ライフサイエンスコーパス: salience

1 h motivation-based theories (e.g., incentive salience).

2 ronizes cortical theta and decreases sensory salience.

3 stent with a role in increasing motivational salience.

4 th these individual differences in incentive salience.

5 ory, contributing to expression of emotional salience.

6 ch reward cues are attributed with incentive salience.

7 frontotemporal connections indexing stimulus salience.

8 o which the CS was attributed with incentive salience.

9 tentially serve as a correlate of perceptual salience.

10 circuit' only if it is imbued with incentive salience.

11 zophrenics suffer from enhanced signaling of salience.

12 ulated by both the reward level and stimulus salience.

13 gnaling of the large reward-predicting cue's salience.

14 diction error, working memory, and incentive salience.

15 t a representation of generalized arousal or salience.

16 dditive and independent effects of value and salience.

17 disrupts maintenance of conditioned stimulus salience.

18 xperienced stimuli acquiring aberrantly high salience.

19 associated with connectivity in the DMN and salience.

20 be important in attribution of motivational salience.

21 ions of striatum and cortex and also encodes salience.

22 ion (corresponding to the highest behavioral salience) across the map.

23 clinical and neural signatures of pleasure, salience, allostasis and withdrawal relate, both in a no

24 hysiological relationships between pleasure, salience, allostasis and withdrawal.

25 uitment to happy faces may reflect increased salience and ambiguity of positive emotional expressions

26 antitative relationship between motivational salience and decision speed, measured by reaction time (

27 by a connectivity disequilibrium between the salience and default-mode networks, a finding of potenti

28 ort these cognitive functions, including the salience and executive control networks.

29 antitative relationship between motivational salience and faster decision speed, they also reveal the

30 ed by a combination of exaggerated incentive salience and habit formation, reward deficits and stress

31 that social stress history increases reward salience and impairs processes that compute predictabili

32 al systems involved in processing emotion or salience and midline cortical regions that may mediate t

33 e coupling relationship between motivational salience and more precise RT.

34 Stimulus salience and reward expectations influence this prioriti

35 othalamic peptide oxytocin in augmenting the salience and rewarding value of social stimuli, includin

36 Indeed by signaling salience and valence, DA is thought to facilitate discri

37 processing governing the interaction between salience and value and the formation of subjective expec

38 use phenotype represents a cause of aberrant salience and, in turn, that aberrant salience (and the r

39 berrant salience and, in turn, that aberrant salience (and the resulting positive symptoms) in schizo

40 perceptual properties of the stimulus (e.g., salience) and its subjective value.

41 rced behavior, such as motivation, incentive salience, and cost-benefit calculations.

42 ponents of the attention, central executive, salience, and default mode networks.

43 motor, speech, semantic, executive control, salience, and default-mode) were extracted, and voxel-wi

44 of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the

45 partially overlapping with the default-mode, salience, and frontoparietal attention networks) and the

46 ciated with executive functioning, incentive salience, and interoceptive processing in cigarette deci

47 Three domains-executive function, incentive salience, and negative emotionality-tied to different ph

48 non-addiction, a pathological, non-adaptive salience attached to food results in withdrawal mediated

49 demonstrate that the neural instantiation of salience attribution in smokers is both more effortful t

50 It has been proposed that aberrant salience attribution is associated with impaired coding

51 ss potentially involving conditioning and/or salience attribution of cocaine reward-related cues.

52 easure of aberrant salience attribution, the salience attribution test, to neural correlates of RPEs

53 sychotic symptoms are the result of abnormal salience attribution, and that the attribution of salien

54 of the orbitofrontal cortex, which processes salience attribution, DA also enables shifting from NOW

55 cts of sensory processing deficits, aberrant salience attribution, prefrontal hypoactivation as well

56 ific link between the constructs of aberrant salience attribution, reduced RPE processing, and potent

57 However, the relationship of aberrant salience attribution, RPE coding, and dopamine synthesis

58 ion between a behavioral measure of aberrant salience attribution, the salience attribution test, to

59 by engaging greater frontal regulation over salience attribution.

60 igated for the default mode, frontoparietal, salience, auditory, sensorimotor and visual networks usi

61 s been suggested that pleasure is related to salience (behavioral relevance), and withdrawal has been

62 stimulation and contextual factors, such as salience, but identifying these components separately ha

63 lt assigned high reward value and hence high salience, but this salience rapidly decreases if the sti

64 sts that naltrexone may be reducing drug cue salience by decreasing the involvement of sensorimotor r

65 outside the neuronal RF while we manipulated salience by varying the time between stimulus presentati

66 EEG components reflecting perceived stimulus salience can be combined with the level of reward to cre

67 e inference to demonstrate how attention and salience can be disambiguated in terms of message passin

68 ine dysfunction in corticostriatal networks (salience, central executive networks, and striatum) and/

69 lt mode) and environmentally driven control (salience, cingulo-opercular) systems.

70 significantly increased activation in reward salience circuitry (ventral striatum, dorsal caudate, an

71 ty of human SN, which underpins value versus salience coding, and impulsive choice versus impulsive a

72 network in decisional impulsivity, while the salience-coding ventral SN network was associated with m

73 ns have been implicated in reward, aversion, salience, cognition, and several neuropsychiatric disord

74 In a multivariate analysis only salience/coherence (beta = 0.65, 95% CI = 0.42-0.88, P <

75 univariate and adjusted univariate analysis (salience/coherence beta = 0.59, 95% CI = 0.45-0.76, P <0

76 that the thalamus-sensorimotor and thalamus-salience connectivity networks were already present in n

77 role in the rapid encoding of intention and salience--critical components of mentalizing and moral e

78 vealed that both groups exploited contextual salience cues in their gaze judgments, and that the aver

79 is of individual subjects' use of contextual salience cues).

80 a, insula) or resting-state networks (e.g., "salience," "default mode").

81 siform, somatosensory cortex, and thalamus), salience detection (anterior insula), and learning and m

82 biological systems subserving fear learning, salience detection, and emotion regulation explaining mu

83 e ventral attentional system responsible for salience detection.

84 s and systems, particularly those supporting salience detection.

85 The pattern was similar for ratings of salience, distress, personal relevance, global threat, a

86 Our results suggest that the contribution of salience dominates at higher levels of the visual system

87 ction for other attention-relevant networks (salience, dorsal attention, and frontoparietal control n

88 Here, we asked whether salience-driven distraction is prevented by suppressing

89 erior cingulate cortex (PCC) signal decision salience during foraging to motivate disengagement from

90 targeting amygdala hypoactivity and blunted salience during positive autobiographical recall could e

91 Crucially, the salience effect modulates attention orienting responses

92 e regions of cortex and striatum and encodes salience (equal response to wins and losses).

93 nt structural covariance was observed in the salience, executive control, auditory, and motor network

94 nal connectivity change over time across the salience, executive, and task-negative networks and how

95 he maturation of networks thought to support salience, executive, integrative, and cognitive function

96 Strikingly, salience-executive control between-network cohesion peak

97 are rapidly reversed upon exposure to a high salience experience such as novel stress or by manipulat

98 antly sensory-attentional (N1), motivational salience (feedback-related negativities [FRN]), and cogn

99 The concept of self-management support had salience for patients, carers and specialist nurses alon

100 Here, we consider attention and salience from the perspective offered by active inferenc

101 linergic systems have been shown to increase salience/gain while suppressing extraneous information.

102 parietal cortex encodes predicted value and salience in superior and inferior compartments, respecti

103 ow that the neural correlate of motivational salience in the basal forebrain (BF), defined independen

104 have recently reported neural correlates of salience in the basolateral amygdala (ABL) of rats durin

105 iming approach behavior and elevating reward salience in the frontostriatal pathway.

106 if conceptually related information acquires salience in the future.

107 ontrary to this idea, novelty affects visual salience in the monkey lateral intraparietal area (LIP)

108 ation, and thus decrease responses driven by salience in the RF.

109 e attention and facilitate memory, enhancing salience in ways that could underlie, for example, prefe

110 e it is generally believed that motivational salience increases decision speed, the quantitative rela

111 ork shows that neural correlates of stimulus salience interact with value information to yield neural

112 This maintenance of salience is a necessary precursor for these stimuli to g

113 t misophonia is a disorder in which abnormal salience is attributed to particular sounds based on the

114 t such reward-related modulation of stimulus salience is conceptually similar to an "attentional habi

115 Here, we report that stressor salience is critical for bidirectionally modifying presy

116 nce attribution, and that the attribution of salience is largely mediated through the prefrontal cort

117 As aberrant salience is primarily a dopaminergic phenomenon, the mod

118 f these response changes in FEF suggest that salience is represented much earlier (<100 ms following

119 In brief, we suggest that salience is something that is afforded to actions that r

120 suggest a role of learning, while incentive salience (IS) models argue that the DA signal imbues sti

121 ling is implicated may be caused by aberrant salience leading to a change in the nature of the inform

122 d porthole, suggesting that higher incentive salience made that cue more attractive.

123 Finally, we show that bottom-up salience, manipulated through varying stimulus contrast,

124 ate how neural representations on the visual salience map are processed in parallel, thus facilitatin

125 with the experimental modulation of a visual salience map.

126 Difficulties in valuating emotional salience may contribute to inabilities to appreciate the

127 We show that salience--measured in saccades and LIP responses--was en

128 Individual variability in aberrant salience measures related negatively to ventral striatal

129 ding motivation, prediction error, incentive salience, memory consolidation, and response output.

130 n voice-selective STS and reward, affective, salience, memory, and face-processing regions during mot

131 lso how reinforcement learning and incentive salience models may shed light on the disorder.

132 vity of the default-mode, executive control, salience, motor, and auditory networks in UHR individual

133 in brain regions including a key node of the salience network (anterior insula) increased linearly ac

134 Regions of the salience network (dorsal anterior cingulate, insula, and

135 network [e.g., dorsolateral (dl)PFC], and a salience network (e.g., insula).

136 , LA increased in the visual system, and the salience network (i.e., cingulate and insular cortices)

137 th decreased connectivity within the ventral salience network (ie, middle frontal gyrus) and the left

138 e auditory cortex, prefrontal cortex and the salience network (insula and anterior cingulate cortex).

139 d eight weaker circuits including within the salience network (insula seeds) and between temporal pol

140 ant reductions in D2 receptor binding in the salience network (insular cortex and anterior cingulate

141 iation networks [default-mode network (DMN), salience network (SAL), dorsal attention network, and fr

142 functional neuroimaging: a cingulo-opercular salience network (SN) and a frontoparietal executive net

143 Interactions between the Salience Network (SN) and the Default Mode Network (DMN)

144 work (DN), frontoparietal network (FPN), and salience network (SN) while recording evoked responses i

145 The salience network (SN), anchored in the anterior insula a

146 n network (DAN), default-mode network (DMN), salience network (SN), and executive control network (EC

147 that cross-network interactions between the salience network (SN), central executive network, and de

148 nd that connectivity involving the so-called salience network (SN), default-mode network (DMN), and f

149 work (DN), frontoparietal network (FPN), and salience network (SN), in seven subjects undergoing inva

150 cingulate cortex (dACC) are key nodes of the salience network (SN), which integrates internal and ext

151 cifically vulnerable in bvFTD, including the salience network (SN), with key nodes in the frontoinsul

152 twork (CEN), default mode network (DMN), and salience network (SN).

153 hizophrenic core symptoms highlight aberrant salience network activity (insula and anterior cingulate

154 ectivity networks (the default mode network, salience network and central executive network) in older

155 Specifically, diminished activity in the salience network and enhanced activity in a cortico-cere

156 Dopaminergic differences in the salience network and the medial temporal lobe contribute

157 role of the sgACC, default mode network, and salience network as predictors of TMS response and sugge

158 d decreased connectivity with regions of the salience network compared with the other groups.

159 Furthermore, these decreases in right insula/salience network connectivity correlated with baseline t

160 In C9orf72 carriers, salience network connectivity reduction correlated with

161 ces in three networks: DMN, ECN and anterior salience network connectivity, as well as a whole brain

162 a syndrome in C9orf72 carriers by disrupting salience network connectivity.

163 Single-patient analyses revealed salience network disruption and default mode network con

164 ing that coordination of activity within the salience network dynamically tracks arousal.

165 For example, the salience network exhibited a transient increase in netwo

166 owing biobehavioral mechanisms: 1) the brain salience network favoring adaptive social approach behav

167 Results revealed decreased right insula/salience network functional connectivity under MDMA.

168 ther showed diminished connectivity with key salience network hubs.

169 e findings indicate the vulnerability of the salience network in PD and its potential role in memory

170 ngs support roles for several regions of the salience network in the pathophysiology of FND.

171 ctional neurological disorder (FND), and the salience network is implicated in the pathophysiology of

172 ed with optimal noradrenergic signaling, the salience network is optimally able to engage the executi

173 ight insular disintegration (ie, compromised salience network membership) as a neurobiological signat

174 Results demonstrate that cohesion within the salience network monotonically increases with arousal, w

175 ealed increased coupling between default and salience network regions (bilateral insula) at the begin

176 status and affective symptoms would map onto salience network regions and that patients with FND woul

177 creased integration of the cingulo-opercular/salience network significantly moderated the robust effe

178 Deficits in the salience network suggest an impaired ability to process

179 own signaling from all major clusters of the salience network to early visual cortex only in the eyes

180 o predictive control modes, from the brain's salience network to the default mode network.

181 rfaces with the anterior-cingulo-insular or "salience network" demonstrated to be transdiagnostically

182 ior insular cortex (AIC), a core hub of the "salience network" that is critical for perception of int

183 auditory cortex, prefrontal cortex, and the salience network) as well as reduced deactivation of the

184 ault mode network, dorsal attention network, salience network, and executive control network).

185 These results suggest that the salience network, and its attention-control function, ar

186 ry encoding, storage, and retrieval, and the salience network, associated with attention and executiv

187 between three key large-scale networks: the salience network, dorsal attention network, and default

188 cluding precuneus and angular gyrus, and the salience network, including insula, putamen and thalamus

189 tion, predominantly of the cingulo-opercular/salience network, increased with age.

190 arousal, and within-network cohesion in the salience network, indicating that coordination of activi

191 memory encoding and retrieval tasks, and the salience network, typically engaged during attention, mo

192 hat is important in cognitive control is the salience network, which includes dorsal anterior cingula

193 in a domain general system, specifically the salience network, with residual language performance in

194 rk degeneration were identified, including 2 salience network-predominant subgroups (frontal/temporal

195 ted increased amygdala connectivity with the salience network.

196 work, the executive control network, and the salience network.

197 ers have on the default mode network and the salience network.

198 connectivity between the hippocampus and the salience network.

199 l network that partially overlapped with the salience network.

200 effects of heroin abuse on cognition and the salience network.

201 ircuit; anterior insula and cingulate of the salience network; and a subregion of fusiform gyrus asso

202 functional integrity of a cingulo-opercular "salience" network.

203 f the right-lateralized dorsal attention and salience networks and (2) complicated anxiety-related hy

204 bic and limbic nodes of the default mode and salience networks that support attentional, executive, a

205 nctions (default mode, central executive and salience networks) and externally-driven, specialized se

206 "hub" areas of the default mode and cortical salience networks, respectively.

207 f the left-lateralized ventral attention and salience networks.

208 aker inhibition between the default mode and salience networks.

209 rom the ventral attention, default mode, and salience networks.

210 c mechanisms by which oxytocin increases the salience of acoustic social stimuli.

211 togenetic silencing of IPN neurons increases salience of and interaction with familiar stimuli withou

212 d it has been proposed that OT increases the salience of both positive and negative social cues.

213 ns are offered to improve the visibility and salience of clinical significance in nursing science.

214 aimed at evaluating behavioral shifts in the salience of cocaine now vs money later, we found that ke

215 t low levels of D2 autoreceptors enhance the salience of cocaine-paired cues and can contribute to th

216 d activity of BLA neurons is to maintain the salience of conditioned stimuli that precede it.

217 or nonreinforcement causes reductions in the salience of conditioned stimuli, rendering these stimuli

218 pal lesion resulted in the loss of incentive salience of cues in sign trackers.

219 erences in facial features may influence the salience of cues.

220 tential to improve the neural and perceptual salience of degraded sensory stimuli through immersive c

221 vioral symptoms including enhanced incentive salience of drug-associated cues, but also a negative af

222 gest that reward can increase the perceptual salience of environmental stimuli, ensuring that potenti

223 migration were based on working conditions, salience of family, and the desire for knowledge, skill,

224 reased affinity may potentiate the incentive salience of food cues and counteract the effects of sati

225 The revised model recognizes the salience of individual cognition as well as acknowledgin

226 exerts control over behavior by biasing the salience of mnemonic representations and adjudicating am

227 ng-term memory associations by assessing the salience of mnemonormation to the immediate sensory inpu

228 This operation enhances the salience of odor-evoked activity without changing cortic

229 limbic system, in tracking context-dependent salience of old and new information.

230 ty and pupil size reflected task-conditional salience of old and new stimuli, but, unexpectedly, this

231 Thus, L2/3 circuits can adjust the salience of output in accordance with momentary behavior

232 s from the body potentiates the motivational salience of reward cues through the recruitment of hedon

233 nsory processing, selectively increasing the salience of reward-associated stimuli.

234 ned how vHipp CB1R signaling may control the salience of rewarding or aversive emotional memory forma

235 t are involved in representing the emotional salience of sensory information.

236 erarching role of oxytocin in regulating the salience of social cues through its interaction with the

237 ur results indicate the CA2 can increase the salience of social signals.

238 al competition is influenced by motivational salience of sounds is, however, not well-understood.

239 sting alterations (biases) in the behavioral salience of specific spatial locations.

240 ces in the thalamus may serve to enhance the salience of speech signals that are degraded as they asc

241 ynamic, within-trial changes in the relative salience of task-relevant and task-irrelevant features.

242 of unresolved harmonics is sensitive to the salience of temporal envelope cues.

243 contextual information about the behavioral salience of the angular error, namely, the bias and vari

244 ck the ability to increase the physiological salience of the events that provide the convergent cross

245 ers were also more sensitive to the featural salience of the images, suggesting a more pervasive role

246 d with impact than either the credibility or salience of the knowledge.

247 al stimulation and the abrupt appearance, or salience, of the presentation.

248 ation for sucrose-paired cues (ie, incentive salience or 'wanting').

249 th perceptual processing, increased physical salience or associated value attenuates action-related i

250 in cognitive control and those that support salience or emotion processing may relate to deficits re

251 evious work implicated the CeMA in incentive salience, our results isolate the investigation to a spe

252 hat require sex analysis and give it special salience over other sources of biological variance can d

253 ntion-emotion interactions, which could bias salience processing and associative learning in youth wi

254 r not driving adaptation we dissociate error-salience processing from error-based adaptation.

255 Postmovement beta-power may reflect error-salience processing independent of sensorimotor adaptati

256 nal integration of brain regions involved in salience processing is differentially modulated by singl

257 Disrupted salience processing is proposed as central in linking dy

258 and the rest of the brain during an oddball salience processing task.

259 d modulation of the beta-rebound may reflect salience processing, independent of sensorimotor adaptat

260 executive control, conflict monitoring, and salience processing, making it difficult to interpret th

261 pain processing--not executive, conflict, or salience processing.

262 ward value and hence high salience, but this salience rapidly decreases if the stimulus signals a neg

263 and physical) pain reflect the processing of salience, rather than hurt.

264 This salience reduction was stimulus-specific, long-lasting,

265 In our foraging tasks, salience refers to the difference between decision thres

266 Decreases in emotion- and salience-related limbic activity, including the insula a

267 e signals and reconcile them with the recent salience report.

268 limbic structures associated with vigilance, salience, reward, and motivation, and mentalizing networ

269 rocessing related to the default mode (DMS), salience/reward (SRS), and frontoparietal (FPS) subnetwo

270 and dorsal anterior cingulate) and classic 'salience/reward/learning' regions (eg, ventral striatum)

271 ty analyses enabled group comparisons of the salience, sensorimotor, and default mode networks.

272 -trial neural activity of perceived stimulus salience, showing that this activity can be combined wit

273 he functional impairment of the motivational salience signal encoded by the poorly understood nonchol

274 re we tested whether this dopamine-dependent salience signal is altered in rats with neonatal ventral

275 Artificially augmenting the BF motivational salience signal via electrical stimulation led to faster

276 p is dictated largely by the BF motivational salience signal.

277 Salience signals were stronger in poor foraging contexts

278 gnals are localized in TS along with general salience signals, while VS dopamine reliably encodes rew

279 distributions with stronger BF motivational salience signals.

280 ightly coupled with stronger BF motivational salience signals.

281 temporal properties of interactions between salience (SN), default mode (DMN), and central executive

282 mode, fronto-parietal, cingulo-opercular and salience systems-engage dynamically in cohesive network

283 ia dopamine-dependent, cue-driven, incentive salience systems.

284 magnetic resonance imaging (fMRI) studies of salience tasks have located alterations in prefrontal an

285 ire motivational properties (i.e., incentive salience) that cause them to have a powerful influence o

286 zed that the rapid presentation would reduce salience (the sudden appearance within the visual field)

287 e, more than passively representing value or salience, the signal appears to play a versatile and act

288 rant learning, but were more prone to assign salience to a cue that predicts reward (sign-tracking) i

289 the inappropriate or spurious attribution of salience to cues in the environment.

290 uch as the propensity to attribute incentive salience to reward cues that is modeled in rats by sign-

291 kers (STs)] are prone to attribute incentive salience to reward cues, which can manifest as a propens

292 amine release, causing the misattribution of salience to stimuli, which are then misinterpreted by th

293 These policy debates lend particular salience to studies evaluating the health effects of ins

294 increases in firing could reflect novelty or salience, variables also correlated with dopamine activi

295 dependence-related alterations in incentive salience/'wanting'.

296 the potentiation of subthreshold fear memory salience was blocked by DA receptor antagonism, CB1-medi

297 y difference was not observed when the cue's salience was diminished after extinction learning.

298 halography, a recognized marker of incentive salience, was used to track motivated attention to drug

299 s show increased connectivity in the DMN and salience when neocortical Tau levels are low, whereas ab

300 ch, when combined with the variable stimulus salience, yields uncertainty in the choice.