ライフサイエンスコーパス: DLPFC

1 DLPFC activity is modulated by the ascending cholinergic

2 DLPFC GABA content did not predict performance sensitivi

3 DLPFC may be an important target for neurostimulation th

4 DLPFC neurons encoded signals related to both task-relev

5 DLPFC rTMS reduced punishment for wrongful acts without

6 Altered DLPFC activation is implicated in a number of human psyc

7 groups had significantly decreased amygdala-DLPFC FC.

8 No effects on n-back-related activation and DLPFC-hippocampus resting-state connectivity were observ

9 tional connectivity between the left ARC and DLPFC in a sample of musicians with and without AP.

10 DLPFC NAA and anterior cingulate cortex and DLPFC Glu levels.

11 ry patterns within and between the DMPFC and DLPFC in human epilepsy patients with intracranial EEG e

12 ma oscillations within and between DMPFC and DLPFC.

13 rity, increased activation in the insula and DLPFC, and decreased DLPFC Glx.

14 gnitude of LDX-induced change in insular and DLPFC activation.

15 fficulties include modulation of insular and DLPFC recruitment as well as decrease in DLPFC Glx conce

16 tly changed, in parvalbumin interneurons and DLPFC gray matter.

17 e on working memory performance measures and DLPFC activation.

18 OFC and DLPFC neurons tended to show the largest changes in firi

19 xibility, and thus the collaboration between DLPFC and TPJ might serve as a more appropriate mechanis

20 Our findings reveal a link between DLPFC structure and an individual's propensity to gain f

21 ecreased repetition suppression in bilateral DLPFC.

22 to be differentially expressed, and in both DLPFC and hippocampus none of the individual immune path

23 HD-tDCS than under sham stimulation in both DLPFC groups.

24 itional, yet crucial role of TPJ: a combined DLPFC/TPJ activity predicted flexibility, regardless of

25 in humans and implicate factors controlling DLPFC GABA content in the neural mechanisms of WM and it

26 Among controls, DLPFC stimulation led to a reciprocal attenuation of MPF

27 pathways in dorsolateral prefrontal cortex (DLPFC) (144 schizophrenia and 196 control subjects) and

28 group in the dorsolateral prefrontal cortex (DLPFC) (MR, 0.26 mm; P = .001) and temporal cortex (MR,

29 hored on the dorsolateral prefrontal cortex (DLPFC) and a salience system anchored on the anterior in

30 t IFG to the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex under three conditi

31 ncluding the dorsolateral prefrontal cortex (DLPFC) and appear to arise during the protracted maturat

32 ver the left dorsolateral prefrontal cortex (DLPFC) and cathodal tDCS over the right DLPFC for 30 min

33 cells in the dorsolateral prefrontal cortex (DLPFC) appears to contribute to cognitive dysfunction in

34 of the left dorsolateral prefrontal cortex (DLPFC) as well as left M1.

35 of the left dorsolateral prefrontal cortex (DLPFC) as well as on the integrity of the left arcuate f

36 of the left Dorsolateral Prefrontal Cortex (DLPFC) can improve implicit, procedural learning of word

37 of the left dorsolateral prefrontal cortex (DLPFC) can produce analgesic effects on postoperative an

38 sfunction of dorsolateral prefrontal cortex (DLPFC) circuitry.

39 ted that the dorsolateral prefrontal cortex (DLPFC) contributes in this process.

40 of the human dorsolateral prefrontal cortex (DLPFC) decreased the effect of honesty concerns on behav

41 urons in the dorsolateral prefrontal cortex (DLPFC) encode a diverse array of sensory and mnemonic si

42 ), and right dorsolateral prefrontal cortex (DLPFC) evident only in SZ.

43 es on normal dorsolateral prefrontal cortex (DLPFC) function.

44 signal, and dorsolateral prefrontal cortex (DLPFC) glutamate+glutamine (Glx) were measured using a c

45 CS) over the dorsolateral prefrontal cortex (DLPFC) has been effective in modulating attention.

46 Although the dorsolateral prefrontal cortex (DLPFC) has long been considered critical for WM, we stil

47 how that the dorsolateral prefrontal cortex (DLPFC) implements a flexible value code based on object-

48 ested in the dorsolateral prefrontal cortex (DLPFC) in MDD (F21,59=2.32, P=0.006).

49 plicated the dorsolateral prefrontal cortex (DLPFC) in norm-based judgments, the relative contributio

50 nsity in the dorsolateral prefrontal cortex (DLPFC) in schizophrenia.

51 (TMS) of the dorsolateral prefrontal cortex (DLPFC) is an established treatment for depression, but i

52 mes that the dorsolateral prefrontal cortex (DLPFC) is causally involved in this adjustment.

53 sed genes of dorsolateral prefrontal cortex (DLPFC) neurons.

54 orted in the dorsolateral prefrontal cortex (DLPFC) of schizophrenia subjects.

55 of the right dorsolateral prefrontal cortex (DLPFC) on working memory performance, while measuring ta

56 he extent of dorsolateral prefrontal cortex (DLPFC) plasticity in Alzheimer disease (AD) and its asso

57 The dorsolateral prefrontal cortex (DLPFC) plays a pivotal role in automating this process o

58 The dorsolateral prefrontal cortex (DLPFC) plays a pivotal role in executive function, inclu

59 The dorsolateral prefrontal cortex (DLPFC) plays an important role in appetite and food inta

60 of the left dorsolateral prefrontal cortex (DLPFC) predicted an individual's response to training.

61 a, and right dorsolateral prefrontal cortex (DLPFC) regions supported the stress processing and react

62 zed that the dorsolateral prefrontal cortex (DLPFC) regulates craving during changes in intertemporal

63 Dorsolateral prefrontal cortex (DLPFC) retrieval activation for the working memory load

64 the primate dorsolateral prefrontal cortex (DLPFC) supports a range of cognitive functions.

65 ack from the dorsolateral prefrontal cortex (DLPFC) to V1.

66 red from the dorsolateral prefrontal cortex (DLPFC) using combined transcranial magnetic stimulation

67 The dorsolateral prefrontal cortex (DLPFC) was chosen as control site.

68 ex and right dorsolateral prefrontal cortex (DLPFC) were compared via 4-tesla proton single volume ma

69 ver the left dorsolateral prefrontal cortex (DLPFC) would reduce cue craving for cigarettes compared

70 la, pACC and dorsolateral prefrontal cortex (DLPFC)) to test the effects of forest, urban green, wate

71 in the left dorsolateral prefrontal cortex (DLPFC), a region of the brain that plays a key role in t

72 ortex (OFC), dorsolateral prefrontal cortex (DLPFC), and anterior cingulate cortex (ACC) in cost-bene

73 e, bilateral dorsolateral prefrontal cortex (DLPFC), and bilateral middle temporal gyrus.

74 to the right dorsolateral prefrontal cortex (DLPFC), and fMRI and functional connectivity analyses [s

75 geted to the dorsolateral prefrontal cortex (DLPFC), anodal, facilitatory tDCS has been shown to impr

76 at the left dorsolateral prefrontal cortex (DLPFC), cathode electrode at the right supraorbital area

77 phrenia (the dorsolateral prefrontal cortex (DLPFC), hippocampus and caudate) in a much larger set of

78 t: bilateral dorsolateral prefrontal cortex (DLPFC), medial frontal/cingulate gyrus, posterior cingul

79 nd the right dorsolateral prefrontal cortex (DLPFC), mirroring clinical evidence of disturbed memory

80 post-mortem dorsolateral prefrontal cortex (DLPFC), we found striking decreases in tyrosine phosphor

81 (L5) of the dorsolateral prefrontal cortex (DLPFC), we sought to determine if transcriptome alterati

82 ncluding the Dorsolateral Prefrontal Cortex (DLPFC).

83 tDCS) of the dorsolateral prefrontal cortex (DLPFC).

84 cells in the dorsolateral prefrontal cortex (DLPFC).

85 (DMPFC) and dorsolateral prefrontal cortex (DLPFC).

86 erved by the dorsolateral prefrontal cortex (DLPFC).

87 of GAD25 in dorsolateral prefrontal cortex (DLPFC).

88 ction of the dorsolateral prefrontal cortex (DLPFC).

89 the primate dorsolateral prefrontal cortex (DLPFC).

90 essed in the dorsolateral prefrontal cortex (DLPFC): UNC5C, ENC1, and TMEM106B.

91 genes in the dorsolateral prefrontal cortex (DLPFC, comprised of Brodmann areas 9 and 46) from 19 ind

92 d (bilateral dorsolateral prefrontal cortex, DLPFC) rsFC analysis was performed.

93 ation in the insula and DLPFC, and decreased DLPFC Glx.

94 to theta coupling in the reverse direction (DLPFC to DMPFC).

95 and a potential treatment target to enhance DLPFC function and working memory in patients with AD.

96 theta power increase that causally entrained DLPFC theta activity (DMPFC to DLPFC).

97 These results point to a causal role for DLPFC in honest behavior.

98 findings reveal a selective, causal role for DLPFC in norm enforcement: representational integration

99 medicated patient group demonstrated higher DLPFC activation (P = .02) and better behavioral perform

100 ficial and middle laminar zones of the human DLPFC.

101 s superficial and middle layers of the human DLPFC.

102 ions of each PV neuronal population to human DLPFC function requires a detailed examination of their

103 Participants with AD had impaired DLPFC plasticity (mean [SD] potentiation, 1.18 [0.25]) c

104 ne whether participants with AD had impaired DLPFC plasticity compared with healthy control participa

105 matic responses that are related to impaired DLPFC activation.

106 In DLPFC L3 and L5 pyramidal cells, transcriptome alteratio

107 In DLPFC, 23 immune genes were found to be differentially e

108 ndings suggest that molecular alterations in DLPFC L3 and L5 pyramidal cells might be characteristic

109 le inefficiency model of risk association in DLPFC and suggests that other neurobiological mechanisms

110 he activity of excitatory pyramidal cells in DLPFC layer 3 and, to a lesser extent, in layer 5.

111 Individual pyramidal cells in DLPFC layers 3 or 5 were captured by laser microdissecti

112 c single-neuron and population value code in DLPFC that advances from reward experiences to economic

113 modest increases in NAA/Cr and choline/Cr in DLPFC in people with schizophrenia.

114 and DLPFC recruitment as well as decrease in DLPFC Glx concentration.

115 ated inhibitory neurotransmission deficit in DLPFC could lead to hyperexcitability and, potentially n

116 any studies have profiled gene expression in DLPFC gray matter in schizophrenia, little is known abou

117 r-specific and cell type-specific fashion in DLPFC deep layer 3.

118 These oscillations are generated in DLPFC layer 3 (L3) via reciprocal connections between py

119 (D2L) ratio were significantly increased in DLPFC of patients with SCZ relative to controls (P<0.000

120 in the proportion of intragenic novel L1s in DLPFC of PDS.

121 e ARP2/3 complex were significantly lower in DLPFC layer 3 and 5 pyramidal cells in schizophrenia.

122 ate that blockade of muscarinic receptors in DLPFC creates deficits in working memory representation

123 errors and showed significant reductions in DLPFC activation.

124 tin cytoskeleton, was previously reported in DLPFC gray matter from subjects with schizophrenia.

125 terrogating gene expression, specifically in DLPFC layer 3 or 5 pyramidal cells, would reveal new and

126 2 splice variants and the DRD1 transcript in DLPFC, hippocampus and caudate nucleus in a large cohort

127 r memory-related cortical regions, including DLPFC, thus supporting a specific hippocampal contributi

128 orm a reward-based foraging task, individual DLPFC neurons signal the value of specific choice object

129 white matter structural integrity between L-DLPFC and thalamus, two key components of the neuromodul

130 .0001), and a positive correlation between l-DLPFC GABA levels, but not Glx, and minimal oxygen satur

131 , there was a negative correlation between l-DLPFC GABA levels, but not Glx, and SDB severity by AHI

132 n the left dorsolateral prefrontal cortex (l-DLPFC) and bilateral hippocampal regions of 19 older adu

133 Left dorsolateral prefrontal cortex (L-DLPFC) tDCS induced an analgesic effect, which was expla

134 In subjects with SDB, levels of l-DLPFC GABA, but not Glx, were significantly lower than i

135 higher task-related frontal activation (left DLPFC, N2>N0), which disappeared after real-rTMS.

136 orsal anterior cingulate cortex (dACC), left DLPFC, hippocampus, and left insula, suggested a stress

137 ncreased withdrawal symptoms, decreased left DLPFC and increased PCC BOLD percent signal change (abst

138 79 TT genotype had significantly higher left DLPFC activation than those with the GG/GT genotypes.

139 Patients showed significantly higher left DLPFC retrieval activation on working memory load 3, low

140 However, left DLPFC underactivation was significantly more pronounced

141 tion of abstinence-induced decreases in left DLPFC activation and reduced suppression of PCC may be a

142 up-regulating the cortical function in left DLPFC and left M1 with tDCS.

143 ving simultaneous anodal stimulation of left DLPFC and cathodal stimulation of right DLPFC (bipolar-b

144 that underlies the analgesic effects of left DLPFC rTMS, and to examine how the function of this circ

145 changes following tDCS over left M1 or left DLPFC in learning a complex bimanual task.

146 loxone immediately before sham and real left DLPFC rTMS on the same experimental visit.

147 These preliminary results suggest that left DLPFC rTMS drives top-down opioidergic analgesia.

148 er repeated anodal tDCS targeted at the left DLPFC (compared with sham tDCS) has an immediate effect

149 We collected MRS measurements in the left DLPFC and left striatum during tDCS and an additional MR

150 orrelated with Glx concentration in the left DLPFC at baseline.

151 term tDCS.Short-term anodal tDCS of the left DLPFC did not have an immediate effect on ad libitum foo

152 nd an additional MRS measurement in the left DLPFC immediately after the end of stimulation.

153 eling (ASL), during tDCS applied to the left DLPFC in healthy humans.

154 l effects of anodal tDCS applied to the left DLPFC in terms of modulating functional connectivity bet

155 We conclude that cathodal tDCS over the left DLPFC might facilitate the relaxation of learned constra

156 Magnetic Stimulation was applied to the left DLPFC or to the control site before the Hebb task.

157 n of high-frequency rTMS (10 Hz) of the left DLPFC significantly reduced subjective craving induced b

158 r gamma-aminobutyric acid levels in the left DLPFC.

159 cient neurovascular coupling within the left DLPFC.

160 cal activity) or sham tDCS aimed at the left DLPFC.

161 ng cathodal, anodal or sham tDCS to the left DLPFC.

162 Smokers showed lower DLPFC NAA, Cr, mI and Glu concentrations and lower lenti

163 We found that individuals with lower DLPFC GABA showed greater performance degradation with h

164 We used fMRI to measure DLPFC/TPJ activity recruited during moral flexibility, a

165 athway were assessed in laser-microdissected DLPFC layer 3 and 5 pyramidal cells and layer 3 parvalbu

166 athway were assessed in laser-microdissected DLPFC layer 3 and 5 pyramidal cells and layer 3 parvalbu

167 h previous ultrastructural studies in monkey DLPFC where Type I PV-IR synapses were not identified in

168 Supporting this interpretation, in monkey DLPFC, higher minor-to-major variant ratios predicted lo

169 cance (P<0.05) in an independent post-mortem DLPFC data set (182 schizophrenia and 212 control subjec

170 ed with smaller fALFF in bilateral ACC/mPFC, DLPFC, and posterior parietal cortex in both groups.

171 1) recent findings regarding alterations of DLPFC layer 3 circuitry in schizophrenia, 2) the develop

172 tion was thereafter completed by coupling of DLPFC gamma power to DMPFC theta oscillations.

173 emonstrated greater age-related decreases of DLPFC NAA and anterior cingulate cortex and DLPFC Glu le

174 arly theta (4-8 Hz) modulated enhancement of DLPFC gamma-band (30-100 Hz) activity constituted a prer

175 tions indicated heterozygosity in genomes of DLPFC cells.

176 These results confirm the involvement of DLPFC GABA in WM load processing in humans and implicate

177 gnitive control, but that the involvement of DLPFC in control is not restricted to the left or right

178 e findings indicate a crucial involvement of DLPFC in the normalization processes of emotional attent

179 The magnitude of DLPFC engagement to rewards administered in the laborato

180 the use of DLPFC plasticity as a measure of DLPFC function and a potential treatment target to enhan

181 The presumptive added modulation of DLPFC circuitry by the thalamus in human may contribute

182 Plasticity of DLPFC was positively associated with working memory perf

183 ) and fMRI to determine the specific role of DLPFC function in norm-enforcement behavior.

184 Using laser microdissection, samples of DLPFC deep layer 3 were collected from 56 matched pairs

185 , or found to a lesser degree, in samples of DLPFC gray matter from the same subjects, suggesting tha

186 ay profiling to analyze the transcriptome of DLPFC L3 PV cells in 36 matched pairs of SZ and unaffect

187 The findings support the use of DLPFC plasticity as a measure of DLPFC function and a po

188 differences in the effect of amphetamine on DLPFC BPND (mean [SD], BPND in HC: -7.5% [11%]; SCZ: +1.

189 ergic stimulation has detrimental effects on DLPFC representations of task attributes.

190 tDCS was applied over DLPFC while subjects performed a computerized test of er

191 ver DLPFC, sham tDCS over M1, sham tDCS over DLPFC, or no stimulation.

192 nodal tDCS applied over M1, anodal tDCS over DLPFC, sham tDCS over M1, sham tDCS over DLPFC, or no st

193 To refine optimal stimulation parameters, DLPFC stimulation using two common electrode montages wa

194 carbachol onto neurons in dorsolateral PFC (DLPFC) of male rhesus macaques performing rule-guided pr

195 la and ventral PFC (VPFC), dorsolateral PFC (DLPFC), and dorsal anterior cingulated cortex (dACC) amo

196 group interaction in right dorsolateral PFC (DLPFC), manifesting as a relative activation increase in

197 ciated with the schizophrenia risk phenotype DLPFC hyperactivation commonly considered a measure of b

198 cence-activated cell sorting from postmortem DLPFC of 36 PDS and 26 age-matched controls.

199 tation was related to increased postresponse DLPFC gamma-band activity and to theta coupling in the r

200 aptic signals, their effect on local primate DLPFC neuronal activity in vivo during cognitive tasks r

201 Proper DLPFC activity is, in part, maintained by two population

202 e AX-CPT, both patient groups showed reduced DLPFC activity compared with the control group (P = .02

203 Given the roles of PV neurons in regulating DLPFC microcircuits and of PNNs in regulating PV cellula

204 e an equal involvement of the left and right DLPFC in adaptive control, whereas stimulation of a cont

205 left DLPFC and cathodal stimulation of right DLPFC (bipolar-balanced montage) showed reduced vigilanc

206 es novel evidence for a causal role of right DLPFC regions in subserving error awareness and marks an

207 ed to four HD-tDCS conditions: left or right DLPFC or left or right primary motor cortex (M1).

208 Anodal tDCS over right DLPFC was associated with a significant increase in the

209 caused by dysconnectivity between the right DLPFC and several cortical regions.

210 0) functional connectivity between the right DLPFC and the right caudate nucleus and bilateral (para)

211 tex (DLPFC) and cathodal tDCS over the right DLPFC for 30 minutes, one of the most common montages us

212 ation of anodal direct currents to the right DLPFC represents a promising option for reducing both ca

213 ion was observed on BOLD signal in the right DLPFC such that TD increased activation in high ACE subj

214 n and functional connectivity with the right DLPFC were calculated.

215 repetitive electric stimulation of the right DLPFC would lower food intake behavior in humans.

216 , real-rTMS (10 Hz) was applied to the right DLPFC.

217 The left, not the right, DLPFC is also involved in affective go/no-go performance

218 rovement was negatively associated with rsFC DLPFC-putamen changes across all subjects.

219 his study, we tested whether an individual's DLPFC gamma-aminobutryic acid (GABA) content predicts in

220 ings, and fMRI revealed punishment-selective DLPFC recruitment, suggesting that these two facets of n

221 Differences were a more severe DLPFC dysfunction in ADHD and a disorder-specific fronto

222 nteers received 20 minutes of active or sham DLPFC stimulation before completing computerized emotion

223 ance sensitivity to other components tested; DLPFC glutamate + glutamine and visual cortical GABA con

224 t serve as a more appropriate mechanism than DLPFC alone.

225 The finding that DLPFC tDCS acutely alters the processing of threatening

226 We hypothesized that DLPFC deficits would appear during the antisaccade prepa

227 These findings indicate that DLPFC builds up value signals based on knowledge of drug

228 Finally, we show that DLPFC rTMS affects punishment decision making by alterin

229 The DLPFC-disrupted group showed enhanced learning of the no

230 the anterior cingulate cortex (ACC) and the DLPFC during REM sleep.

231 theta and beta activities in the ACC and the DLPFC, two relatively distant but reciprocally connected

232 uced anticorrelated connectivity between the DLPFC and medial prefrontal DMN nodes.

233 dulating functional connectivity between the DLPFC and thalami, as has been hypothesized previously.

234 d a significant decrease in rsFC between the DLPFC and the left putamen and insula.

235 d a significant decrease in rsFC between the DLPFC and the left superior frontal gyrus (SFG) and ante

236 at explicit memory processes mediated by the DLPFC can indirectly interfere with implicit recognition

237 Tissue samples containing the DLPFC (Brodmann area 46) were Golgi-stained, and basilar

238 , we focused on connectivity seeded from the DLPFC and the subgenual cingulate, a key region closely

239 related via excitatory projections from the DLPFC to the ventral mesencephalon, the location of dopa

240 Data from the DLPFC were obtained from 12 patients.

241 Across the sample, higher NAA and Glu in the DLPFC and NAA concentrations in multiple lobar gray matt

242 found in patients with schizophrenia in the DLPFC and the amygdala of males, while the pattern is op

243 ge change in binding potential (BPND) in the DLPFC following amphetamine, BOLD activation during the

244 for the major PNN protein, aggrecan, in the DLPFC from schizophrenia and matched comparison subjects

245 in the capacity for dopamine release in the DLPFC in SCZ and suggest a more widespread deficit exten

246 tion between BPND and BOLD activation in the DLPFC in the overall sample including patients with SCZ

247 support the idea that spine deficits in the DLPFC may contribute to subcortical hyperdopaminergia in

248 uption of the regulation of the GluRs in the DLPFC of females with MDD, with more specific GluR alter

249 We analyzed the neuronal activity in the DLPFC of monkeys performing a probabilistic reversal tas

250 xpression of t-DARPP-32 was increased in the DLPFC of patients with schizophrenia and bipolar disorde

251 ayer 3 and/or layer 5 pyramidal cells in the DLPFC of schizophrenia subjects.

252 hermore, conflict-related activations in the DLPFC of those CHR individuals who ultimately developed

253 tal evidence that modulating activity in the DLPFC reduces vigilance to threatening stimuli.

254 Furthermore, dopamine release in the DLPFC relates to working memory-related activation of th

255 of neural signals are flexibly routed in the DLPFC so as to favor actions that maximize reward.

256 ence of generalized neural mechanisms in the DLPFC subserving the comparison of sensory signals.

257 Dendritic spine loss in the DLPFC was seen in both individuals with schizophrenia an

258 Pools of L3 and L5 pyramidal cells in the DLPFC were individually captured by laser microdissectio

259 corded activity of individual neurons in the DLPFC while monkeys performed a memory-guided decision t

260 and staining intensity were compared in the DLPFC, as well as separately in Brodmann areas 9 and 46.

261 In the DLPFC, cortical inhibition was significantly decreased i

262 e DLPFC in the control group, but not in the DLPFC-disrupted group.

263 ly higher full-length GAD1 expression in the DLPFC.

264 pect to the lateralization of control in the DLPFC.

265 ing regional specificity of pathology in the DLPFC.

266 schizophrenia-associated alterations in-the DLPFC circuitry that subserves working memory could prov

267 Indeed, the DLPFC of schizophrenia cases exhibit increased PSD-95 an

268 Inactivation of the DLPFC also reduced craving-related signals in the anteri

269 CS, to clarify the causal involvement of the DLPFC in conflict adaptation.

270 ies have suggested causal involvement of the DLPFC in this phenomenon, such evidence is currently lac

271 Plasticity of the DLPFC measured as potentiation of cortical-evoked activi

272 ial direct current stimulation (tDCS) of the DLPFC reduces food cravings, we hypothesized that repeti

273 cortex was attenuated by inactivation of the DLPFC, particularly when cigarettes were immediately ava

274 n-containing basket cells) in layer 3 of the DLPFC.

275 ed with executive functions that rely on the DLPFC in the control group, but not in the DLPFC-disrupt

276 ese observations indicate that tDCS over the DLPFC has fast excitatory effects, acting on prefrontal

277 mulation (1 mA, 20 min) was applied over the DLPFC.

278 Since the DLPFC and the ACC are implicated in memory and emotional

279 estigated the possibility of suppressing the DLPFC by transcranial direct current stimulation (tDCS)

280 timulation (HD-tDCS) to demonstrate that the DLPFC is causally involved in conflict adaptation in hum

281 n sum, the present results indicate that the DLPFC plays a causal role in adaptive cognitive control,

282 , counter to current prevailing thought, the DLPFC is active during REM sleep and likely interacting

283 ntal cortex across all contexts, whereas the DLPFC most strongly encoded intertemporal availability i

284 Results showed reduced connectivity with the DLPFC for the risk allele carriers mainly in the Stroop

285 xecutive control network associated with the DLPFC might be an integral part of mind-wandering neural

286 g the posterior supratemporal plane with the DLPFC.

287 the neural elements and pathways within the DLPFC that support WM in humans.

288 ural phenotype appears correlated within the DLPFC with the development of psychosis and with functio

289 The subjects then had their DLPFC GABA content measured by single-voxel proton magne

290 V neurons and their PNNs could contribute to DLPFC dysfunction in schizophrenia.

291 lly entrained DLPFC theta activity (DMPFC to DLPFC).

292 r during the antisaccade task, is related to DLPFC dysfunction.

293 The dorsal striatal BOLD response to DLPFC stimulation however was not significantly differen

294 yer 3 parvalbumin interneurons, and in total DLPFC gray matter.

295 yer 3 parvalbumin interneurons, and in total DLPFC gray matter.

296 This study demonstrated impaired in vivo DLPFC plasticity in patients with AD.

297 l and dorsolateral prefrontal cortex (VLPFC, DLPFC).

298 th AD and controls, and to determine whether DLPFC plasticity was associated with working memory.

299 ond step, in the subset of participants with DLPFC DNA methylation data (n = 648), we found that resi

300 ird step, in the subset of participants with DLPFC RNA sequencing data (n = 469), brain transcription