutants from

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

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

137 Productive viral gene expression in trigeminal ganglia is readily detected from 2 to 7 days

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 In trigeminal ganglia, neurons expressing trkB receptor wer

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

154 In trigeminal ganglia of acutely infected calves (1, 7, or

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

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

157 here were significantly fewer neurons in the trigeminal ganglia of bcl-2(-/-) embryos at E16 and E18.

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

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

160 levels of infectious virus in the brains and trigeminal ganglia of challenged mice.

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

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

163 903 induces increased levels of apoptosis in trigeminal ganglia of infected rabbits compared to LAT+

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

165 In trigeminal ganglia of latently infected calves, an sncRN

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

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

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

169 In trigeminal ganglia of mice acutely infected with the wil

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

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

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

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

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

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

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

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

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

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

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

181 During acute infection of trigeminal ganglia or following dexamethasone-induced re

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

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

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

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

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

187 ns and over the arachnoid layers surrounding trigeminal ganglia supports suggestions that TNF has a d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 Trigeminal ganglia (TG) from rabbits latently infected w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 his study the NnAChRs were identified in rat trigeminal ganglia (TG) using RT-PCR and immunocytochemi

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

228 le in viral reactivation, RNA from explanted trigeminal ganglia (TG) was analyzed by differential dis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 1 establishes latency in sensory neurons of trigeminal ganglia (TG).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 -length and polyadenylated IE transcripts in trigeminal ganglia was not efficient compared to that of

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

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

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

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

281 5, 11, 23, and 37 days postinfection (dpi), trigeminal ganglia were examined for beta-galactosidase-

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

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

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

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

286 ary, pterygopalatine, superior cervical, and trigeminal ganglia were incubated with antisera to neuro

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

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

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

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

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

292 LAT is produced, and during latency in mouse trigeminal ganglia, where both LATs are expressed.

293 N and KLN vectors in latently infected mouse trigeminal ganglia, where high levels of beta-NGF protei

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

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

299 In vivo, L/ST-4BS was reactivated from mouse trigeminal ganglia with reduced efficiency and delayed k

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