ライフサイエンスコーパス: BDNF

1 BDNF also improved expression of genes in muscle known t

2 BDNF and GDNF production were increased in the astrocyte

3 BDNF and its high-affinity receptor TrkB are reduced in

4 BDNF expression was virtually absent in RA neurons of SD

5 BDNF levels among the smokers who were Val allele carrie

6 BDNF mRNA expression increased in the medial prefrontal

7 BDNF signaling in hypothalamic circuitries regulates mam

8 BDNF signaling thru TrkB receptor tyrosine kinase is one

9 BDNF signaling via its transmembrane receptor TrkB has a

10 BDNF(Val66Met) was not associated with connectivity in a

11 BDNF-evoked glutamate release and synapsin phosphorylati

12 BDNF/TrkB variant carriers exhibited learning difficulti

13 LTD of ovBNST neurons was prevented by a BDNF scavenger or in the presence of TrkB inhibitors, in

14 horylation, and increased transcription of a BDNF-dependent program of gene expression containing CRE

15 We conclude by proposing a BDNF stress-sensitivity hypothesis, which posits that di

16 AAV2-BDNF promoted significant functional diaphragm recovery,

17 AAV2-BDNF promotes respiratory axon plasticity and recovery o

18 Furthermore, AAV2-BDNF significantly increased numbers of putative monosyn

19 nges include persistent neuronal activation, BDNF-dependent increase in the excitatory synapse marker

20 Additionally, BDNF is secreted by skeletal muscle and muscle-specific

21 expression is essential to precisely adjust BDNF levels that are dysregulated in various neurologica

22 e trained by physical exercise in the adult, BDNF expression in motor cortex is reinduced, especially

23 the regulation of BDNF by CREB family after BDNF-TrkB signaling is generally conserved between rat a

24 reatment increased adenylyl cyclase (AC) and BDNF gene expression in LCLs.

25 factor beta1), interleukin-1, TNF-alpha, and BDNF signaling pathways.

26 nd memory formation such as Egr-1, Arc1, and BDNF specifically in the cerebral cortex, impacting beha

27 is differentially perturbed by cocaine, and BDNF may be required to link D2R to neuroplasticity in c

28 rsued 4 genes of large effect size: EGR1 and BDNF (decreased by isolation) and FKBP5 and UTS2B (incre

29 ted the effect of solo isolation on EGR1 and BDNF, but not on FKBP5 and UTS2B nor on circulating cort

30 e metabolism, the HPA axis, neurogenesis and BDNF, epigenetics, and obesity.

31 ng the effects of coculturing WT neurons and BDNF-deficient astrocytes.

32 s between smoking, cognitive performance and BDNF in a normal Chinese Han population.

33 ung tissue, and SNPs in the NTRK2 [TrkB] and BDNF genes linked to asthma.

34 Growth factor genes, including VEGFA and BDNF were significantly down-regulated in cells from dep

35 nimal models of BDNF deficiency in vivo, and BDNF is a common downstream intermediary for environment

36 on of an AMPA receptor antagonist or an anti-BDNF neutralizing antibody.

37 latory actions toward growth factors such as BDNF.

38 xpression of promyelinating factors, such as BDNF.

39 ion, and provided a new method that boosting BDNF expression through blocking the function of Pdcd4 i

40 Further, both BDNF and IGF-1 expressions are decreased in MeCP2 T158A

41 rain DHA, which results in increase of brain BDNF.

42 uired for the signaling cascade initiated by BDNF and its receptors at the plasma membrane to modulat

43 rylation and potentiation of GluN2B NMDAR by BDNF at lamina I synapses.

44 everal inflammatory cytokines, such as CD31, BDNF, TFF3, Serpin E-1, VCAM-1, Vitamin D BP, and PDGF-A

45 beta-cell BDNF-TrkB.T1 signaling triggers calcium release from int

46 Upregulation of cancer cell BDNF was required to promote full invasiveness of 4T1BR5

47 ted with nicotine addiction, and circulating BDNF is a biomarker of memory and general cognitive func

48 ggest that for quantification of circulating BDNF blood collected in K2EDTA tubes and plasma stored u

49 d repeated freeze-thaw cycles on circulating BDNF concentrations was evaluated.

50 lude observations that the functional common BDNF Val66Met polymorphism modulates stress susceptibili

51 Moreover, the non-competitive BDNF/TrkB inhibitor ANA-12 reduced E2-induced 4T1BR5 BM

52 L-3'-UTRs containing BDNF messenger RNAs, which migrate to distal dendrites o

53 ly unrecognized role of Pdcd4 in controlling BDNF mRNA translation, and provided a new method that bo

54 Reduced expression of cortical BDNF in 3-month-old mice results in impaired motor learn

55 fferents from motor cortex and that cortical BDNF is essential for motor learning.SIGNIFICANCE STATEM

56 learning in mice depends on corticostriatal BDNF supply, and regulation of BDNF expression during mo

57 SD-mediated effects on hippocampal cAMP-CREB-BDNF, cAMP-PKA-LIMK1-cofilin, and RhoA-ROCK2 pathways.

58 ng toward the calcium-dependent guidance cue BDNF, with STIM1 functioning to sustain calcium signals

59 lls differentially expressed CXCL-10, CXCR3, BDNF and ERBB4 in the developing organoids and in respon

60 r mechanisms behind TrkB signaling-dependent BDNF mRNA induction and show that CREB family transcript

61 To better understand how promoter IV-derived BDNF controls HC-PFC connectivity and fear expression, w

62 Our data suggest that muscle-derived BDNF may be a key factor mediating increased glucose met

63 CREB specific inhibitor (666-15) diminished BDNF and GDNF production induced by n-3 PUFA, suggesting

64 Notably, disrupting BDNF production from promoter IV-derived transcripts enh

65 afficking to the soma and blocked downstream BDNF- and TrkB-dependent signaling to the nucleus.

66 DS BDNF protein positively correlated with perseverative an

67 in vivo in the adult rat hippocampus during BDNF-induced LTP.

68 In cells, the E183K BDNF variant resulted in impaired processing and secreti

69 pharmacological inhibitor of HDAC3, elevated BDNF expression and BRD4 binding to the BDNF promoter, e

70 , which posits that disruption of endogenous BDNF activity by common factors (such as the BDNF Val66M

71 eby stress hormones interact with endogenous BDNF-TrkB signaling to alter brain homeostasis.

72 II and V neurons in the motor cortex express BDNF as a potential regulator of plasticity in corticost

73 lized with neural cell markers and expressed BDNF, TGF-beta1, GFAP, and IL-6.

74 Finally, we show that extensive BDNF transcriptional autoregulation, encompassing all ma

75 GFR(hi) cells induce the neurotrophic factor BDNF, which contributes to T cell resistance, as does NG

76 r, CXCR3, brain-derived neurotrophic factor (BDNF) and a receptor tyrosine-protein kinase, ERBB4, in

77 lation of brain-derived neurotrophic factor (BDNF) and somatostatin (SST), a marker of inhibitory gam

78 s well as brain-derived neurotrophic factor (BDNF) and total percent DNA methylation of Th and Bdnf g

79 s rich in brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) receptor.

80 driven by brain-derived neurotrophic factor (BDNF) and Tropomyosin receptor kinase B (TrkB).

81 th plasma brain-derived neurotrophic factor (BDNF) concentrations.

82 in muscle brain-derived neurotrophic factor (BDNF) correlate with neuromuscular deficits in mouse mod

83 rved that brain-derived neurotrophic factor (BDNF) enhances co-localization of dendritic ZBP1 and PAT

84 enhancing brain-derived neurotrophic factor (BDNF) expression and improved memory following HDAC inhi

85 ations of brain-derived neurotrophic factor (BDNF) have been linked to cancer, neuropsychiatric, diab

86 lation of brain-derived neurotrophic factor (BDNF) in astrocytes, and subsequent activation of tumor

87 eptor and brain-derived neurotrophic factor (BDNF) in the antidepressant-like effects of 5-HT(1A) rec

88 ess total brain-derived neurotrophic factor (BDNF) in the cortex and/or hippocampus at 1 and/or 21 da

89 Brain-derived neurotrophic factor (BDNF) influences the differentiation, plasticity, and su

90 port that brain-derived neurotrophic factor (BDNF) is a fasting-induced myokine that controls metabol

91 Brain-derived neurotrophic factor (BDNF) is a growth factor that plays vital roles in the n

92 Brain-derived neurotrophic factor (BDNF) is a key regulator of the morphology and connectiv

93 Brain-derived neurotrophic factor (BDNF) is a potent modulator of brain synaptic plasticity

94 Brain-derived neurotrophic factor (BDNF) is generated by proteolytic cleavage of a prodomai

95 Brain-derived neurotrophic factor (BDNF) is widely accepted for its involvement in resilien

96 d whether brain-derived neurotrophic factor (BDNF) mediates a transsynaptic effect from HVC to RA in

97 rate that brain-derived neurotrophic factor (BDNF) might be associated with nicotine addiction, and c

98 ility and brain-derived neurotrophic factor (BDNF) modulates glutamate plasticity in these circuits,

99 educed in brain-derived neurotrophic factor (BDNF) mutants, which are severely obese and have diminis

100 Brain-derived neurotrophic factor (BDNF) plays a central pivotal role in the development of

101 owed that brain-derived neurotrophic factor (BDNF) signaling in the mesolimbic dopamine (DA) circuit

102 Brain-derived neurotrophic factor (BDNF) signaling regulates synaptic plasticity in the hip

103 ates that brain-derived neurotrophic factor (BDNF) signaling through the TrkB receptor plays a critic

104 icity and brain-derived neurotrophic factor (BDNF) signaling.

105 Brain-derived neurotrophic factor (BDNF) signals through its high affinity receptor Tropomy

106 izes with brain-derived neurotrophic factor (BDNF), a key player in the pathophysiology of major depr

107 or (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and glial cell line-derive

108 ticularly brain-derived neurotrophic factor (BDNF), on airway contractility [ via increased airway sm

109 (MSK1), a brain-derived neurotrophic factor (BDNF)-activated enzyme downstream of the mitogen-activat

110 ttenuates brain-derived neurotrophic factor (BDNF)-induced pTRKB in cortical neurons in culture.

111 KOR), and brain-derived neurotrophic factor (BDNF).

112 CREB), and brain-derived neurotropic factor (BDNF) by up-regulating the microRNA miR-34a.

113 t that a muscle-derived neurotrophic factor, BDNF, rescues synaptic and muscle function in a muscle-t

114 duce astrocyte-derived neurotrophic factors, BDNF and IGF-1, and the glutamate transporter, GLT-1 aft

115 the astrocyte-derived neurotrophic factors, BDNF and IGF-1, as well as the astrocytic glutamate tran

116 PAT1 is essential for BDNF-stimulated neuronal growth cone development and den

117 e in the phosphorylation of the receptor for BDNF, TrkB, in the ventral hippocampus (vHipp) 30 or 60

118 ated that the avidity of heparan sulfate for BDNF increased with sulfation at the 2-O position of idu

119 of the tyrosine-related kinase B (TrkB) for BDNF, prevented the increase in RA neuron firing rate in

120 signaling, and activates transcription from BDNF promoter IV by recruiting CBP.

121 ns and knock-in mice with a loss of function BDNF SNP (Val66Met), the functionality of this circuit w

122 In conclusion, human loss of function BDNF/TrkB variants that impair hippocampal synaptogenesi

123 Furthermore, BDNF deletion reduces motor end plate volume without aff

124 Furthermore, BDNF/TrkB signaling mediated long-term depression (LTD)

125 the brain-derived neurotrophic factor gene (BDNF Val66Met), in a way that recapitulates the hallmark

126 The association between higher BDNF levels and cognitive impairment, mainly attention i

127 Hippocampal BDNF levels and cortical mTOR expression were found to b

128 rment occurred despite preserved hippocampal BDNF content and could be reversed by stimulation of BDN

129 However, BDNF's broad functionality has manifested a heterogeneou

130 ossibility, transgenic mice expressing human BDNF in skeletal muscle were crossed with '97Q' KD mice.

131 The ex vivo human BDNF model may thus form a translational bridge between

132 paraventricular nucleus of the hypothalamus (BDNF(PVH)).

133 ivation of Ocn-Cre(+) dDG neurons identified BDNF, which was required for Ocn-Cre(+) dDG neurons medi

134 Our data identify BDNF/TrkB signaling as a critical regulator of synaptic

135 knock-in mice (Ntrk2tm1Ddg/J) with impaired BDNF signaling were chronically exposed to ovalbumin (OV

136 n hippocampal-medial-frontal connectivity in BDNF(Val66Met) could be also found in elderly subjects w

137 le mice with a muscle-specific deficiency in BDNF (MBKO mice) were unable to switch the predominant f

138 development of this circuit is disrupted in BDNF Met carriers due to insufficient BDNF bioavailabili

139 served functional cAMP-responsive element in BDNF promoter IXa in humans renders the human promoter r

140 situ hybridization confirmed an increase in BDNF expression in HVC neurons of birds switched to a lo

141 results suggest a critical role for PAT1 in BDNF-induced beta-actin mRNA transport during postnatal

142 characterised a de novo missense variant in BDNF and seven rare variants in TrkB identified in a lar

143 of differentially expressed genes, including BDNF.

144 been implicated in schizophrenia (including BDNF and GABAergic-related transcripts).

145 eting of BRD4 to the BDNF promoter increased BDNF mRNA.

146 suggest that BDNF-TrkB signaling may induce BDNF gene expression in a distinct manner compared with

147 od-brain barrier during sepsis and inhibited BDNF-mediated LTP.

148 Hook1 depletion inhibited BDNF trafficking to the soma and blocked downstream BDNF

149 r, decreased Rab5 or Rab11 activity inhibits BDNF-induced dendritic branching.

150 ted in BDNF Met carriers due to insufficient BDNF bioavailability, specifically during a peri-adolesc

151 Intriguingly, BDNF's ameliorative effects differed between muscle type

152 and 2) smooth muscle-specific BDNF knockout (BDNF(fl/fl)/SMMHC11(Cre/0)) mice.

153 ignaling, suggesting the presence of a local BDNF inhibitor.

154 ry vein AR duration were associated with low BDNF in CAD.

155 ional autoregulation, encompassing all major BDNF transcripts, occurs also in vivo in the adult rat h

156 red for the early induction of all the major BDNF transcripts, whereas CREB itself directly binds onl

157 affect the quantity of BDNF measured as mean BDNF concentrations generally fell within our calculated

158 brain-derived neurotrophic factor-mediated (BDNF-mediated) process responsible for spatial memory fo

159 receptors at the plasma membrane to modulate BDNF-dependent gene expression and neuronal dendritic gr

160 stimulus-specific distal enhancer modulating BDNF gene expression.

161 Muscle BDNF expression was also affected in KD patients, reinfo

162 sease (KD), suggesting that restoring muscle BDNF might restore function.

163 In sum, muscle BDNF slows disease progression, rescuing select cellular

164 Given that muscle BDNF had divergent therapeutic effects that depended on

165 We found that muscle BDNF slowed disease, doubling the time between symptom o

166 diated transsynaptically by the neurotrophin BDNF.

167 DPSC-CM contained significant levels of NGF, BDNF, NT-3 and GDNF.

168 rimentally disentangle the causal actions of BDNF in stress responses, which likely interact to poten

169 h functions are likely through activation of BDNF.

170 Plasma concentrations of BDNF were significantly affected by the type of plasma s

171 Deletion of BDNF(PVH) blunts the effects of leptin on innervation.

172 wing for inducible, reversible disruption of BDNF receptor kinase activity by administration of 1NMPP

173 lutamate receptors, as well as disruption of BDNF-TrkB signaling.

174 that hippocampal PKMzeta acts downstream of BDNF and controls AMPAR synaptic insertion to elicit rec

175 igate whether mGluR5 might act downstream of BDNF to critically regulate VMH neuronal activity and me

176 that hippocampal PKMzeta acts downstream of BDNF to regulate AMPAR recycling during ORM reconsolidat

177 rylation of signaling proteins downstream of BDNF, including mTOR, ERK, 4EBP1, and p70S6K.

178 rited Alzheimer Network (DIAN) the effect of BDNF(Val66Met) on resting-state fMRI assessed functional

179 sults contribute to the emerging evidence of BDNF as a potential diagnostic value in CAD that might l

180 ses the mRNA level and protein expression of BDNF and IGF-1 in MeCP2 T158A mice.

181 report for the first time that expression of BDNF, but not other members of the neurotrophin family,

182 B.T1 identifies a new regulatory function of BDNF on metabolism that is independent of CNS activity.

183 physical exercise leads to the induction of BDNF, and identify lactate as a potential endogenous mol

184 Infusion of BDNF protein adjacent to the RA of SD birds caused an in

185 NF-expressing cortical neurons and levels of BDNF protein are highest in juvenile mice when adult mot

186 understanding of the intricate mechanism of BDNF transcriptional autoregulation.SIGNIFICANCE STATEME

187 se changes, which involved the mechanisms of BDNF, muscarinic receptors, and beta3-adrenoceptor expre

188 have also been observed in animal models of BDNF deficiency in vivo, and BDNF is a common downstream

189 Hook1 significantly reduced the motility of BDNF-signaling endosomes without affecting the motility

190 a contemporary update on the neurobiology of BDNF including new data from the behavioral neuroscience

191 nance errors, suggesting mPFC-DS overflow of BDNF during withdrawal.

192 we demonstrate how neurochemical pathways of BDNF and FGF2, through the MAPK, PI3K, and JNK cascades,

193 e in HDAC3 inhibitor-induced potentiation of BDNF expression, neuroplasticity, and memory.SIGNIFICANC

194 l complexity is increased in the presence of BDNF and is dependent upon BDNF/TrkB.T1 signaling.

195 ant decrease in the flux and processivity of BDNF-Qdots along the mid-axon, an effect specific for Ho

196 did not significantly affect the quantity of BDNF measured as mean BDNF concentrations generally fell

197 In support of this, in vitro reduction of BDNF induced axonal hypersensitivity to PlexinA4 signali

198 pathway, which resulted in the reduction of BDNF protein expression.

199 could be reduced by genetic co-reduction of BDNF.

200 r constructs indicate that the regulation of BDNF by CREB family after BDNF-TrkB signaling is general

201 rticostriatal BDNF supply, and regulation of BDNF expression during motor learning is highest in cort

202 rstanding of stimulus-specific regulation of BDNF gene expression is essential to precisely adjust BD

203 Ergo regulators of BDNF availability, such as the Val66Met polymorphism, ma

204 y identifying novel epigenetic regulators of BDNF expression, these data may lead to new therapeutic

205 scription factors are the main regulators of BDNF gene expression after TrkB signaling.

206 We first demonstrate the relevance of BDNF release from astrocytes by evaluating the effects o

207 n the present study, we examined the role of BDNF in allergen-induced airway inflammation using 2 tra

208 The role of BDNF in vulnerability to stress and stress-related disor

209 accumbens, suggesting a dichotomous role of BDNF signaling in striatal regions.

210 recent advances in knowledge on the role of BDNF within the fear circuitry, as well as address mount

211 tent and could be reversed by stimulation of BDNF signaling, suggesting the presence of a local BDNF

212 and selectively repressed the translation of BDNF splice variant IIc mRNA in an eIF4A-dependent manne

213 endogenous inhibitor for the translation of BDNF, and selectively repressed the translation of BDNF

214 Since there is bidirectional transport of BDNF through the BBB, we tested the hypothesis that plas

215 used) to create 5xFAD mice that overexpress BDNF when and where astrogliosis is initiated (5xF:pGB m

216 Next, we crossed 5xFAD mice with pGFAP:BDNF mice (only males were used) to create 5xFAD mice th

217 Plasma BDNF was quantified using a commercially available ELISA

218 n omega-3 index with the increases in plasma BDNF and the erythrocyte index were determined.

219 ively correlated with the increase in plasma BDNF, it negatively correlated with the erythrocyte inde

220 he BBB, we tested the hypothesis that plasma BDNF may be used as biomarker for brain DHA enrichment.

221 These results show that the plasma BDNF is more reliable than the erythrocyte index as biom

222 ially mechanistically linked to the powerful BDNF-TrkB neurotrophic signaling system.

223 e Pdcd4-eIF4A complex substantially promoted BDNF expression and rescued the behavioral disorders whi

224 growth, proliferation and survival proteins (BDNF, Akt, mTOR, p70S6K, ERK and CREB) in the cerebral c

225 CRTC family, are the main regulators of rat BDNF gene expression after TrkB signaling.

226 like effects via activation of AMPA receptor/BDNF/mTOR signaling in mice, which subsequently increase

227 ucocorticoid signaling also acutely recruits BDNF to enhance the expression of fear memory.

228 ese findings suggest that activity regulates BDNF expression differentially in layers II/III and V st

229 Remarkably, BDNF is capable of modulating its own expression levels

230 Remarkably, BDNF stimulates TrkB to phosphorylate APP Y687 residue t

231 tained antidepressant responses that require BDNF expression and calcium mobilization in vmPFC.

232 dynamics (MD) simulations of the 91 residue BDNF prodomain, for both the V66 and M66 sequence.

233 two-dimensional echocardiography, and serum BDNF estimation.

234 Relating serum BDNF levels with two-dimensional echocardiographic indic

235 nificant molecular linkage between the serum BDNF level and cardiovascular function.

236 Notably, the serum BDNF was significantly lower in individuals with CAD (30

237 Particularly, the model with serum BDNF concentration and blood parameters of CAD achieved

238 P1 derivative, and 2) smooth muscle-specific BDNF knockout (BDNF(fl/fl)/SMMHC11(Cre/0)) mice.

239 reted by skeletal muscle and muscle-specific BDNF knockout phenocopies the beta-cell TrkB.T1 deletion

240 ical and therapeutic importance of the STAT3-BDNF-TrkB axis in orchestrating alveolar epithelial rege

241 asticity and survival.SIGNIFICANCE STATEMENT BDNF is a neurotrophic factor that regulates plastic cha

242 Pb-related alterations in behavior, striatal BDNF levels, frontal cortical Th total percentage DNA me

243 rs influencing plasma storage and subsequent BDNF quantification are incompletely understood.

244 Surprisingly, BDNF protein declined in mPFC but was elevated in dorsal

245 factor for several mental illnesses, targets BDNF in disease-implicated brain regions and circuits.

246 We also find that BDNF rescues select molecular mechanisms in slow and fas

247 The finding that BDNF is also secreted by differentiated human muscle cel

248 We first found that BDNF from astrocytes is crucial for dendrite outgrowth a

249 These results indicate that BDNF is sufficient, and TrkB receptor activation is nece

250 These findings indicated that BDNF/TrkB signalling was disrupted in the OC of Nhe6 KO

251 rogeneous literature; likely reflecting that BDNF plays a hitherto under-recognized multifactorial ro

252 We have previously shown that BDNF/TrkB signaling regulates the activity and mobility

253 Our results suggest that BDNF-TrkB signaling may induce BDNF gene expression in a

254 Recent evidence suggests that BDNF has adverse subclinical cardiac remodeling in parti

255 Although the BDNF Met genotype intersects the behavioral and transcri

256 Chronic stress and the BDNF polymorphism Val66Met disrupt the BDNF-dependent GR

257 BDNF activity by common factors (such as the BDNF Val66Met variant) potentiates sensitivity to stress

258 d the BDNF polymorphism Val66Met disrupt the BDNF-dependent GR-PO(4) pathway necessary for preserving

259 machine (SVM) models performed to ensure the BDNF level in the classification of CAD from healthy con

260 Ovariectomized mice heterozygous for the BDNF Met allele (Het-Met) and their matched wild-type (W

261 Furthermore, the BDNF receptor tropomyosin receptor kinase B (TrkB) was e

262 However, the BDNF translational machinery in depression remains unkno

263 Mutations in the BDNF or the TrkB-encoding NTRK2 gene have been found to

264 (seed) to medial-frontal connectivity in the BDNF(Val66Met) carriers compared to BDNF(Val) homozogyte

265 aphic indices will provide insights into the BDNF mediated pathophysiology in coronary artery disease

266 The SAHP version of the BDNF prodomain suggested a protein segmented into three

267 ignaling, we measured the mRNA levels of the BDNF receptor TrkB and of P/Q-type Ca(2+) channel alpha-

268 ndings suggest a synaptic entry point of the BDNF/TrkB system for adaptation to stressful environment

269 on in smokers appears to be dependent on the BDNF Val66Met polymorphism.

270 ith neuroticism, and a locus overlapping the BDNF receptor gene, NTRK2.

271 Here, we show that the BDNF receptor TrkB.T1 is expressed by pancreatic beta-ce

272 riven by TrkB signaling and suggest that the BDNF-TrkB pathway may be a potential target.

273 m male mouse ovBNST in vitro showed that the BDNF/TrkB interaction causes a hyperpolarizing shift of

274 RD4, locus-specific targeting of BRD4 to the BDNF promoter increased BDNF mRNA.

275 ated BDNF expression and BRD4 binding to the BDNF promoter, effects that were abrogated by JQ1 (an in

276 The number of these BDNF-expressing cortical neurons and levels of BDNF prot

277 Thus, BDNF may induce plasticity to deleteriously promote the

278 Alteration to BDNF expression is associated with major depressive diso

279 y in the BDNF(Val66Met) carriers compared to BDNF(Val) homozogytes.

280 ed cell types that selectively contribute to BDNF-dependent behaviors.

281 shifting and these deficits may be linked to BDNF-mediated alterations in glutamate signaling dynamic

282 , whereas CREB itself directly binds only to BDNF promoter IV, is phosphorylated in response to BDNF-

283 howed that stretched axons do not respond to BDNF signaling, suggesting interference between the two

284 romoter IV, is phosphorylated in response to BDNF-TrkB signaling, and activates transcription from BD

285 ans renders the human promoter responsive to BDNF-TrkB-CREB signaling, whereas the rat ortholog is un

286 on provides a clear example of transsynaptic BDNF effects in the adult brain in a functionally releva

287 in effector Hook1 mediates transport of TrkB-BDNF-signaling endosomes in primary hippocampal neurons.

288 ed brain changes are strongly dependent upon BDNF genetic variation, illustrating how drug-induced ps

289 n the presence of BDNF and is dependent upon BDNF/TrkB.T1 signaling.

290 ly and late stages of BM, and E2 upregulated BDNF in ER(+) reactive astrocytes in vitro and in vivo.

291 In V1, BDNF and its high-affinity receptor TrkB are important f

292 ina I synapses and show that a human ex vivo BDNF model of pathological pain processing downregulates

293 However, whether BDNF exerts metabolic effects on peripheral organs is cu

294 derived from embryos of unknown sex, whether BDNF-induced signaling cascades are altered when early a

295 improves the outcome of the therapy in which BDNF could have a role.

296 therapeutic value for CNS diseases in which BDNF signaling is disrupted.SIGNIFICANCE STATEMENT It is

297 and identify a developmental window in which BDNF-based interventions may have therapeutic potential.

298 when adult motor patterns are shaped, while BDNF levels in the adult are low.

299 Additionally, TrkB activation with BDNF increases firing of these PVH neurons.

300 Our complementary reporter assays with BDNF promoter constructs indicate that the regulation of