ライフサイエンスコーパス: limbic

1 lopride binding in the anterior striatum and limbic ACC.

2 reduced ventromedial prefrontal-hypothalamic-limbic activation, but they also showed hyperactivation

3 ietal and visual cortices) and emotional and limbic activity (insula, amygdala).

4 Decreases in emotion- and salience-related limbic activity, including the insula and amygdala, were

5 deposition was frequent in typical (59%) and limbic AD pathologies (67%), but not HpSp AD pathology (

6 n = 19); typical AD pathology (n = 136); and limbic AD pathology (n = 33).

7 induced increases in anxiety associated with limbic AEA deficiency.

8 ortical regions additional to connections to limbic and associative areas.

9 have undergone deep brain stimulation of the limbic and associative subthalamic nucleus.

10 tor availability in the cortex and striatal (limbic and associative) dopamine neuron integrity in 4 g

11 he motivational drive, hunger, and, finally, limbic and cognitive processes that bring about hunger-m

12 rain stem, the ependyma (EP), containing the limbic and cortical areas, which also harbor neural prog

13 glutamate transporter-2 (VGluT2)--project to limbic and cortical regions, but also excite neighboring

14 that, although participants showed enhanced limbic and electrophysiological reactions to emotional d

15 ct patterns of dysfunctional connectivity in limbic and frontostriatal networks.

16 future research on the interactions between limbic and language networks.

17 Deficits in the right orbitofrontal-temporal-limbic and left inferior frontal regions remained in a s

18 structural changes of structures involved in limbic and memory functions predispose to delirium under

19 Connectivity of limbic and motor cortical and striatal nodes mapped onto

20 s the neurochemistry of PH connectivity with limbic and neuroendocrine systems.

21 irectly modulated functional connectivity of limbic and paralimbic areas such as the amygdala and ins

22 reduced volume of the hippocampus and other limbic and paralimbic areas.

23 trum perform similar functions in processing limbic and sensorimotor information, respectively.

24 ch/exo-patch and matrix neurons receive both limbic and sensorimotor information.

25 Increased limbic and striatal activation in adolescence has been a

26 rations in the developmental trajectories of limbic and striatal regions during adolescence may repre

27 in 12 brain regions, including neocortical, limbic and subcortical areas from Alzheimer's disease ca

28 sed 12 brain regions, including neocortical, limbic and subcortical areas, from post-mortem brains of

29 ts reflects performance difference, and that limbic and thalamic dysfunction is critically involved i

30 pes (hippocampal sparing [HpSp]; typical and limbic) and further examine the relationship between TDP

31 ad reduced WM integrity in interhemispheric, limbic, and arcuate WM tracts.

32 integrate inputs from diverse sensorimotor, limbic, and associative regions to guide action-selectio

33 umulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood,

34 nd distributed activity throughout thalamic, limbic, and particularly primary sensory cortical areas

35 ated with more years of smoking in the right limbic area and frontal region.

36 s an antibody-associated inflammation of the limbic area.

37 tal cortex and a large number of subcortical limbic areas (e.g., amygdala, lateral hypothalamus), and

38 Widespread connections of limbic areas and focal connections of eulaminate areas y

39 s glutamatergic neurotransmission in several limbic areas and further indicates that compounds that r

40 opportunity for intracranial recordings from limbic areas has arisen in patients undergoing deep brai

41 regions as well as into several subcortical limbic areas implicated in social play.

42 The role of distinct limbic areas in emotion regulation has been largely infe

43 ar responses across each of the cortical and limbic areas signal movement during the TST and open fie

44 immmunohistochemistry and neurochemistry in limbic areas such as the amygdala (Amy), Hippocampus (Hi

45 read of tau neurofibrillary tangles from the limbic areas to the cortex.

46 ore in specific brain areas, especially some limbic areas, while full-length amyloid-beta42 tended to

47 ansmission and decreased astrocyte number in limbic areas.

48 ing the prefrontal, associative, sensory and limbic areas.

49 vailability of 5-HT1AR receptors in the same limbic areas.

50 band oscillations in the vStr and associated limbic areas.SIGNIFICANCE STATEMENT The ventral striatum

51 ty of frontal-striatal circuitry involved in limbic arousal and executive control in 36 individuals-1

52 ut that the 'set point' for mobilizing their limbic arousal system has been elevated-an interpretatio

53 ioid enkephalin, patches (or striosomes) are limbic-associated subcompartments enriched in mu opioid

54 ter integrity, with the strongest effects in limbic association tracts such as the anterior cingulum,

55 conducted in non-human primates dissociating limbic, associative and motor frontal hyper-direct conne

56 are positioned to influence outputs to the 'limbic-associative' striatum, which is distinct from str

57 They further suggest that mesolimbic and non-limbic basal ganglia dopamine circuits are functionally

58 ntly identified key reproductive hormone, on limbic brain activity and behavior.

59 lates of the disorder in patterns of frontal-limbic brain activity and dysregulation of serotonergic

60 ated that kisspeptin administration enhanced limbic brain activity specifically in response to sexual

61 to induce tinnitus and measured auditory and limbic brain activity using manganese-enhanced MRI (MEMR

62 t into serotonin receptor (dys)function in a limbic brain area.

63 neuronal excitability have been observed in limbic brain areas after associative learning, but littl

64 of knowledge regarding these mechanisms: the limbic brain imparting risk, and the mesolimbic learning

65 ed nucleus of the stria terminalis (BNST), a limbic brain region involved in pathological reward and

66 node in the information flow between fronto-limbic brain regions and monoaminergic brainstem nuclei,

67 at dysfunctional dorsolateral prefrontal and limbic brain regions are a hallmark feature of BPD and t

68 uit in vivo activity from eight cortical and limbic brain regions as mice were subjected to the tail

69 Circuits distributed across cortico-limbic brain regions compose the networks that mediate e

70 gene expression data in four interconnected limbic brain regions implicated in depression and its tr

71 functional connectivity between the dmIC and limbic brain regions implicated previously in MDD, inclu

72 to monitor electrophysiological activity in limbic brain regions linked to social behavior.

73 ry-specific representations in olfactory and limbic brain regions suggests that such ensemble pattern

74 ciated with neuronal atrophy of cortical and limbic brain regions, but the molecular mechanisms under

75 structural abnormalities in corticostriatal-limbic brain regions, which may explain the associations

76 and generated along distributed cortical and limbic brain regions.

77 This may point to sex differences in limbic brain regions.

78 eurons with connections to basal ganglia and limbic brain regions.

79 by activating CRF type 1 (CRF1) receptors in limbic brain regions.

80 ynamics in the nucleus accumbens (NAc)-a key limbic brain reward region-in the regulation of aberrant

81 erability factor for specific alterations of limbic brain structure in individuals with adverse child

82 ate that volume and shape of subcortical and limbic brain structures are potential endophenotypic mar

83 Furthermore, kisspeptin's enhancement of limbic brain structures correlated with psychometric mea

84 The limbic brain system has key roles in sexual and emotiona

85 variation in stress cortisol reactivity and limbic brain volumes in children, phenotypes associated

86 ects of genetic variation and life stress on limbic brain volumes, particularly on left amygdala volu

87 eased cortisol reactivity and differences in limbic brain volumes, yet the mechanisms underlying thes

88 modify and potentially alter our emotional (limbic) brain and affect our social interactions.

89 ining stimulus for the circadian system, and limbic centers encoding aversive information are likely

90 be involved in the repetitive movements and limbic changes of autism.

91 cific functional roles within the prefrontal-limbic circuit.

92 with the expression of a distinct cerebello-limbic circuit.

93 ta = -0.01 [P = .02]) and tracts involved in limbic circuitry (fornix crus [AD, beta = 0.02 (P = .046

94 between trauma exposure and altered cortico-limbic circuitry may in part explain the association bet

95 he notion that greater activation in cortico-limbic circuitry predicts better CBT response in GAD and

96 by a smaller set of hedonic hot spots within limbic circuitry.

97 dopamine receptors, is expressed throughout limbic circuits affected in neuropsychiatric disorders,

98 romedial hypothalamus, extended amygdala and limbic circuits are known to encode initiation of aggres

99 dopamine receptors, are expressed throughout limbic circuits, including prefrontal cortex (PFC).

100 state likely to affect sensory processing in limbic circuits.

101 ls hold promise in dissecting well-conserved limbic circuits.

102 connectivity-based parcellation of SN with a limbic, cognitive, motor arrangement.

103 ection between amygdala and PFC and a second limbic connection following the fornix and the anterior

104 increased task-induced deactivation, altered limbic connectivity and increased cortical thickness.

105 Limbic connectivity of the PH was then established by si

106 amic causal modeling) measures of prefrontal-limbic connectivity within the circuit.

107 tive control network, dysfunctional auditory-limbic connectivity, and deafferentation-induced atrophy

108 The vlPAG showed fronto-limbic correlations at rest, whereas during breathlessne

109 f both interictal and PSs in acute models of limbic cortex ictogenesis induced by pharmacological man

110 in a subnetwork that primarily included the limbic cortex, visual cortex, and subcortex during emoti

111 rts of temporal, parietal, sensorimotor, and limbic cortex.

112 ntral to the claustrum, has connections with limbic cortical areas and should be considered part of a

113 These data demonstrate that limbic cortical areas both tune the function of cognitiv

114 ting cognate receptors throughout neurons in limbic cortical networks to alter synaptic functioning.

115 reported using Fos labeling that only a few limbic cortical structures including the retrosplenial c

116 perience of control over drug seeking from a limbic cortical-ventral striatal circuit underlying goal

117 these structures, forming key components of limbic-cortical-striatal-pallidal-thalamic circuitry inv

118 n in the cortex, extending from the simplest limbic cortices to eulaminate areas with elaborate lamin

119 visual, auditory, somatosensory, motor, and limbic cortices via retrograde pathway tracers injected

120 its effects on cognition and emotion through limbic corticostriatal systems.

121 to consist of sensorimotor, associative and limbic domains, their precise demarcations and whether a

122 re considered definitely autoimmune, 10 with limbic encephalitis (antibody specificity: 5 LGI1, 1 con

123 reactivation is well established as causing limbic encephalitis after haematopoietic stem cell trans

124 od B-cell populations from two patients with limbic encephalitis and faciobrachial dystonic seizures

125 ness in 13 patients with VGKC antibodies and limbic encephalitis in 2004.

126 ge: 64.0 +/- 2.55 years, median 4 years post-limbic encephalitis onset; n = 18 controls].

127 and two as stiff person syndrome; five had a limbic encephalitis or epileptic encephalopathy, two had

128 Limbic encephalitis that is associated with anti-voltage

129 -treated LGI1 VGKC-complex antibody-mediated limbic encephalitis were investigated using in vivo ultr

130 Symptoms of limbic encephalitis were observed in all patients, inclu

131 ium channel (VGKC) complex antibody-mediated limbic encephalitis with generalized hippocampal atrophy

132 Limbic encephalitis with leucine-rich, glioma-inactivate

133 ented as classic paraneoplastic syndromes (5 limbic encephalitis, 1 paraneoplastic encephalomyelitis,

134 seen with symptoms suggestive of autoimmune limbic encephalitis, although they can be paucisymptomat

135 h VGKC antibodies described in patients with limbic encephalitis, and the subsequent seminal paper de

136 otein-2 (CASPR2), are found in patients with limbic encephalitis, faciobrachial dystonic seizures, Mo

137 -responsive clinical presentations including limbic encephalitis, Morvan's syndrome and acquired neur

138 romyotonia (NMT), Morvan syndrome (MoS), and limbic encephalitis.

139 Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void

140 onal network formations during the course of limbic epileptogenesis (LE).

141 tegrating stress-related signals between the limbic forebrain and hypothalamo-pituitary-adrenal (HPA)

142 ) is a brain structure receiving inputs from limbic forebrain areas and innervating major midbrain mo

143 onal stressors activate a stereotyped set of limbic forebrain cell groups implicated in constraining

144 of GABA and glutamate neurons throughout the limbic forebrain express ESR1, with ESR1-GABAergic neuro

145 g stress-induced activation of hindbrain and limbic forebrain neurons.

146 le aversive situations activate a network of limbic forebrain regions thought to mediate such changes

147 eurons and their downstream hypothalamic and limbic forebrain targets.

148 ting behavioral processes and connecting the limbic forebrain with neuroendocrine systems.

149 a cannabinoid CB1 receptors in hypothalamus, limbic forebrain, and brainstem.

150 ssion in central autonomic components of the limbic forebrain, the locus coeruleus and cerebellar Pur

151 r stress-sensitive projection targets in the limbic forebrain.

152 dels suggest a pronounced effect on ventral 'limbic' FST systems, although recent work in patients wi

153 Hypoactivation in executive circuitry and limbic hyperactivation to threat could reflect partly in

154 ced tinnitus may play a role in auditory and limbic hyperactivity, the non-auditory effects of blast

155 edication-free samples were characterized by limbic hyperactivity, whereas no such group differences

156 n stress-related pathologies associated with limbic-hypothalamic dysfunction.

157 sive protection of the newborn decreases the limbic-hypothalamic-pituitary-adrenal (LHPA) axis activi

158 ts have alterations in the components of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis, with

159 ation results in activation of the posterior limbic (including the retrosplenial cortex) and parahipp

160 These results suggest that enkephalin gates limbic information flow in dorsal striatum, acting via a

161 The role of the claustrum in processing limbic information, however, is poorly understood.

162 laterodorsal tegmental nucleus (LDT) convey limbic information.

163 analyses revealed divergent stress-activated limbic input to the PH, emanating predominantly from the

164 udies suggest patches preferentially receive limbic inputs and project to dopamine neurons in substan

165 To investigate the role of TANs in motor-limbic interaction processes, we recorded 169 TANs in th

166 e endophenotype for OCD, possibly reflecting limbic interference with and neural inefficiency within

167 pe of autoimmune encephalitis with prominent limbic involvement and seizures that is rarely associate

168 stiff-person syndrome (one with seizures and limbic involvement), and two had opsoclonus-myoclonus.

169 In particular, limbic kindling appears to enhance dendritic inhibition,

170 Paul Broca's concept of the "great limbic lobe" has had a huge impact on neuroscience.

171 s 32, 24, 14, and 25 (mPFC) form part of the limbic memory system, but little is known about their fu

172 at metabolism within a tripartite prefrontal-limbic-midbrain circuit mediates some of the inborn risk

173 then identified a fully connected prefrontal-limbic model comprising the IFG, vmPFC, and amygdala.

174 sociated with differential engagement of the limbic modulatory network.

175 ve hippocampal projections on targets in the limbic neocortex could contribute to components of schiz

176 terictal and ictal discharges induced in the limbic network by intracortical and brief arterial infus

177 e of the right frontoinsular cortex-thalamic-limbic network in a mother's proclivity to engage in men

178 frontoinsular cortex (RFIC) and subcortical limbic network would be associated with independent obse

179 The results stress the importance of the limbic network's increased response to neutral facial st

180 development and plasticity of the prefrontal-limbic network, which therefore may increase the vulnera

181 ating function in components of the anterior limbic network.

182 sion scores and activity within the anterior limbic network.

183 of PTSD as a disorder specific to the fronto-limbic network.

184 development and plasticity of the prefrontal-limbic network.

185 del emerges in which we propose that cortico-limbic networks interact to support parental brain respo

186 nectivity among sensorimotor, executive, and limbic networks.

187 aberrant prefrontal regulation of downstream limbic networks.

188 in somatomotor, thalamic, basal ganglia, and limbic networks.

189 tructural differences in corticostriatal and limbic networks.

190 ed maladaptive transcriptional regulation in limbic neural circuits contributes to the development of

191 We hypothesized that targeting limbic neural pathways would modulate the affective sphe

192 ing serotonergic innervation of the cortical-limbic neuronal circuit, RGS6 exerts powerful anxiogenic

193 youthful brain regions in key paralimbic and limbic nodes of the default mode and salience networks t

194 Brain abnormalities of subcortical and limbic nuclei are common in patients with schizophrenia,

195 t link between vomeronasal sensory input and limbic output-are intrinsically rhythmogenic.

196 l link between vomeronasal sensory input and limbic output.

197 tional connectivity of prefrontal areas with limbic-paralimbic structures and enhanced connectivity w

198 n were identified starting in frontotemporal limbic/paralimbic and neocortical regions (phase I).

199 disease tau neuropathology may originate in limbic/paralimbic cortices.

200 ture tau pathology markers in frontotemporal limbic/paralimbic regions compared to neocortical region

201 y volunteers, the medial prefrontal and core limbic parts of the emotional network (for example, ante

202 This reticular-limbic pathway may thus function in processing aversive

203 Limbic pathways were investigated in relation to seizure

204 visual, somatosensory, motor, cognitive, and limbic pathways.

205 e classified as either typical AD (n = 100), limbic-predominant (n = 33), or hippocampal-sparing (n =

206 fine these patients, who may have underlying limbic-predominant, non-amyloid-related pathologies.

207 btypes of Alzheimer's disease (AD): typical, limbic-predominant, or hippocampal-sparing.

208 ociated with reward conferred them a role in limbic processes.

209 nfraslow autorhythmicity is likely to affect limbic processing of pheromonal information.

210 ns that indicate that this probiotic reduces limbic reactivity.

211 differences in neuronal activity in one key limbic region, the basolateral amygdala (BLA), whose act

212 PAG receives strong projections from higher limbic regions and from the anterior cingulate, insula,

213 Overall, these studies identified limbic regions associated with stress circuits providing

214 of the ventral striatum, midbrain, and other limbic regions for neutral cues, neutral outcomes, and n

215 of the ventral striatum, midbrain, and other limbic regions for rewards and positive prediction error

216 volume loss in the mesial temporal lobe and limbic regions in subjects with Parkinson's disease with

217 ectivity of the striatum with prefrontal and limbic regions may be a biomarker for improvement in sym

218 ty along the auditory pathway and in certain limbic regions of rats with tinnitus compared to age-mat

219 ngulate, dorsolateral prefrontal cortex, and limbic regions such as the hippocampus and anterior insu

220 e brain areas, including amygdala and fronto-limbic regions, compared with placebo.

221 BOLD and CBVw fMRI signals in VTA-innervated limbic regions, including the ventral striatum (nucleus

222 lutamatergic inputs arising from the PFC and limbic regions, such as the hippocampus (HP).

223 ssociate distinct roles for three prefrontal-limbic regions, wherein the IFG provides evaluation of s

224 ssociate distinct roles for three prefrontal-limbic regions, wherein the inferior frontal gyrus provi

225 y-a critical cortical pathway to subcortical limbic regions-and aggression in medication-naive childr

226 strates may involve mesial temporal lobe and limbic regions.

227 ype3, small reductions localized to anterior limbic regions.

228 ) by provoking a release of serotonin in key limbic regions; and (2) by increasing the availability o

229 the striatum, and excitatory input from the 'limbic' regions of the subthalamic nucleus.

230 n piriform (olfactory) cortex, as well as in limbic-related brain areas, including amygdala and hippo

231 dhood experiences, complemented by increased limbic responsiveness to emotional interpersonal stimuli

232 Strikingly, activity in limbic, right inferior frontal, and inferior parietal ar

233 is a therapeutic target for the treatment of limbic seizures and possibly for other neurological cond

234 a new piece of evidence to the proposal that limbic seizures can be supported by GABAergic hyperactiv

235 ) degradation versus synthetic CB agonist on limbic seizures induced by maximal dentate activation (M

236 tion of tonic current and protection against limbic seizures, our findings provide novel implications

237 e sst2A receptor and, consequently, modulate limbic seizures.

238 six-hertz (6 Hz) model of pharmacoresistant limbic seizures.

239 is a therapeutic target for the treatment of limbic seizures.

240 after global ischemia and CA3 neurons after limbic seizures.

241 aBST-projecting neurons in limbic sites implicated in HPA axis inhibition tended to

242 We demonstrate in two models of acute limbic SLE that PS events are different from interictal

243 perfusion of either BMI or 4AP induced focal limbic SLEs.

244 The medial SN connects with limbic striatal and cortical regions and encodes value (

245 act measureable physiological alterations in limbic striatal circuitry that vary as a function of dop

246 der was associated with structural change in limbic, striatal, and prefrontal cortical regions from e

247 tum), 0.7781 (associative striatum), 1.0344 (limbic striatum), and 1.0189 (sensorimotor striatum) in

248 In the central nucleus of amygdala (CeA), a limbic structure critically involved in the affective di

249 the central nucleus of the amygdala (CeA), a limbic structure implicated in the emotional components

250 ceives inputs from medial pallium-originated limbic structures (e.g., the medial prefrontal cortex [m

251 ructural and functional connectivity between limbic structures and pre-frontal cortices.

252 the expression pattern of Pcdh19 and Ncdh in limbic structures at four postnatal stages of C57BL/6J m

253 sing functional neuroanatomy that only a few limbic structures including the retrosplenial cortex (RS

254 nal injury on white matter tracts connecting limbic structures involved in memory processing.

255 increased functional connectivity affecting limbic structures such as the anterior/posterior cingula

256 Memory processing relies on limbic structures such as the hippocampus, parahippocamp

257 interconnectivity of cortical, striatal, and limbic structures that regulate alcohol intake, it has b

258 d with reductions in activity in caudate and limbic structures, respectively.

259 est connectivity to ARAS structures included limbic structures, thalamus and certain neocortical area

260 ontralateral projections to sensorimotor and limbic structures.

261 to ventromedial prefrontal cortex and other limbic structures.

262 involving prefrontal cortex, paralimbic, and limbic structures.

263 including between the prefrontal cortex and limbic structures.

264 rigins are located in the frontotemporal and limbic structures.

265 Scientists have long investigated how "limbic" structures, such as the amygdala, process affect

266 ough a distributed network of prefrontal and limbic subcortical regions implicated in cognitive contr

267 (effect size: .85; t36 = 2.54, p = .015) and limbic subdivisions (effect size: .74; t36 = 2.23, p = .

268 dicate that altered connectivity in a visual-limbic subnetwork during emotional face processing may b

269 tion is associated with anterior associative-limbic subthalamic nucleus and right dorsolateral prefro

270 ight specificity of the anterior associative-limbic subthalamic nucleus in decisional impulsivity.

271 cuitry with DREADDs normalized PFC-dependent limbic synchrony in stress-susceptible animals and resto

272 aventricular and centromedian thalamus), and limbic system (amygdala and nucleus accumbens).

273 ew DMRs distinguished regions of the cortex, limbic system and brain stem.

274 The rat limbic system contains head direction (HD) cells that fi

275 at emphasize stress pathways and accelerated limbic system development.

276 Head direction (HD) cells in the rat limbic system fire according to the animal's orientation

277 A detailed analysis of the limbic system highlight clear expression boundaries betw

278 long-lasting alterations in the function of limbic system structures, including the nucleus accumben

279 both, Ncdh and Pcdh19, in structures of the limbic system with overlapping expression patterns parti

280 ve degeneration of neurons in the neocortex, limbic system, and nucleus basalis, among others.

281 volving the occipital lobes, temporal lobes, limbic system, cerebellum, and frontoparietal cortices,

282 volving the occipital lobes, temporal lobes, limbic system, cerebellum, and frontoparietal cortices,

283 including heteromodal association areas and limbic system, demonstrate the high variability.

284 h include the basal ganglia and parts of the limbic system, have key roles in learning, motor control

285 ressant efficacy have largely focused on the limbic system, leaving it unclear whether this signaling

286 with the ventromedial prefrontal cortex and limbic system, together with dorsal and fronto-striatal

287 ceive input from different structures of the limbic system.

288 tified abnormal activation in the prefrontal-limbic system.

289 y as inhibitory components of the prefrontal-limbic system.

290 bnormal volumes are densely connected to the limbic system.

291 on the mechanisms of ketamine on a disrupted limbic system.

292 aminergic and glutamatergic functions in the limbic system.

293 l, as well as of the hypothalamus and of the limbic system.

294 ely late-developing ventrolateral prefrontal-limbic-temporal regions that are known to mediate late-d

295 contribution supports the emerging view that limbic thalamic nuclei may contribute critically to adap

296 Furthermore, this refocus on the limbic thalamus, as well as the rest of Papez circuit, w

297 apez circuit), which critically involves the limbic thalamus.

298 and involved a pattern of prefronto-temporo-limbic volume reductions and premotor, somatosensory and

299 ifying factors that influence prefrontal and limbic volume, such as midbrain BPnd, may be important f

300 Estimates of heritability in subcortical and limbic volumes ranged from .45 in the right hippocampus