ライフサイエンスコーパス: sensory ganglia

1 ptive behavior and increase pain peptides in sensory ganglia.

2 transcript expressed during latency in human sensory ganglia.

3 e the majority of the neurons of the cranial sensory ganglia.

4 tebrates, NeuroD is expressed in all cranial sensory ganglia.

5 protein is expressed during latency in human sensory ganglia.

6 ted the stable 2.0-kb LAT intron only in the sensory ganglia.

7 ntrols the virus and limits it to latency in sensory ganglia.

8 distribution of ENT1 in rat dorsal horn and sensory ganglia.

9 causes varicella and establishes latency in sensory ganglia.

10 lla-zoster virus (VZV) pathology in skin and sensory ganglia.

11 m cell bodies situated in two distinct vagal sensory ganglia.

12 but not neuronal, maintenance in developing sensory ganglia.

13 e in apoptosis and severe loss of neurons in sensory ganglia.

14 ns of gene expression between RGCs and other sensory ganglia.

15 ce of a neural crest contribution to cranial sensory ganglia.

16 ance of a latent infection within neurons in sensory ganglia.

17 it induces a rash and establishes latency in sensory ganglia.

18 neurons whose cell bodies reside in cranial sensory ganglia.

19 ly with SP from the somata of neurons within sensory ganglia.

20 e paired sense organs and neurons in cranial sensory ganglia.

21 ia of splanchnic or vagus circuitry prior to sensory ganglia.

22 g neurons in the nodose and petrosal cranial sensory ganglia.

23 gh thoracic dorsal root ganglia and in vagal sensory ganglia.

24 s in either the dorsal root ganglia or vagal sensory ganglia.

25 distribution in and reactivation from human sensory ganglia.

26 (NT-3) are born with deficits in almost all sensory ganglia.

27 tions with other regulatory factors found in sensory ganglia.

28 ection of the vaginal mucosa, but not of the sensory ganglia.

29 e of neurons is often observed in peripheral sensory ganglia.

30 ally, in the spinal gray, but not in primary sensory ganglia.

31 lpha herpesvirus that establishes latency in sensory ganglia.

32 trophic effects on the development of spinal sensory ganglia.

33 ually resulting in fusion of sympathetic and sensory ganglia.

34 I produces an increase in MIF release within sensory ganglia.

35 ipolar tail neurons as homologues of cranial sensory ganglia.

36 he development of the heart, mammary glands, sensory ganglia.

37 differences in neuronal gene expressions in sensory ganglia.

38 lateral craniofacial mesenchyme, retina and sensory ganglia.

39 ment of HSV infections or of dysfunctions of sensory ganglia.

40 y humans and establish a latent infection in sensory ganglia.

41 inergic receptor-operated channel in SGCs of sensory ganglia.

42 increased expression of nociceptive genes in sensory ganglia.

43 e switch between neuronal and glial fates in sensory ganglia.

44 ation channel subfamily member M8 (TRPM8) in sensory ganglia.

45 ding the establishment of latency within the sensory ganglia.

46 establishes latent reservoirs in neurons in sensory ganglia.

47 primary infection and establishes latency in sensory ganglia.

48 cted most frequently in latently infected RM sensory ganglia.

49 s process for pathogenesis in human skin and sensory ganglia.

50 lved to infect areas innervated by different sensory ganglia.

51 immunodeficient mice models the infection of sensory ganglia.

52 pesvirus that infects skin, lymphocytes, and sensory ganglia.

53 the geniculate, petrosal, and nodose cranial sensory ganglia.

54 d under the LAT promoter in vivo in infected sensory ganglia.

55 at are normally found in the CNS, but not in sensory ganglia.

56 f infectious herpes simplex virus (HSV) from sensory ganglia.

57 SVV DNA and transcripts were detected in sensory ganglia 3 dpi, before the appearance of rash.

58 D4 and CD8 T cells were also detected in the sensory ganglia 3 dpi.

59 e tissue can induce the formation of ectopic sensory ganglia adjacent to the developing dorsal mesenc

60 ebate whether macrophage accumulation in the sensory ganglia after peripheral nerve injury is due to

61 increase in the number of macrophages in the sensory ganglia after SNI is a consequence of the prolif

62 t the number of macrophages increased in the sensory ganglia after the spared nerve injury (SNI) mode

63 cines to protect both the vaginal mucosa and sensory ganglia against HSV-2.

64 Similarly, optimal protection of the sensory ganglia against reinfection with HSV-2 was depen

65 rug selection and establish latency in human sensory ganglia alone or together with wild-type virus.

66 atic origin could be found in the celiac and sensory ganglia along with metastases to the spinal cord

67 ow that Nageotte nodules are abundant in DPN sensory ganglia and account for 25% of all neurons.

68 on of Trpa1(+)EECs directly stimulates vagal sensory ganglia and activates cholinergic enteric neuron

69 rophages and neutrophils infiltrate infected sensory ganglia and are responsible for driving the prod

70 placodes contribute to all sense organs and sensory ganglia and arise from a common pool of Six1/Eya

71 e taste bud and taste receptor expression in sensory ganglia and brain.

72 VZV establishes latency in the sensory ganglia and can reactivate later in life to caus

73 SGCs tightly ensheath neurons of sensory ganglia and can regulate neuronal excitability i

74 la-zoster virus (VZV) establishes latency in sensory ganglia and causes herpes zoster upon reactivati

75 g of muscle, we show that neutrophils invade sensory ganglia and confer mechanical hypersensitivity o

76 SV-1) virions travel via axonal transport to sensory ganglia and establish a lifelong latent infectio

77 include a severe reduction in the number of sensory ganglia and fibres.

78 at higher levels than xefiltin in peripheral sensory ganglia and in structures caudal to the mesencep

79 ves, but these senses remain separate in the sensory ganglia and in their first central relays.

80 -2 in the developing neural tube, peripheral sensory ganglia and limb buds, and shows that the two cF

81 They give rise to the cranial sensory ganglia and much of the craniofacial skeleton, a

82 m next to the neural tube that contribute to sensory ganglia and organs in the vertebrate head, inclu

83 tem express Kv1.1, including neuronal cells (sensory ganglia and outer aspect of cerebral hemispheres

84 ZV) is a human alphaherpesvirus that infects sensory ganglia and reactivates from latency to cause he

85 imary infection, the virus remains latent in sensory ganglia and reactivates upon weakening of the ce

86 os leads to an early loss of placode-derived sensory ganglia and reduced number of NC-derived postgan

87 r fast synaptic transmission, whereas in the sensory ganglia and sensory neurons, they may be involve

88 ergic communication within rodent peripheral sensory ganglia and show that it can modulate transmissi

89 HSV-specific CD4(+) T cells were present in sensory ganglia and spinal cords coincident with HSV-1 c

90 ectoderm that invaginate or ingress to form sensory ganglia and the paired sense organs.

91 rget-derived BMP signaling in development of sensory ganglia and the sensory innervation of the skin

92 ld-type VZV persists in a latent form in the sensory ganglia, and can re-activate to cause herpes zos

93 rating neural crest cells to localize in the sensory ganglia, and induces the expression of sensory n

94 within the developing brain and spinal cord, sensory ganglia, and olfactory epithelium.

95 ZV) causes varicella, establishes latency in sensory ganglia, and reactivates as herpes zoster.

96 rane tyrosine kinases, in rat sciatic nerve, sensory ganglia, and spinal cord 0-30 d postaxotomy.

97 ctory epithelium, the inner ear, the cranial sensory ganglia, and the anterior pituitary arise from a

98 pathway, the branchial arches, the gut, the sensory ganglia, and the nerves.

99 llance of HSV-1 latently infected neurons in sensory ganglia, and their functional properties are inf

100 ough all neuronal populations within primary sensory ganglia appear to be capable of supporting a pro

101 SGCs in sensory ganglia are activated by numerous types of nerve

102 in the promoters of genes that are silent in sensory ganglia are also not occupied in vivo.

103 Neurons of cranial sensory ganglia are derived from the neural crest and ec

104 We found that trigeminal sensory ganglia are formed from early-born and late-born

105 Although the sensory ganglia are the primary pathological target of t

106 Neurons of the vertebrate cranial sensory ganglia arise from both neural crest and a serie

107 the intermediolateral cell column but not in sensory ganglia as compared to controls: spinal-intact a

108 Ps may limit both the final neuron number in sensory ganglia as well as the extent of innervation of

109 FIV vectors from peripheral nerve endings to sensory ganglia, as evidenced by HuMOR expression in neu

110 ings indicate that in neurons of the cranial sensory ganglia, as in DRG neurons, cGMP signals are nec

111 has an important role in the development of sensory ganglia, as well as red nucleus, inferior olive,

112 ich are ectodermal thickenings that form the sensory ganglia associated with cranial nerves, but the

113 ults for SVV DNA, no VZV DNA was detected in sensory ganglia at necropsy.

114 By profiling sensory ganglia at single-cell resolution, we find that

115 on appears to be conserved in more posterior sensory ganglia but not in the CNS neurons that express

116 dent apoptotic pathways are activated in the sensory ganglia but only the Caspase-dependent apoptotic

117 both peripheral taste organs and innervating sensory ganglia, but the underlying mechanisms remain po

118 mpathetic ganglia/adrenal gland, enteric and sensory ganglia by immunohistochemical methods.

119 the unique role of macrophages in peripheral sensory ganglia by using a translational model of sleep

120 neurons in sympathetic, parasympathetic and sensory ganglia can be mapped in detail by using tissue

121 has provided insights into the diversity of sensory ganglia cell types in rodents, nonhuman primates

122 pretreatment, but not posttreatment, of the sensory ganglia, combined with ChABC modification of CSP

123 CB1 in sensory ganglia controls visceral sensation, and transcr

124 Although jawless vertebrates have sensory ganglia, convention has it that trunk sympatheti

125 dal specification and function of trigeminal sensory ganglia depends on the timing of neurogenesis.

126 developmental decrease in neuron numbers in sensory ganglia depends upon BMP signaling, and that BMP

127 umber of apoptotic neurons within individual sensory ganglia despite tight control of total number in

128 head, crucial parts of the sense organs and sensory ganglia develop from special regions, the crania

129 fusion of GABA or GABA reuptake inhibitor to sensory ganglia dramatically reduced acute peripherally

130 ights into host-pathogen interactions in the sensory ganglia during acute varicella and demonstrate t

131 d from tissues in the vicinity of peripheral sensory ganglia during embryogenesis, exert synergistic

132 In sensory ganglia, ENT1 was localized to a high proportion

133 onents of the inner ear and specific cranial sensory ganglia fail to form.

134 re effectively trafficked in axons to either sensory ganglia following initial infection or back out

135 novel sympathetic sprouting observed within sensory ganglia following peripheral nerve injury.

136 erns of viral infection, we colabeled murine sensory ganglia for evidence of HSV infection and for th

137 remains in a latent form within innervating sensory ganglia for the life of the host.

138 Sensory ganglia from the 3- and 7-day-exercised animals

139 to the paired sensory organs and the cranial sensory ganglia generating a wide variety of cell types

140 l viral gene expression in latently infected sensory ganglia gives rise to a unique, functionally act

141 e strongly labeled in neurons of all cranial sensory ganglia (gV, gVII, gVIII, gIX, and gX).

142 riction of herpes virus latency to mammalian sensory ganglia has led to a search for tissue-specific

143 Vertebrate cranial sensory ganglia have a dual origin from the neural crest

144 Neurons within sensory ganglia have been proposed to communicate via no

145 Spinal sensory ganglia have been shown to contain neuronal subp

146 function in satellite glial cells (SGCs) of sensory ganglia have not been explored.

147 xus and adrenal medulla and in somata of the sensory ganglia implies an extensive involvement of this

148 e injury leads to sNAMs proliferation in the sensory ganglia in a CX3CR1-dependent manner accounting

149 elial surface would allow rAAV to traffic to sensory ganglia in a manner similar to that seen with HS

150 e the somatic excitability of neurons within sensory ganglia in inflammatory pain states.

151 mutant to infect neuronal cells in vitro or sensory ganglia in mice after intramuscular inoculation

152 Hence, we systematically studied primary sensory ganglia in rat to determine if the peripheral di

153 velopment of neurogenic placodes and cranial sensory ganglia in the dogfish, with a focus on the epib

154 the cartilage, bone, connective tissue, and sensory ganglia in the head.

155 Neuronal counts of sensory ganglia in the trkC mutant mice reveal less seve

156 delaminate from epithelial placodes to form sensory ganglia in the vertebrate head.

157 Cranial sensory ganglia in vertebrates develop from the ectoderm

158 t of cranial neurogenic placodes and cranial sensory ganglia in vertebrates, we cloned and analysed t

159 The cranial sensory ganglia, in contrast to those of the trunk, have

160 establishes a latent infection in neurons of sensory ganglia, including those of the trigeminal gangl

161 hemokines expressed by two tissues (skin and sensory ganglia) infected with a common viral pathogen (

162 ection, the bulk of virus replication in the sensory ganglia is controlled by macrophages and gammade

163 the topographical representation of cranial sensory ganglia is established by entrance order, with t

164 evolutionary origin of placodes and cranial sensory ganglia is hampered by the anatomical difference

165 V and its host during acute infection in the sensory ganglia is not well understood due to limited ac

166 that DLK is essential for reactivation from sensory ganglia isolated from infected mice.

167 ial nerves IX, X, XI, and XII and associated sensory ganglia IX and X in all embryos as well as the l

168 Viscera receive innervation from sensory ganglia located adjacent to multiple levels of t

169 Sensory ganglia located anteriorly project more medially

170 within the cell body and, if administered to sensory ganglia, may be employed to rapidly and selectiv

171 Netrin-3 is expressed in sensory ganglia, mesenchymal cells, and muscles during t

172 ated HSV reactivation from latency both in a sensory ganglia model system and in vivo.

173 GFRalpha1-deficient dopaminergic and nodose sensory ganglia neurons no longer respond to GDNF or to

174 Rat primary afferent and sensory ganglia neurons--trigeminal ganglia (Vg), and do

175 nificant in the brainstem and nodose cranial sensory ganglia (NGs), structures critical for cardiores

176 t wall and establishes a latent infection in sensory ganglia (nodose ganglia) of the tenth cranial ne

177 e, endogenous Brn3a expression levels in the sensory ganglia of Brn3a(+/+) and Brn3a(+/-) mice are si

178 omparable to the latent transcription in the sensory ganglia of control RMs.

179 GL-3 accumulation in the small intestine and sensory ganglia of Gla KO mice provides a model for stud

180 against Na(V)1.7 subtype gene into the vagal sensory ganglia of guinea pigs in vivo.

181 ing the neuronal damage and loss observed in sensory ganglia of HIV-infected individuals have not bee

182 peripheral lesions, do not accumulate in the sensory ganglia of immunocompetent patients receiving mu

183 en reported to establish latent infection of sensory ganglia of mice, in that HSV latency-associated

184 We have previously shown that SVV latency in sensory ganglia of nondepleted juvenile RMs is associate

185 rprisingly, p21Waf-1/Cip-1 is induced in the sensory ganglia of Rb-mutant embryos in a p53-independen

186 virus (VZV)-was determined in autonomic and sensory ganglia of the head and neck obtained from forma

187 ndependently distributed among autonomic and sensory ganglia of the human head and neck.

188 establishment of latent virus in peripheral sensory ganglia of the latently infected host.

189 surround primary sensory neurons located in sensory ganglia of the peripheral nervous system also ex

190 ls, neural crest cells then form the cranial sensory ganglia of the peripheral nervous system.

191 Sympathetic axons are also seen invading the sensory ganglia of transgenic mice; these fibers form pe

192 e (plus-end) motion, these viruses travel to sensory ganglia or peripheral tissue at specific stages

193 Infectious HSV-2 was not detected in the sensory ganglia or spinal cord of HSV-immune mice deplet

194 Several cranial sensory ganglia originating from neurogenic placodes, su

195 mic relay neurons (which expressed alpha1G), sensory ganglia, pituitary, and dentate gyrus granule ne

196 ed that neuroimmune-glia interactions at the sensory ganglia play a critical role in the genesis of h

197 polar tail neurons are homologous to cranial sensory ganglia rather than derivatives of neural crest(

198 ese afferent nerves are located in the vagal sensory ganglia referred to as nodose and jugular gangli

199 Many aspects of VZV infection of sensory ganglia remain poorly understood, due to limited

200 he formation of parasympathetic and visceral sensory ganglia, respectively.

201 Vertebrate cranial sensory ganglia, responsible for sensation of touch, tas

202 ervous system, primarily brain, spinal cord, sensory ganglia, retina, and nasal epithelia, as well as

203 c are required for the proper development of sensory ganglia, retinal ganglion cells, and inner ear h

204 The resident macrophages of the sensory ganglia (sensory neuron-associated macrophages,

205 deletion of numb and numblike in developing sensory ganglia show a severe reduction in axonal arbori

206 ctates mature neuron function within cranial sensory ganglia: specifically, gustatory neurons derive

207 rpes simplex virus 1 (HSV-1) from neurons in sensory ganglia such as the trigeminal ganglia (TG) is i

208 nhanced IL-20R1 expression in the trigeminal sensory ganglia, suggesting a lesion-associated and epid

209 dditionally, VZV DNA was not detected in the sensory ganglia, suggesting that viremia might be requir

210 tron was significantly more efficient in the sensory ganglia than in other tissues.

211 ime the neuroimmune-glia interactions in the sensory ganglia that account for the development of acut

212 examined the neuroimmune interactions at the sensory ganglia that account for the genesis of herpetic

213 Sensory ganglia that innervate taste buds and gustatory

214 nin gene-related peptide (CGRP) increased in sensory ganglia that projected to the wounded skin, but

215 ollowing reactivation from latently infected sensory ganglia, the majority never develop a recurrent

216 (HSV) travels from the corneal epithelium to sensory ganglia then returns to the stroma to cause dise

217 sorimotor circuit transmits information from sensory ganglia through the cerebellum to vPPNs to regul

218 HE TRPV1 cells are distributed in sensory ganglia throughout the neuraxis, with higher num

219 In cranial sensory ganglia, Tlx3 is highly expressed in differentia

220 co-released ATP and substance P (SP) within sensory ganglia to further advance the hypothesis of non

221 ranscriptome analysis of the star-nosed mole sensory ganglia to identify novel candidate mammalian to

222 We used in vivo calcium imaging of sensory ganglia to investigate how the activity of perip

223 They then grow in association with sensory ganglia, to their targets, the muscles of the br

224 application of GABA receptor antagonists to sensory ganglia triggered or exacerbated peripherally in

225 s maintained in a latent state in neurons of sensory ganglia until complex stimuli reactivate viral l

226 We found that after dissociation of adult sensory ganglia, up to 27% of neurons die within 4 days

227 Within sensory ganglia, VRL-1 is most prominently expressed by

228 A minor disturbance of sensory ganglia was found.

229 aration of embryonic chicken spinal cord and sensory ganglia was used to test the influence of ventra

230 ay rami to the spinal nerves near the lumbar sensory ganglia, we avoided widespread sympathetic dener

231 of VEGF on endothelial cells and neurons in sensory ganglia, we used explanted mouse dorsal root gan

232 Large neurons in cranial nerve sensory ganglia were also labeled.

233 Varicella severity and viral latency within sensory ganglia were comparable in RMs infected with SVV

234 anial motor axons, while explants of cranial sensory ganglia were weakly chemoattractive.

235 1 (HSV-1) establishes latency in neurons of sensory ganglia, where the only abundant viral gene prod

236 ristic latent viral transcription profile in sensory ganglia, where we detected 68 out of 69 SVV-enco

237 ded retrograde transport to the cell body in sensory ganglia, whereas addition of these proteins was

238 eficits of monoaminergic neurons and cranial sensory ganglia, whereas expression of the pan-neuronal

239 erm regulates the differentiation of cranial sensory ganglia, which coordinates the cranial nerves wi

240 ease in the population of macrophages in the sensory ganglia, which have been implicated in different

241 o the function and proposed roles of KARs in sensory ganglia, which include promotion of neurite outg

242 epibranchial placode-derived distal cranial sensory ganglia, while the phenotype appears less severe

243 through sensory systems serviced by cranial sensory ganglia, whose neurons arise predominantly from

244 dependent wave of lytic gene expression from sensory ganglia will ultimately permit the development o

245 he establishment of lifelong latency in host sensory ganglia with occasional reactivation causing rec

246 imarily restricted to nociceptors in primary sensory ganglia, with minimal expression in a few discre

247 whereas nearby epibranchial placodes produce sensory ganglia within branchial clefts.