ライフサイエンスコーパス: thalamocortical

1 These findings underscore the importance of thalamocortical activation of mPFC gamma-aminobutyric ac

2 ) range consistent with known frequencies of thalamocortical activation.

3 ury that result in the generation of altered thalamocortical activity and a persistent neuropathic pa

4 Disrupting thalamocortical activity patterns has proven to be a pro

5 and non-anesthetized mice to manipulate the thalamocortical activity.

6 ABAA receptor function and thereby influence thalamocortical activity.

7 receive dense but transient innervation from thalamocortical afferents during the first postnatal wee

8 Thalamocortical anatomical connectivity was compared bet

9 it mediates reciprocal interactions between thalamocortical and corticofugal axons to form the IC.

10 lopment of forebrain connectivity, ascending thalamocortical and descending corticofugal axons first

11 e approaches indicated increased spontaneous thalamocortical and hippocampal network activity in muta

12 Here, we optogenetically isolated the thalamocortical and intracortical excitatory inputs to i

13 These data identify Sema7A as a regulator of thalamocortical and local circuit development in layer 4

14 In thalamocortical and thalamic reticular nucleus neurons,

15 that invasion of monoamine, basal forebrain, thalamocortical, and corticocortical axons is mainly res

16 Findings indicate that deficits in thalamocortical, as well as corticocortical, connectivit

17 They are linked to pathology of the thalamocortical axis and a thalamic mechanism has been e

18 erentiation of barrel neurons and individual thalamocortical axon (TCA) arbors that synapse with them

19 rons were located in barrel rings encircling thalamocortical axon (TCA) clusters while mGluR5 knock-o

20 lipid-interacting molecule, is important for thalamocortical axon guidance.

21 ccompanied by a broadening of 5-HT-sensitive thalamocortical axon projections.

22 y information reaches the cortex after brief thalamocortical axonal delays, corticothalamic axons can

23 Some thalamocortical axons (TCAs) also fail to leave the dien

24 rincipal neurons, GABAergic interneurons and thalamocortical axons (TCAs) are essential elements of t

25 In early brain development, ascending thalamocortical axons (TCAs) navigate through the ventra

26 ipients of ascending sensory information via thalamocortical axons (TCAs).

27 ositioning of "corridor" guidepost cells for thalamocortical axons by Frizzled3.

28 w that proper routing of corticothalamic and thalamocortical axons in the internal capsule requires F

29 Thus, Linx guides the extension of thalamocortical axons in the ventral forebrain, and subs

30 Therefore, although thalamocortical axons invade appropriate cortical region

31 that the frequency selectivity of individual thalamocortical axons is surprisingly heterogeneous, eve

32 d selective loss of Ctip1 in cortex deprives thalamocortical axons of their receptive "sensory field"

33 tion of polarized dendritic outgrowth toward thalamocortical axons relaying sensory information, (3)

34 high-throughput viral approach to visualize thalamocortical axons with high sensitivity.

35 of different axon tracts (i.e., striatal and thalamocortical axons).

36 rridor and on corticofugal axons, but not on thalamocortical axons, and that mice with a null mutatio

37 maging of visually driven calcium signals in thalamocortical axons.

38 ependent modulator of Netrin-1 attraction in thalamocortical axons.

39 cal boutons typically form a single synapse, thalamocortical boutons in S1 usually formed multiple sy

40 Unlike M1, where thalamocortical boutons typically form a single synapse,

41 Following each training session, a thalamocortical brain slice was generated, and inhibitor

42 rtical signatures consistent with widespread thalamocortical burst firing such as increased delta osc

43 rent subtypes of cortical neurons to unitary thalamocortical bursts are mostly unknown.

44 SOM-mediated, distally directed inhibition, thalamocortical bursts could momentarily enhance the sal

45 ic GABA-ARs reduced the firing of individual thalamocortical cells but did not abolish slow oscillati

46 d GABAergic synaptic currents disappeared in thalamocortical cells when the presynaptic, reticular th

47 ticothalamic neurons monosynaptically excite thalamocortical cells, but also indirectly inhibit them

48 e estimation of dynamical characteristics of thalamocortical cells, such as dynamics of ion channels

49 l alpha by silencing a specialized subset of thalamocortical cells, thought to generate occipital alp

50 Seminal studies of the thalamocortical circuit in the visual system of the cat

51 The basal ganglia thalamocortical circuit may play a key role in the expre

52 t a fundamental computation performed by the thalamocortical circuit to accentuate salient tactile in

53 to synapses of a single cell-type within the thalamocortical circuit, is sufficient to remodel synchr

54 d auditory-evoked activities in the auditory thalamocortical circuit.

55 avior-related computation implemented by the thalamocortical circuit.

56 pecific neurons or pathways-for example, the thalamocortical circuitry, layer 4-3 (L4-L3) synapses, o

57 ts toward the involvement of cortico-striato-thalamocortical circuitry.

58 arallel and largely segregated basal ganglia thalamocortical circuits (ie, the motor circuit).

59 amus, which lead to hyperexcitability in the thalamocortical circuits and obsessive-compulsive disord

60 his study will increase our understanding of thalamocortical circuits and will improve computational

61 Basal ganglia-thalamocortical circuits are critical for motor control

62 Although the dynamics of the thalamocortical circuits are traditionally thought to un

63 Thalamocortical circuits are traditionally thought to un

64 PCP activates thalamocortical circuits in a bottom-up manner by reduci

65 izure resistance, and (2) hyperexcitation of thalamocortical circuits leading to non-convulsive absen

66 maladaptive changes involving nAChRs within thalamocortical circuits partially underpin the difficul

67 ly sculpt subplate circuits before permanent thalamocortical circuits to layer 4 are present, and dis

68 supporting the involvement of basal ganglia-thalamocortical circuits, representing emotional, cognit

69 1 spines integrate signals from associative thalamocortical circuits, their column-specific eliminat

70 feature of long-distance corticocortical and thalamocortical circuits.

71 nt connectivity models for intracortical and thalamocortical circuits.

72 ractions between most nodes of basal ganglia-thalamocortical circuits.

73 visual cortical input, and innervates visual thalamocortical circuits.

74 foundation for functional investigations of thalamocortical circuits.

75 rough modulation of both olivocerebellar and thalamocortical circuits.

76 e effects correspond to important changes in thalamocortical coding properties.

77 tico-cortical communication, while enhancing thalamocortical communication in this frequency band.

78 Thalamocortical conduction times are short, but layer 6

79 FP signature of the single-axon monosynaptic thalamocortical connection as measured by spike-trigger-

80 However, the development of thalamocortical connections and how such development rel

81 arly infancy, functional integration through thalamocortical connections depends on significant funct

82 Thalamocortical connections from the hand and face repre

83 The thalamocortical connections in the pallid bat are organi

84 uired for several key steps in wiring up the thalamocortical connections to form the cortical somatos

85 Preterm birth impacts on the development of thalamocortical connections to inferior frontal and medi

86 predominantly distributed in subcortical and thalamocortical connections.

87 tracortical circuitry and thereby can sculpt thalamocortical connections.

88 e intervals, similar to results reported for thalamocortical connections.

89 tworks and determine the correlation between thalamocortical connectivity and cognitive performance a

90 This paracrine signal may ensure thalamocortical connectivity and dispersion of inhibitor

91 To better understand the rules governing thalamocortical connectivity and the origin of cortical

92 ys a role in establishing the specificity of thalamocortical connectivity and the receptive fields (R

93 To define functional thalamocortical connectivity at the normal time of birth

94 maging data revealed a strong distinction in thalamocortical connectivity between the dorsal and vent

95 on the behavioral importance of the emerging thalamocortical connectivity during infancy.

96 However, no investigation has tested whether thalamocortical connectivity is altered in individuals a

97 haracterize the age-dependent development of thalamocortical connectivity patterns by examining the f

98 he functional significance of this extensive thalamocortical connectivity remains largely unknown.

99 onsciousness where movement ceases, coherent thalamocortical delta oscillations (1-5 Hz) develop, dis

100 suggests that Dgcr8-microRNA-Drd2-dependent thalamocortical disruption is a pathogenic event underly

101 us in slow oscillation, but global slow-wave thalamocortical dynamics have never been experimentally

102 ine magnetic resonance images, we identified thalamocortical dysconnectivity in the 243 individuals a

103 Thalamocortical dysconnectivity is present in both chron

104 ical oscillatory activity, a self-sustaining thalamocortical dysrhythmia, and the constant perception

105 Tinnitus and chronic pain may reflect thalamocortical dysrhythmia, which results from abnormal

106 iated with altered thalamic burst firing and thalamocortical dysrhythmia.

107 associated with altered thalamic firing and thalamocortical dysrhythmia.

108 tex progressively increased to exceed direct thalamocortical excitation.

109 gnitive testing is associated with increased thalamocortical FC, thus suggesting that neuroplasticity

110 rewards, which may be a product of increased thalamocortical feedback.

111 Developing thalamocortical fibers both in PRG-2 full knockout (KO)

112 aware patients (ie, specific damage to motor thalamocortical fibers), highlight the importance of the

113 (LPA), which failed to repel PRG-2-deficient thalamocortical fibers.

114 ity, which should play a significant role in thalamocortical function.

115 ogram, as thalamic damage and alterations in thalamocortical functional connectivity (FC) are importa

116 By performing graph-theoretic analyses on thalamocortical functional connectivity data collected f

117 tion, we revealed clear evidence of distinct thalamocortical functional connectivity pattern originat

118 cific disruption of synaptic transmission at thalamocortical glutamatergic projections in the auditor

119 nstrate the real-time capability to estimate thalamocortical hidden properties with high precision un

120 evaluates a real-time estimation system for thalamocortical hidden properties.

121 bsequently, responses appeared in the future thalamocortical input layer 4, and sound-evoked spike la

122 We also show that thalamocortical input to layer 1 includes collaterals fr

123 ts in infragranular layers, prolonging local thalamocortical input via positive feedback between infr

124 These complex thalamocortical input-output transformations significant

125 g of intrinsic connections in area 3b or the thalamocortical inputs does not contribute to large-scal

126 e, without significantly affecting bottom-up thalamocortical inputs indexed by the early cortical com

127 recurrently connected neurons were driven by thalamocortical inputs of similar magnitude indicating t

128 erneuron network, the synaptic maturation of thalamocortical inputs onto parvalbumin interneurons is

129 d and face representations, or any change in thalamocortical inputs to these areas.

130 eurons within the same layers receive weaker thalamocortical inputs, yet are strongly innervated by s

131 processed auditory information may modulate thalamocortical inputs.

132 order cognitive circuits, and the underlying thalamocortical interaction mechanism has attracted incr

133 ere evoked either by auditory or electrical (thalamocortical, intracortical) stimulation while random

134 t of structures throughout the basal ganglia-thalamocortical loop in the lesioned hemisphere of hemip

135 e rat somatosensory system contains multiple thalamocortical loops (TCLs) that altogether process, in

136 nsic and circuit-level specializations among thalamocortical loops may determine their involvement in

137 h synchronize the cortex through large-scale thalamocortical loops.

138 approximately 20Hz) throughout basal ganglia-thalamocortical loops.

139 The presence of identical thalamocortical malformations in two independent ciliary

140 Equivalent sensory thalamocortical manipulations showed that behaviour was

141 Here we uncovered a thalamocortical mechanism in which cortical fast-spiking

142 ic stimulation and further highlight a novel thalamocortical modulatory capacity that may explain the

143 t modulators of pathological oscillations in thalamocortical network activity during absence seizures

144 aves can only be achieved by considering the thalamocortical network as a single functional and dynam

145 ring natural sleep a dynamically fluctuating thalamocortical network controls the duration of sleep s

146 se oscillatory dynamics in the somatosensory thalamocortical network depended on the behavioral conte

147 of oscillatory dynamics of the somatosensory thalamocortical network in perception and decision makin

148 of high beta oscillations throughout the BG-thalamocortical network in the behaving parkinsonian rat

149 on dynamics of synaptic connectivity in the thalamocortical network model implementing spike-timing-

150 tion by creating the first conductance based thalamocortical network model of N2 sleep to generate bo

151 A thalamocortical network model suggested that observed di

152 her speculate that the intrinsic dynamics of thalamocortical network oscillations are crucial for ear

153 ose that these deficits cooperate to enhance thalamocortical network synchrony and generate pathologi

154 when applied to the brain-wide basal ganglia-thalamocortical network, DCM accurately reproduced the e

155 using biophysically realistic models of the thalamocortical network, we identified the critical intr

156 DOWN states in the component neurons of the thalamocortical network.

157 bnormal low-frequency oscillations (LFOs) in thalamocortical networks of patients in the interictal p

158 ce of abnormal low-frequency oscillations in thalamocortical networks of patients in the interictal p

159 nate sources of GABAergic control in nascent thalamocortical networks.

160 ltered in chronic schizophrenia involves the thalamocortical networks.

161 that NMDA-R blockade in RtN would disinhibit thalamocortical networks.

162 f low-frequency oscillations (LFO; <4 Hz) in thalamocortical networks.

163 sized corticothalamic EPSPs propagate within thalamocortical neuron dendrites and how different spati

164 s to act as synchrony-dependent "drivers" of thalamocortical neuron firing.

165 ffects of corticothalamic synaptic inputs on thalamocortical neuron membrane potential and allow thes

166 However, in thalamocortical neurones of the mouse ventrobasal (VB) t

167 However, in thalamocortical neurones of the mouse ventrobasal (VB) t

168 Here we focused on ventrobasal thalamocortical neurones, which contribute to behavioura

169 ated each of a diverse group of postsynaptic thalamocortical neurons (TCs).

170 erminals in contact with distal dendrites of thalamocortical neurons and GABAergic interneurons elici

171 s are highly conserved between glutamatergic thalamocortical neurons and GABAergic thalamic reticular

172 , the numerically dominant synaptic input to thalamocortical neurons comes from the cortex, which pro

173 more, uncaging of MNI glutamate reveals that thalamocortical neurons have postsynaptic voltage-depend

174 Thalamocortical neurons have thousands of synaptic conne

175 We find that thalamocortical neurons have voltage- and synchrony-depe

176 ing glutamatergic synaptic transmission from thalamocortical neurons in mice and found that eliminati

177 ond order trigemontothalamic and third order thalamocortical neurons in rats.

178 formed by networks of reciprocally connected thalamocortical neurons in the ventrobasal nucleus (VB)

179 nd thalamus, we found that M1-CT neurons and thalamocortical neurons in the ventrolateral (VL) nucleu

180 ed how rat dorsal lateral geniculate nucleus thalamocortical neurons integrate excitatory corticothal

181 real-time, mode-switching approach to drive thalamocortical neurons into or out of a phasic firing m

182 Toggling between phasic and tonic firing in thalamocortical neurons launched and aborted absence sei

183 tions reflect phasic information transfer in thalamocortical neurons projecting from lateral genicula

184 Thalamocortical neurons relay sensory and motor informat

185 Thalamocortical neurons relay sensory and motor informat

186 significantly increase the responsiveness of thalamocortical neurons to cortical excitatory input and

187 In hyperpolarized thalamocortical neurons, T-type Ca(2+)channels produce n

188 asynaptic GABAARs control the firing mode of thalamocortical neurons, we examined tonic GABAAR curren

189 ions of sensory input in mouse somatosensory thalamocortical neurons, we show that membrane excitabil

190 by recording and sampling from glutamatergic thalamocortical neurons, which receive major synaptic in

191 ng of cortical LFPs on spontaneous spikes of thalamocortical neurons.

192 nd temporal input patterns are integrated by thalamocortical neurons.

193 l neurons in mice and found that eliminating thalamocortical neurotransmission prevented the formatio

194 graded control of thalamic output, enabling thalamocortical operations to dynamically match ongoing

195 Sleep spindles, a defining thalamocortical oscillation of non-rapid eye movement st

196 Sleep spindles are thalamocortical oscillations in non-rapid eye movement (

197 Sleep spindles are thalamocortical oscillations in nonrapid eye movement sl

198 neural connectivity manifesting in increased thalamocortical oscillations in sleep is one particular

199 us is a major factor in the amplification of thalamocortical oscillations, making it a strong candida

200 us is a major factor in the amplification of thalamocortical oscillations, making it a strong candida

201 amus plays a critical role in the genesis of thalamocortical oscillations, yet the underlying mechani

202 fficient GABA-AR activation to control major thalamocortical oscillations.

203 pain pathway that likely underpins increased thalamocortical oscillatory activity, a self-sustaining

204 nder corticothalamic SWO UP and DOWN states, thalamocortical output can exhibit maximum alpha power a

205 ite in the deafferented FBS, we examined the thalamocortical pathway in 2 forelimb-amputated rats.

206 by disruptions thalamic metabolic growth and thalamocortical pathway maturation, particularly in extr

207 ceptor-mediated inhibition in the trigeminal thalamocortical pathway of mice lacking active Met in th

208 ific alterations in the lateral thalamus and thalamocortical pathways in extremely preterm neonates e

209 differences in the synaptic organization of thalamocortical pathways in striate and extrastriate are

210 In sensory thalamocortical pathways, thalamic recruitment of feedfo

211 c NAA/Cho and microstructural alterations in thalamocortical pathways.

212 ted thalamocortical silent states and evoked thalamocortical persistent activity; conversely, mild he

213 Thus, a synchronous thalamocortical phasic firing state is required for abse

214 This model suggests that blocking thalamocortical phasic firing would treat absence seizur

215 t in vivo characterization of sensory-driven thalamocortical potentials in V1.

216 Several challenges to current views of thalamocortical processing are offered here.

217 aneous and evoked firing rate of third order thalamocortical projection neurons, but not second order

218 ly outside the cortical region receiving the thalamocortical projection, implying that it indeed prov

219 ion might reflect synaptic depression in the thalamocortical projection.

220 tions, the auditory cortex receives parallel thalamocortical projections from the medial geniculate n

221 Such locally varied thalamocortical projections may be useful in enabling ra

222 Drd2 in the thalamus, which renders 22q11DS thalamocortical projections sensitive to antipsychotics

223 In adult mammals, ascending thalamocortical projections target layer 4, and the onse

224 uditory thalamus, an abnormal sensitivity of thalamocortical projections to antipsychotics, and an ab

225 2 elevation and hypersensitivity of auditory thalamocortical projections to antipsychotics.

226 with the available evidence on interoceptive thalamocortical projections, and also with the tensile a

227 Furthermore, Linx binds to thalamocortical projections, and it promotes outgrowth o

228 Cell counts reveal that, similar to thalamocortical projections, many more cells are present

229 tions, we constructed a comprehensive map of thalamocortical projections.

230 rated topographic organizations in all three thalamocortical projections.

231 The thalamocortical ratio remained strongly prognostic (P <

232 lar (RT) neurons or heightened inhibition of thalamocortical relay (TC) neurons by RT.

233 e sole descending cortical synaptic input to thalamocortical relay cells and reticular interneurons a

234 the SRTT task, which is linked to hypocretin-thalamocortical responses.

235 To disentangle their roles in thalamocortical rhythms, we focally deleted synaptic, ga

236 anesthesia rapidly and reversibly eliminated thalamocortical silent states and evoked thalamocortical

237 ce, cooling also prevented the generation of thalamocortical silent states.

238 ultures plated on multielectrode arrays; (2) thalamocortical slices examined by field potential recor

239 sed laser-scanning photostimulation in acute thalamocortical slices of mouse auditory cortex during t

240 g optogenetically guided recordings in mouse thalamocortical slices, we achieved the first reported p

241 thetized or naturally sleeping mice disrupts thalamocortical slow oscillation and induces the activat

242 site effect; it increases the rhythmicity of thalamocortical slow oscillation.

243 haracterized by reversible disruption of the thalamocortical slow-wave pattern rhythmicity and the ap

244 activity; conversely, mild heating increased thalamocortical slow-wave rhythmicity.

245 ompared between cortical responses to single thalamocortical spikes and bursts.

246 ortical slow oscillations (SO; 0.5-1 Hz) and thalamocortical spindle activity (12-15 Hz) during sleep

247 nt glioma group, high thalamic SUVs and high thalamocortical SUV ratios were associated with short su

248 lts in a profound, long-lasting reduction in thalamocortical synapses accompanied by a transient incr

249 How thalamocortical synapses are formed and maintained in th

250 Under anesthesia, depression at thalamocortical synapses disrupted the fidelity of senso

251 input to the middle cortical layer and that thalamocortical synapses form a small fraction (M1: 12%;

252 sory areas, which raises the question of how thalamocortical synapses formed in M1 in the mouse compa

253 ent plasticity mediated by NMDA receptors at thalamocortical synapses in acute PFC slices.

254 e of presynaptic 5-HT2A receptors located at thalamocortical synapses in the control of thalamofronta

255 glutamatergic transmission and plasticity at thalamocortical synapses remains largely unexplored.

256 naptic responses to hypocretin, a measure of thalamocortical synapses, compared with its effects on 5

257 ic impairment of neurotransmitter release at thalamocortical synapses, or a selective reduction of se

258 levels depress intracortical but facilitate thalamocortical synapses, whereas low levels potentiate

259 determine the organization and plasticity of thalamocortical synapses.

260 t it indeed provides a very local measure of thalamocortical synaptic activation.

261 To determine whether thalamocortical synaptic circuits differ across cortical

262 We investigated somatosensory thalamocortical synaptic communication in mice deficient

263 ecreted protein hevin is required for normal thalamocortical synaptic connectivity in the mouse corte

264 However, thalamocortical synaptic properties remain poorly unders

265 -frequency (delta/theta) oscillations in the thalamocortical system are elevated in schizophrenia dur

266 esults indicate that bifacial maps along the thalamocortical system do not offer a functional advanta

267 Synchronous neuronal activity in the thalamocortical system is critical for a number of behav

268 e used a detailed computational model of the thalamocortical system to report that interaction betwee

269 In the thalamocortical system, gap junctions couple inhibitory

270 f the traditionally implicated basal ganglia thalamocortical system, in particular, the pedunculopont

271 nchrony, and rhythmogenesis in the mammalian thalamocortical system, similar to chemical synaptic pla

272 In the thalamocortical system, the topographical sorting of dis

273 ircuit, corticothalamic loop, and cortico-BG-thalamocortical system.

274 nd systems neuroscientists interested in the thalamocortical system.

275 d the generation of rhythmic activity in the thalamocortical system.

276 ize the consequences of bifacial maps in the thalamocortical system.

277 means that the extent of backpropagation in thalamocortical (TC) and thalamic reticular nucleus (TRN

278 02 caused a reduction in the total number of thalamocortical (TC) axons innervating the somatosensory

279 , we measured somatic activity of excitatory thalamocortical (TC) cells together with axonal activity

280 lamina and averaged on spontaneous spikes of thalamocortical (TC) cells.

281 In primary sensory cortices, thalamocortical (TC) inputs can directly activate excita

282 of the nucleus reticularis thalami (NRT) and thalamocortical (TC) neurons discharge high-frequency bu

283 Further, although the RE inhibits thalamocortical (TC) neurons, decreased RE firing causes

284 Auditory thalamocortical (TC) projections recently emerged as a n

285 ty between retinal ganglion cells (RGCs) and thalamocortical (TC) relay neurons is thought to be esse

286 Previous in vitro studies have proposed that thalamocortical (TC) synapses are stronger than corticoc

287 hat in adults visual deprivation strengthens thalamocortical (TC) synapses in A1, but not in primary

288 We explored STP variability across thalamocortical (TC) synapses, measuring whole-cell resp

289 the anatomical organization of the auditory thalamocortical (TC) system is fundamental for the under

290 ses, and Type I PV-IR synapses from putative thalamocortical terminals comprised the remaining approx

291 OFC exceeded in size and specialization even thalamocortical terminals from the prefrontal-related th

292 enerated optogenetic stimulation of auditory thalamocortical terminals were also attenuated, suggesti

293 In contrast with the thalamocortical theory, it also predicts that reducing t

294 ilia in the formation of the corticothalamic/thalamocortical tracts by establishing the correct cellu

295 stigate the formation of the corticothalamic/thalamocortical tracts in mice mutant for Rfx3, which re

296 and the corticothalamic, corticospinal, and thalamocortical tracts.

297 n of these neurons in regulating the gain of thalamocortical transfer of sensory information dependin

298 x is thought to be dependent on the onset of thalamocortical transmission to layer 4 as well as the e

299 , a group of GABAergic neurons that regulate thalamocortical transmission, sleep rhythms, and attenti

300 In addition to the primary thalamocortical visual relay in the lateral geniculate n