ライフサイエンスコーパス: BDNF

1 BDNF and TrkB are both highly expressed in the dorsal ra

2 BDNF is involved in many brain functions and plays key r

3 BDNF mRNA expressing neurons mostly increased in the are

4 BDNF mRNA levels, assessed by quantitative PCR and in si

5 BDNF serum levels were significantly higher in children

6 BDNF signaling through TrkB receptors differentially mod

7 ts ( approximately 30% survival; p < 0.001), BDNF and phosphorylated ERK expression were increased in

8 creases in OH-PAHs were associated with >16% BDNF decreases.

9 Patients (N=71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%

10 In summary, HDACi and a BDNF mimetic are sufficient to rescue retinal cell death

11 ion model on organotypic slice culture, in a BDNF-dependent manner.

12 mice, we investigated the effectiveness of a BDNF-mimetic treatment with 7,8-dihydroxyflavone at alle

13 In addition, intra-mPFC infusion of a BDNF-neutralizing antibody was performed to test the nec

14 increased by PTN (12.7:1) when compared to a BDNF + GDNF choice.

15 hibitor, PP2, into the PrL cortex prior to a BDNF infusion, immediately after the end of the last coc

16 Notably, sole treatment with a BDNF mimetic, 7,8-dihydroxyflavone hydrate, significantl

17 obligatory precursor of biologically active BDNF, becomes readily detectable.

18 tion predominately possessing lower activity BDNF genotypes (Val/Met, Met/Met).

19 We analyzed BDNF serum levels with ELISA and their correlation with

20 , interleukin [IL]-6, IL-8 and IL-1beta) and BDNF levels were also measured.

21 Activity-dependent and BDNF-dependent neuroplasticity within the OFC coordinate

22 evels of neurotrophic factors NT-3, GDNF and BDNF.

23 epair cell markers, including Shh, GDNF, and BDNF.

24 rotrophic factor (BDNF) BDNF-IX, BDNF-IV and BDNF-I transcripts and increased vascular endothelial gr

25 Plasma ketamine levels and BDNF genotypes were assessed.

26 plasticity by recruitment of AMPAR, mTOR and BDNF signaling in both mouse mesencephalic and human ind

27 Changes in cAMP/cGMP levels, PKA/PKG and BDNF expression were also prevented by BAY.

28 scopolamine-induced behavioral responses and BDNF-tropomyosin receptor kinase B signaling, suggesting

29 e-related changes in estradiol secretion and BDNF Val(66)Met genotype on measures of hippocampal func

30 epressant, ketamine, to BDNF translation and BDNF-dependent signaling, has re-emphasized the importan

31 cortical axons, they normalized anterograde BDNF transport, restored retrograde BDNF transport, and

32 ntal cortex (intra-mPFC) infusion of an anti-BDNF nAb or in mice with a knock-in of the BDNF Val66Met

33 uated responses to scopolamine and that anti-BDNF antibody infusions into the mPFC prevented the anti

34 ctivation of synaptic growth factors such as BDNF, NGF, and IGF.

35 that carrageenan, interleukin 6, as well as BDNF-induced hyperalgesia and priming are reduced specif

36 Furthermore, there were changes at BDNF exon I gene promoter, in concert with overall BDNF

37 ogether, our results suggest that attenuated BDNF release and signaling in the dentate gyrus may acco

38 trophic factor-tropomyosin-related kinase B (BDNF-TrkB) signaling in the actions of GLYX-13.

39 pal brain-derived neurotrophic factor (BDNF) BDNF-IX, BDNF-IV and BDNF-I transcripts and increased va

40 , exercise-induced expression of total BDNF, BDNF splice variants 1, 2, 4, 6 and fibronectin type III

41 of the last cocaine SA session, would block BDNF's ability to suppress reinstatement of cocaine-seek

42 Inhibition of SFKs using PP2 blocked BDNF-mediated phosphorylation of GluN2A, GluN2B, and ERK

43 , but not the negative control, PP3, blocked BDNF's suppressive effect on context-induced relapse aft

44 Z, especially the decreased peripheral blood BDNF levels in SCZ patients validated by several meta-an

45 I is accompanied by reduced peripheral blood BDNF levels, supporting an association between the decre

46 also show that this process is controlled by BDNF signaling.

47 ity, and this process is likely initiated by BDNF-TrkB pathway activation.

48 233.68, g = 0.54 (0.31, 0.77)], moderated by BDNF genotype, with met(66) carriers showing larger gain

49 n-acronymic), which is robustly regulated by BDNF/TrkB signaling, is downregulated in hippocampus (ma

50 platforms, demonstrate an ovarian hormone-by-BDNF interaction on working memory-related hippocampal f

51 Our findings thus indicate that cerebellar BDNF is derived primarily from excitatory neurons--prece

52 We show that within the cerebellum, BDNF-expressing cells are restricted to the internal gra

53 ght to quantitatively summarize the clinical BDNF data in patients with AD and mild cognitive impairm

54 e, we describe a key role for a constitutive BDNF feed forward signaling pathway in regulating synapt

55 By contrast, BDNF is undetectable in mouse megakaryocytes, in line wi

56 actors (e.g., for WM: COMT val(158)met, DAT, BDNF val(66)met).

57 MCI subjects showed a trend for decreased BDNF levels compared with HC subjects (14 studies, Hedge

58 itro experiments were performed to delineate BDNF-dependent mechanisms underlying the effects of scop

59 ify an essential role for activity-dependent BDNF release in the rapid antidepressant effects of scop

60 ested the hypothesis that activity-dependent BDNF release within the mPFC is necessary for the antide

61 ument the effects of sex and genotype (i.e., BDNF Val66Met) on acute stress-induced gene expression.

62 els of the mRNA species leading to efficient BDNF translation rapidly increase.

63 g electron microscopy to localize endogenous BDNF to dendrites and spines of hippocampal CA1 pyramida

64 These data indicate that endogenous BDNF signalling in the NTS is integral for the maintenan

65 reagent-mediated reductions in mHTT enhanced BDNF delivery to restore the trophic status of BACHD str

66 with the TrkB-Fc scavenger for extracellular BDNF or TrkB antagonism, but were eliminated by neutrali

67 as brain derived neurotrophic growth factor (BDNF), vascular endothelial growth factor-A (VEGF-A), in

68 ated with brain-derived neurotrophic factor (BDNF) (p < 0.05), and interquartile range (IQR) increase

69 Brain-derived neurotrophic factor (BDNF) and its high affinity receptor, tropomyosin recept

70 Brain-derived neurotrophic factor (BDNF) and its receptor TrkB are crucial for many forms o

71 ticularly brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are crucial modulato

72 icity via brain-derived neurotrophic factor (BDNF) and protein neo-synthesis.

73 kines and brain-derived neurotrophic factor (BDNF) are biomarkers for BP.

74 mones and brain-derived neurotrophic factor (BDNF) are highly convergent on brain function.

75 5-HT) and brain-derived neurotrophic factor (BDNF) are two signaling molecules that have important re

76 ppocampal brain-derived neurotrophic factor (BDNF) BDNF-IX, BDNF-IV and BDNF-I transcripts and increa

77 retion of brain-derived neurotrophic factor (BDNF) by pulp fibroblasts.

78 d lowered brain-derived neurotrophic factor (BDNF) expression (0.6-fold) in the stroke-affected gastr

79 crease in brain-derived neurotrophic factor (BDNF) expression and a reduction in the expression and f

80 tained PL brain-derived neurotrophic factor (BDNF) expression is required for memory consolidation, r

81 n between brain-derived neurotrophic factor (BDNF) expression, nerve density, and increased survival

82 nt in the brain-derived neurotrophic factor (BDNF) gene generates a truncated mRNA transcript in naiv

83 depend on brain-derived neurotrophic factor (BDNF) genotype and dose.

84 d colonic brain-derived neurotrophic factor (BDNF) has been reported to be associated with abdominal

85 e member, brain-derived neurotrophic factor (BDNF) has drawn much attention due to its pleiotropic ro

86 icking of brain-derived neurotrophic factor (BDNF) in DIV7 cultures of E18 cortical neurons was marke

87 ssions of brain-derived neurotrophic factor (BDNF) in the BCCAO rats treated with LIP ultrasound were

88 e role of brain-derived neurotrophic factor (BDNF) in the regenerative ability of adult brain, after

89 including brain-derived neurotrophic factor (BDNF) induction and increased phosphorylated cyclic-AMP

90 Brain-derived neurotrophic factor (BDNF) is a critical effector of depression-like behavior

91 nction of brain-derived neurotrophic factor (BDNF) is a possible contributor to the pathology and sym

92 , we show brain-derived neurotrophic factor (BDNF) is required for the antimanic-like effects of lith

93 ances the brain-derived neurotrophic factor (BDNF) level in the brain; (2) reduces both microglia/mac

94 red their brain-derived neurotrophic factor (BDNF) levels as a proxy of neuronal plasticity.

95 including brain-derived neurotrophic factor (BDNF) play a role in chronic inflammatory skin diseases

96 Brain-derived neurotrophic factor (BDNF) plays a key role in the pathophysiology and treatm

97 ype 1 and brain-derived neurotrophic factor (BDNF) protein levels were measured.

98 vation of brain-derived neurotrophic factor (BDNF) receptor TrkB, facilitation of mammalian target of

99 on of the brain-derived neurotrophic factor (BDNF) receptor trkB.T1, a truncated isoform of BDNF.

100 Brain-derived neurotrophic factor (BDNF) regulates neuronal survival and growth and promote

101 ar level, brain derived-neurotrophic factor (BDNF) represents an important player that supports EE-as

102 Brain-derived neurotrophic factor (BDNF) signaling in the dorsolateral striatum (DLS) keeps

103 s (GR) by brain-derived neurotrophic factor (BDNF) signaling integrates both pathways for remodeling

104 show that brain-derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (TrkB) recepto

105 role for brain-derived neurotrophic factor (BDNF) that is produced in the brain of mice housed in EE

106 d for pro-brain-derived neurotrophic factor (BDNF) to induce long-term depression, and with the BDNF

107 dy on the Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism, a genetic variant linked to

108 encoding brain-derived neurotrophic factor (BDNF) was associated with ADHD at Bonferroni corrected l

109 ession of brain-derived neurotrophic factor (BDNF) was markedly decreased in the hippocampus of patie

110 Brain-derived neurotrophic factor (BDNF), a key player in regulating synaptic strength and

111 Y (NPY), brain-derived neurotrophic factor (BDNF), as well as neuroinflammatory markers including io

112 level of brain-derived neurotrophic factor (BDNF), but the underlying mechanism still remains unclea

113 r (GDNF), brain-derived neurotrophic factor (BDNF), pleiotrophin (PTN), and NT-3 in asymmetrically gu

114 d release brain-derived neurotrophic factor (BDNF), which is vital for neuronal survival, development

115 ) secrete brain-derived neurotrophic factor (BDNF), which significantly stimulated axonal growth from

116 levels of brain-derived neurotrophic factor (BDNF).

117 stream of brain-derived neurotrophic factor (BDNF).

118 effect of brain-derived neurotrophic factor (BDNF).

119 gene for brain derived neurotrophic factor (BDNF).

120 -survival brain derived neurotrophic factor (BDNF).

121 tsynaptic brain-derived neurotrophic factor (BDNF)/TrkB and presynaptic cyclic AMP (cAMP)/PKA signali

122 KG and the brain derived neurotropic factor (BDNF) levels in hippocampus and cortex were detected wit

123 ssion and secretion of neurotrophic factors- BDNF and NT3 was quantified.

124 nd axonal permissive factors including FGF2, BDNF, and NGF.

125 d flow PET in 39 healthy women genotyped for BDNF Val(66)Met, and a confirmatory data set was obtaine

126 indicate that SFK activity is necessary for BDNF-mediated suppression of cocaine-seeking and reversa

127 tropomyosin-related kinase B, a receptor for BDNF, can improve neurological function after TBI.

128 these findings demonstrate a requirement for BDNF in the antimanic action of lithium and identify enh

129 not effective, indicating a crucial role for BDNF in oleandrin's protective and antitumor functions.

130 also suggest a non-cell autonomous role for BDNF in the DRN in mediating antidepressant efficacy.

131 The most significant gene BDNF was also associated with osteoporotic fractures.

132 the brain-derived neurotrophic factor gene (BDNF) provides examples of how such a vertically integra

133 ons between variants within candidate genes (BDNF, OXTR, RORA, GRM8, CHRNA4, IL-1A, CRHR1, MTHFR, DRD

134 creases the expression of AD-relevant genes: BDNF, alpha-secretase (ADAM10), MINT2, FE65, REST, SIRT1

135 Behaviourally, only heterozygous BDNF Val66Met females exhibit spatial memory impairment,

136 not observed in ovariectomized heterozygous BDNF Val66Met females, suggesting that circulating ovari

137 eover, a significant increase in hippocampal BDNF was detected in APPSWE /PS1dE9 mice exposed to EE,

138 sues related to BDNF biology, as well as how BDNF may function as a downstream mediator of newer phar

139 Our results implicate BDNF as a genetic risk factor for ADHD, potentially by v

140 oal-directed response selection, implicating BDNF-expressing OFC projection neurons in selecting acti

141 Most importantly, BDNF- tyrosine receptor kinase B (TrkB) signalling in th

142 In BDNF-deficient mice (bdnftm1Jae/J) and in glioma cells s

143 oral effects of scopolamine were assessed in BDNF Val/Met knock-in mice, in which BDNF processing and

144 dings suggest that age-dependent decrease in BDNF signaling may cause synaptic alterations through an

145 There was no difference in BDNF levels of filaggrin-positive or filaggrin-negative

146 ed two novel functional AP-1 cis-elements in BDNF promoter I, responsible for the activation of the p

147 ed swimming test in BDNF(Val/Val) but not in BDNF(Met/Met) mice.

148 ntal period due in part to a perturbation in BDNF-TrkB signaling, and could contribute to the alterat

149 ntidepressant efficacy, which was reduced in BDNF floxed mice injected in dHc with AAV-Cre, and in NB

150 ther, these results implicate a reduction in BDNF-TrkB signalling in the dmNTS during CHF that contri

151 Attenuation of responses in BDNF Met mice indicates that patients with the Met allel

152 es were found between AD and MCI subjects in BDNF levels (11 studies, Hedges' g=0.058, 95% CI=-0.120

153 mobility time in the forced swimming test in BDNF(Val/Val) but not in BDNF(Met/Met) mice.

154 -induced increase in myostatin and increased BDNF expression in skeletal muscle.

155 fect of exercise was paralleled by increased BDNF expression in trisomic mice, we investigated the ef

156 ia nigra (SN) dopamine neurons and increases BDNF in the nigrostriatal system and primary motor corte

157 eurotoxicants in animal models and increases BDNF.

158 These results suggest that STN DBS increases BDNF-trkB signaling to contribute to the neuroprotective

159 over, silencing C5L2 significantly increases BDNF secretion by LTA-stimulated pulp fibroblasts.

160 tudy, we found that 5-HT treatment increases BDNF receptor, TrkB (tropomyosin related kinase B), leve

161 Inhibiting BDNF's receptor, TrkB, ERK/MAP kinase activation, or NMD

162 -derived neurotrophic factor (BDNF) BDNF-IX, BDNF-IV and BDNF-I transcripts and increased vascular en

163 ment, which reflect GABA circuit maturation, BDNF, and circadian Clock genes.

164 part by increasing both pro-BDNF and mature BDNF levels.

165 To this end, we microinjected BDNF or the highly selective TrkB receptor antagonist [N

166 ver, how tau pathology specifically modifies BDNF signaling and affects neuronal function during earl

167 MAOA, MAOB, BCHE and TH), neurodevelopment (BDNF and others), the SNARE system and other forty genes

168 minergic (COMT, ANKK1) and the neurotrophic (BDNF, NGFR) system, associations with the Nogo-P3 as wel

169 otein-coupled 5-HT2 receptor activation, new BDNF synthesis, and MEK/ERK signaling (the Q pathway).

170 megakaryocytes, in line with the absence of BDNF in mouse serum.

171 , cell biological and biochemical aspects of BDNF biology has now been established, certain aspects r

172 inhibition eliminates the retrograde bias of BDNF/TrkB trafficking.

173 ren with AD, and there was no correlation of BDNF with IL-31 and Th2 cytokines including IL-4 and IL-

174 However, depletion of BDNF by transfecting lentivirus-derived shBDNF in hippoc

175 ance of understanding the precise details of BDNF biology at the synapse.

176 GDP-Rab3a and thus impairing the docking of BDNF vesicles on plasma membranes of astrocytes.

177 However, the effect of BDNF in autosomal dominant Alzheimer's disease is unknow

178 and p70s6 kinase (p70s6k) and expression of BDNF and membrane GluR1 and GluR2 in the CA1.

179 Over-expression of BDNF in the hippocampus of THC-treated DN-DISC1 mice pre

180 of PSD mice and upregulate the expression of BDNF in the hippocampus.

181 BSJYD inhibited the expression of BDNF, Ras, ERK1/2, and c-fox mRNA in LVH.

182 ced by upregulation of protein expression of BDNF.

183 e PCR were used to assess the expressions of BDNF, Ras, ERK1/2, and c-fox levels.

184 re absent or reduced in the dentate gyrus of BDNF(Met/Met) mice.

185 A dose-dependent increase of BDNF was evident following completion of an NMES protoco

186 ily members, participate in the induction of BDNF exon I, III, and VI transcripts.

187 esults of this study imply that induction of BDNF following adolescence THC exposure may serve as a h

188 As previously reported, infusion of BDNF into the PrL cortex blocked cocaine SA-induced deph

189 ic effect of a PUFA, while the inhibition of BDNF resulted in the reduction of global hypothalamic ce

190 Inhibition of BDNF signaling prevented induction of structural plastic

191 found that the tonic sympatho-inhibition of BDNF was withdrawn in the CHF state, thus contributing t

192 monstrate that pharmacological inhibitors of BDNF-TrkB signaling or of L-type voltage-dependent Ca(2+

193 NF) receptor trkB.T1, a truncated isoform of BDNF.

194 SBP group had significantly lower levels of BDNF (P = 0.005) and TGF-beta1 (P = 0.02).

195 association between the decreasing levels of BDNF and the progression of AD.

196 ecreased baseline peripheral blood levels of BDNF compared with healthy control (HC) subjects (24 stu

197 es report reduced peripheral blood levels of BDNF in AD, but findings are inconsistent.

198 However, protein levels of BDNF remained elevated for a longer period after fractur

199 short-term synaptic facilitation and loss of BDNF surge in the hippocampus of DN-DISC mice, but not i

200 However, local manipulation of BDNF signaling yields divergent effects, depending on th

201 library of small molecules for modulators of BDNF-induced Arc expression in primary cortical neurons.

202 ibody was performed to test the necessity of BDNF release in driving scopolamine-induced behavioral r

203 ly, conditioning results in new occupancy of BDNF chromatin by DNA insulator protein CCCTC-binding fa

204 To identify the cellular origin of BDNF in platelets, we established primary cultures of me

205 Moreover, quantifications of BDNF protein in the hypothalamus, prefrontal cortex, and

206 genetic mechanisms involved in regulation of BDNF expression induced by fluoxetine.

207 inly supported by the abnormal regulation of BDNF in SCZ, especially the decreased peripheral blood B

208 L2 indicates that the negative regulation of BDNF secretion by C5L2 correlates with C5aR activation a

209 identifying C5L2 as a negative regulator of BDNF secretion by pulp fibroblasts under carious teeth.

210 d to the precise localization and release of BDNF at the synapse have remained obscure.

211 e findings indicate that enhanced release of BDNF through exocytosis caused by activation of VDCCs an

212 processing and activity-dependent release of BDNF.

213 Replacement of BDNF selectively in the mOFC in Bdnf(+/-)mice rescued be

214 ogether, these results highlight the role of BDNF in brain repair processes and reinforce the value o

215 Here, we investigated the moderating role of BDNF polymorphism on sleep and next-morning learning abi

216 Studies examining the role of BDNF-TrkB signaling in depression and antidepressant eff

217 pulp nerve regeneration in the secretion of BDNF by pulp fibroblasts under sites of carious injury.

218 have shed light on the question-the site of BDNF release at the synapse.

219 injury (TBI), suggesting that stimulation of BDNF signaling pathways may facilitate functional recove

220 Pharmacological stimulation of BDNF signaling rescued synaptic plasticity and memory de

221 e expression level of transcript variants of BDNF, NTRK2, and selected BDNF-coexpressed genes in youn

222 homeostatic plasticity that was dependent on BDNF and its receptor tropomyosin receptor kinase B (Trk

223 NF pathway (P = 1.73E-10), and its effect on BDNF secretion was sigma 1 receptor (S1R) dependent.

224 ion of microtubule dynamics has no effect on BDNF/TrkB motility, suggesting that dendritic kinesin mo

225 proliferation in vitro in response to FBS or BDNF compared with WT astrocytes.

226 xon I gene promoter, in concert with overall BDNF levels in the hippocampus of drug-treated animals c

227 ology to safely engineer NSCs to overexpress BDNF.

228 explore the relationship between peripheral BDNF levels and autism spectrum disorder (ASD), but the

229 lysis provided evidence of higher peripheral BDNF levels in ASD compared with controls [standardized

230 r memory consolidation, retrieval engages PL BDNF to regulate excitatory and inhibitory synaptic prot

231 We confirm the presence of postsynaptic BDNF using electron microscopy to localize endogenous BD

232 es neuroadaptations in the DLS that preclude BDNF's ability to gate alcohol self-administration in ra

233 on, occurring in part by increasing both pro-BDNF and mature BDNF levels.

234 Under these conditions, pro-BDNF, the obligatory precursor of biologically active BD

235 d suggest SORCS2 as the link between proBDNF/BDNF signaling and mental disorders.

236 ls of these patients can release and produce BDNF.

237 viously reported, requires coincident, rapid BDNF translation and release.

238 ng confirmed the existence of all novel rare BDNF variants.

239 Further, phospho-TRBP recapitulates BDNF-induced neuronal dendritic spine growth in a Lin28a

240 brain-derived neurotrophic factor receptor (BDNF), contributes to gliosis after SCI, but little is k

241 dentified as factors that potentially reduce BDNF secretion, brain plasticity, and memory.

242 a TrkB receptor agonist, suggesting reduced BDNF-TrkB signaling as a contributing factor.

243 wever, the mechanism by which 5-HT regulates BDNF signaling is unknown.

244 d the importance of fluoxetine in regulating BDNF expression which could represent a potential strate

245 ase-dead mutant of PERK (PERK-K618A) rescues BDNF and PSD95 levels in the pericontusional cortex by r

246 erograde BDNF transport, restored retrograde BDNF transport, and normalized lysosomal transport.

247 script variants of BDNF, NTRK2, and selected BDNF-coexpressed genes in younger and older subjects.

248 Stress-sensitive BDNF Val66Met mice of both sexes show a pre-stressed tra

249 pathophysiology of AD, suggesting that serum BDNF which correlates with disease severity contributes

250 A single BDNF infusion into the PrL cortex following a final coca

251 dnf transcripts are associated with specific BDNF-dependent molecular, cellular, and behavioral pheno

252 nts show that scopolamine rapidly stimulates BDNF release and tropomyosin receptor kinase B-extracell

253 eomic analysis of dye eye extracts suggested BDNF-TrkB and Akt signaling as mediators of HDACi rescue

254 gnalling and on postsynaptically synthesized BDNF.

255 delivery of small interfering RNAs targeting BDNF or TrkB mRNA, and MEK/ERK (U0126) or PI3 kinase/Akt

256 via autocrine influence on sensory terminal BDNF.

257 e.g. GRIN2A, DRD1, DRD2, HTR2A, CACNA1C, TH, BDNF, SLC6A3, P2RX7, DRD3, and DRD4) and also highlighte

258 endent on TrkB receptor activation, and that BDNF rescues theta-LTP and cocaine-associated memory def

259 integral for the maintenance of BRS and that BDNF/TrkB signalling is impaired in the NTS in the CHF s

260 We argue that BDNF-ERK1/2 in the mOFC is a key regulator of "online" g

261 ain plasticity, and we provide evidence that BDNF signaling represents a potentially new pharmacologi

262 Instead, we found that BDNF derived from excitatory mossy fiber endings control

263 We found that BDNF Met/Met mice have attenuated responses to scopolami

264 Together, these findings indicate that BDNF-TrkB signaling both mediates and reverses cocaine-i

265 It has been reported that BDNF strengthens the proliferative activity of neuronal

266 RNA interference revealed that BDNF knockdown can suppress osteoblast differentiation.

267 zation and immunocytochemistry revealed that BDNF mRNA was restricted to cells identified as mature n

268 We show that BDNF acts cell autonomous and autocrine, as wildtype neu

269 This study is the first to show that BDNF signaling through the cognate tropomyosin receptor

270 istent with these findings we also show that BDNF/Trk/PKA mediated signaling is required for Zn(2+)-i

271 These findings suggest that BDNF and/or KCC2 could represent novel treatment strateg

272 The BDNF surge in response to THC is perturbed in the presen

273 However, advancing age and carrying the BDNF Met allele were both identified as factors that pot

274 hat human and rat megakaryocytes express the BDNF gene.

275 y of the lower functioning Met allele of the BDNF gene.

276 nd older individuals who are carriers of the BDNF Met allele displayed no positive association betwee

277 n subjects carrying at least one copy of the BDNF Met allele, a more consolidated sleep was not assoc

278 monstration in women that the effects of the BDNF Val/Met polymorphism on hippocampal function are se

279 i-BDNF nAb or in mice with a knock-in of the BDNF Val66Met allele, which blocks the processing and ac

280 Less than 10% of the BDNF-positive cells expressed BrdU, but this percentage

281 inding protein, and subsequently reduces the BDNF level after TBI.

282 internal granular layer (IGL), but that the BDNF protein is present within mossy fibers which origin

283 Pridopidine upregulated the BDNF pathway (P = 1.73E-10), and its effect on BDNF secr

284 to induce long-term depression, and with the BDNF receptor tyrosine kinase TrkB to elicit long-term p

285 nt with conventional antidepressants through BDNF/TrkB signaling.

286 methylcytosine dioxygenase 1 (Tet1), bind to BDNF chromatin in naive but dissociate during conditioni

287 17 children with AD and their connection to BDNF.

288 activity and TrkB signaling is imperative to BDNF's suppressive effect on drug-seeking.

289 he rapid-acting antidepressant, ketamine, to BDNF translation and BDNF-dependent signaling, has re-em

290 t of previously unresolved issues related to BDNF biology, as well as how BDNF may function as a down

291 Neurons lacking SorCS2 failed to respond to BDNF by TrkB autophosphorylation, and activation of down

292 reover, exercise-induced expression of total BDNF, BDNF splice variants 1, 2, 4, 6 and fibronectin ty

293 tial, region-specific contributions to total BDNF levels.

294 na, both in steady-state conditions and upon BDNF stimulation.

295 When BDNF was neutralized, there was a significant reduction

296 However, whether BDNF signaling in the SN participates in the neuroprotec

297 ssant action, although it is unknown whether BDNF and TrkB in the dorsal raphe nucleus are involved i

298 ssed in BDNF Val/Met knock-in mice, in which BDNF processing and release are impaired.

299 rated four novel mutant mouse lines in which BDNF production from one of the four major promoters (I,

300 uicide was not significantly associated with BDNF level (beta = 0.28, SE = 1.20, P = 0.82).

301 whose expression positively correlates with BDNF (r>0.575; n=200 genes) and analyzed them for enrich