ライフサイエンスコーパス: TRN

1 TRN dendritic and axonal morphologies are inconsistent w

2 TRN dysfunction has been linked to sensory abnormality,

3 TRN neurons are also coupled to one another by electrica

4 TRN neurons are interconnected by a network of GABAergic

5 TRN-1 bound directly to capsid nanotubes and induced dra

6 TRN-restricted deletion of Ptchd1 leads to attention def

7 TRN-SR2 was originally identified in a yeast two-hybrid

8 TRNs are characterized by the abundance of motifs such a

9 we identify beta-karyopherin Transportin-1 (TRN-1) as a cellular co-factor of HIV-1 infection, which

10 chronous and imprecise rebound bursting; (2) TRN-mediated lateral inhibition that further desynchroni

11 Thus, the FLP neurons can acquire a TRN-like fate but use multiple levels of regulation to e

12 ion factors cause the FLP neurons to acquire TRN-like traits.

13 state, touch stimuli sufficient to activate TRNs induce an average strain of 3.1% at the center of t

14 In addition, TRN-1 promotes the efficient nuclear import of both vira

15 and organization of the TRN MTs and affects TRN axonal morphology.

16 nal modeling to demonstrate how the amygdala-TRN pathway, embedded in a wider neural circuit, can med

17 The model suggests that the amygdala-TRN projection can serve as a unique mechanism for emoti

18 notation of regulatory features of genes and TRN reconstruction are challenging tasks of microbial ge

19 ndle epoch, oscillatory activity in mPFC and TRN increased in frequency from onset to offset, accompa

20 aptic circuits that generate rhythmicity and TRN cell-intrinsic mechanisms that control PF and oscill

21 geted patch-clamp recordings from rat TC and TRN neuron dendrites to measure bAPs directly.

22 spatial influence of bAP signaling in TC and TRN neurons is more restricted, with potentially importa

23 terior Hox proteins transformed the anterior TRN subtype toward a posterior identity both morphologic

24 mmon genes had previously been identified as TRN-specific.

25 By contrast, DSI is not observed at TRN synapses targeting thalamic relay neurons.

26 Ptchd1 deletion attenuates TRN activity through mechanisms involving small conducta

27 Because TRN neurons signal electrically through dendrodendritic

28 ile the reciprocal synaptic circuits between TRN and sensory relay nuclei are known to underlie the g

29 nstrated that the direct interaction between TRN-SR2 and HIV integrase predominantly involves the cat

30 s is supported by direct interaction between TRN-SR2 and HIV-1 integrase (IN).

31 characterization of the interaction between TRN-SR2 and Ran.

32 ability of adaptive behavior differs between TRNs and ERNs.

33 This brain TRN quantitatively predicts with high accuracy gene expr

34 GABAergic synapses formed by TRN neurons contact both thalamic relay cells and neuron

35 rom the ventral posterior nucleus to central TRN cells transmit rapid excitatory currents that depres

36 ow captures different aspects of the E. coli TRN than expression-based approaches, potentially making

37 Under in vitro conditions, TRN neurons can generate slow oscillations in a cell-int

38 c cholinergic receptors, thereby controlling TRN neuronal activity with high spatiotemporal precision

39 unknown role of ErbB4 in regulating cortico-TRN-thalamic circuit function.

40 The anterior subtype maintains a default TRN state, whereas the posterior subtype undergoes furth

41 thalamic nuclei to form molecularly defined TRN-thalamus subnetworks.

42 elated), which ensures, but does not direct, TRN differentiation.

43 tent with a decrease in arousal state during TRN stimulation.

44 he posterior medial thalamic nucleus to edge TRN cells evoke slower, less depressing excitatory curre

45 by restricting variability, and thus ensures TRN differentiation.

46 of the Erbb4 gene in somatostatin-expressing TRN neurons markedly alters behaviors that are dependent

47 ucleus, which similarly innervated extensive TRN sites.

48 By combining the first TRN ensemble recording with psychophysics and connectivi

49 However, existing methods for TRN identification suffer from the inclusion of excessiv

50 Here, we propose methods for TRN inference in a mammalian setting, using ATAC-seq dat

51 utoregulation of mec-3 is not sufficient for TRN differentiation; ALR-1 provides a second positive fe

52 ion was much larger for relay cells than for TRN neurons.

53 A-seq, we compare transcription profiles for TRNs with those of two other sensory neurons, and presen

54 t it is mediated by the release of 2-AG from TRN neurons.

55 Blocking synaptic release from TRN neurons through conditional deletion of vesicular GA

56 ity to deal with the complexity of a genomic TRN, providing a snapshot of the synergistic TFs regulat

57 Here we anatomically identify the human TRN using multiple registered and averaged proton densit

58 nd the absolute expression level to identify TRN connections.

59 Computational approaches to identify TRNs can be applied in any species where quality RNA can

60 tive stress may play a key role in impacting TRN PV neurons at early stages of these disorders.

61 nical findings, our results support impaired TRN-PV neuron activity as a potential cause of schizophr

62 we anticipate that our methods will improve TRN inference in new mammalian systems, especially in vi

63 recorded slow forms of rhythmic activity in TRN neurons, which were driven by fast glutamatergic tha

64 ent functions, including rebound bursting in TRN neurons, with potential implications for schizophren

65 In contrast, in TRN neurons, AP properties are unchanged between LTS bur

66 dence and strength of electrical coupling in TRN was sharply reduced, but not abolished, in KO mice.

67 reases and the generation of burst firing in TRN neurons.

68 ls to powerfully control spike generation in TRN neurons.

69 that intracellular Cl(-) levels are high in TRN neurons, resulting in a Cl(-) reversal potential (E(

70 ther underscore the importance of the HIV-IN TRN-SR2 protein-protein interaction for HIV nuclear impo

71 ns and their axons evokes GABAergic IPSCs in TRN neurons in mice younger than 2 weeks of age but fail

72 GABAergic neurons in TRN exhibited large initial excitatory responses that qu

73 s sufficient to trigger action potentials in TRN neurons.

74 ata, MEC-10, but not MEC-6, formed puncta in TRN neurites that colocalize with MEC-4 when MEC-4 is ov

75 s no effect on spontaneous IPSCs recorded in TRN neurons aged 2 weeks or older while dramatically red

76 specifically, FFLs) in signal propagation in TRNs and the organization of the TRN topology with FFLs

77 n for HIV nuclear import and validate the IN/TRN-SR2 interaction interface as a promising target for

78 Insight into the IN/TRN-SR2 interaction interface is necessary to guide drug

79 mproves the ability to computationally infer TRN from time series expression data.

80 mented in the RegPredict Web server to infer TRN in the model Gram-positive bacterium Bacillus subtil

81 The inferred TRN in B. subtilis comprises regulons for 129 TFs and 24

82 Instead, TRN neuronal organization could facilitate transmission

83 ll as by electrical synapses interconnecting TRN neurons.

84 inent at inhibitory synapses interconnecting TRN neurons.

85 e problem and thus solving it for very large TRNs remains to be a challenge.

86 Next, the regions of the solenoid-like TRN-SR2 molecule that are involved in the interaction wi

87 expressing parvalbumin (PV neurons), a main TRN neuronal population, and associated Wisteria floribu

88 c inhibitory circuitry, neuronal morphology, TRN cell function and electrical coupling requires Cx36.

89 ents evokes near-synchronous firing in mouse TRN neurons that is rapidly desynchronized in thalamic n

90 iggers postsynaptic depolarizations in mouse TRN neurons.

91 d electrophysiological features of the mouse TRN to connectivity and systems-level function.

92 a brain transcriptional regulatory network (TRN) model.

93 The transcriptional regulatory network (TRN) of Bacillus subtilis coordinates cellular functions

94 , by its transcriptional regulatory network (TRN) that coordinates its gene expression to respond to

95 ses is a transcriptional regulatory network (TRN) that modulates gene expression.

96 hrough the transcription regulatory network (TRN).

97 ring of transcriptional regulatory networks (TRN) from genomics data has always represented a computa

98 rks and transcriptional regulatory networks (TRNs) by combining them into more complex circuitries of

99 nstruct transcriptional regulatory networks (TRNs) focus primarily on proximal data such as gene co-e

100 ling of transcriptional regulatory networks (TRNs) has been increasingly used to dissect the nature o

101 logy of transcriptional regulatory networks (TRNs) is an effective way to study the regulatory intera

102 tion of transcriptional regulatory networks (TRNs) is of significant importance in computational biol

103 Transcriptional regulatory networks (TRNs) program cells to dynamically alter their gene expr

104 Transcriptional regulatory networks (TRNs) provide insight into cellular behavior by describi

105 yet the transcriptional regulatory networks (TRNs) that control ILC function are largely unknown.

106 In transcriptional regulatory networks (TRNs), a canonical 3-node feed-forward loop (FFL) is hyp

107 complex transcriptional regulatory networks (TRNs), which are still only partially understood even fo

108 ee-node transcriptional regulatory networks (TRNs), with three different types of gene regulation log

109 through transcriptional regulatory networks (TRNs).

110 ns result in variable touch receptor neuron (TRN) function.

111 two subtypes of the touch receptor neurons (TRNs) in C. elegans, we found that a "posterior inductio

112 scles in mammals and touch receptor neurons (TRNs) in Caenorhabditis elegans nematodes are embedded i

113 n of 15-p MTs in the touch receptor neurons (TRNs) MTs.

114 e well-characterized touch receptor neurons (TRNs) of Caenorhabditis elegans to investigate this ques

115 Using the touch receptor neurons (TRNs) of Caenorhabditis elegans, we find that mec-15(-)

116 fferentiation of the touch receptor neurons (TRNs) of Caenorhabditis elegans.

117 tle touch in the six touch receptor neurons (TRNs) using a mechanotransduction complex that contains

118 h is mediated by six touch receptor neurons (TRNs), and is dependent on MEC-4, a DEG/ENaC channel.

119 ucial markers in the touch receptor neurons (TRNs), we visualized and measured touch-induced mechanic

120 ectly sensitizes the touch receptor neurons (TRNs).

121 number in C. elegans touch receptor neurons (TRNs).

122 d exclusively in six touch receptor neurons (TRNs).

123 extend our previous Th17 TRN, using our new TRN inference methods to integrate all Th17 data (gene e

124 ory systems: the thalamic reticular nucleus (TRN) and extrathalamic inhibitory (ETI) inputs.

125 c neurons in the thalamic reticular nucleus (TRN) and intrinsic interneurons of dLGN.

126 ecordings in the thalamic reticular nucleus (TRN) and medial prefrontal cortex (mPFC) of freely behav

127 volvement of the thalamic reticular nucleus (TRN) come from its unique neuronal characteristics and n

128 t neurons in the thalamic reticular nucleus (TRN) form GABAergic synapses with other TRN neurons and

129 c neurons in the thalamic reticular nucleus (TRN) form powerful inhibitory connections with several d

130 s known that the thalamic reticular nucleus (TRN) gates sensory information en route to the cortex, b

131 The inhibitory thalamic reticular nucleus (TRN) is a hub of the attentional system that gates thala

132 The thalamic reticular nucleus (TRN) is a unique brain structure at the interface betwee

133 The thalamic reticular nucleus (TRN) is hypothesized to regulate neocortical rhythms and

134 The thalamic reticular nucleus (TRN) is hypothesized to regulate thalamo-cortical intera

135 The thalamic reticular nucleus (TRN) is implicated in schizophrenia pathology.

136 ortical (TC) and thalamic reticular nucleus (TRN) neurons remains unknown.

137 ursting in model thalamic reticular nucleus (TRN) neurons.

138 c neurons in the thalamic reticular nucleus (TRN) of mice and rats form two types of GJ-coupled clust

139 , neurons in the thalamic reticular nucleus (TRN) participate in distinct types of oscillatory activi

140 ithin the mature thalamic reticular nucleus (TRN) powerfully inhibit ventrobasal (VB) thalamic relay

141 ic activation of thalamic reticular nucleus (TRN) rapidly induces slow wave activity in a spatially r

142 odality-specific thalamic reticular nucleus (TRN) subnetworks.

143 y neurons of the thalamic reticular nucleus (TRN) that regulate the flow of those data(3-6).

144 The thalamic reticular nucleus (TRN), a brain area rich in gap junctional (electrical) s

145 The thalamic reticular nucleus (TRN), a brain area rich in gap-junctional (electrical) s

146 ion in the mouse thalamic reticular nucleus (TRN), a brain structure essential for sensory processing

147 nsmission in the thalamic reticular nucleus (TRN), a brain structure intimately involved in the contr

148 expressed in the thalamic reticular nucleus (TRN), a group of GABAergic neurons that regulate thalamo

149 s the inhibitory thalamic reticular nucleus (TRN), a key node in the brain's attentional network.

150 The thalamic reticular nucleus (TRN), the major source of thalamic inhibition, regulates

151 c neurons in the thalamic reticular nucleus (TRN).

152 arising from the thalamic reticular nucleus (TRN).

153 eurons, but these cells do not share obvious TRN traits or proteins.

154 r, it remains unclear whether alterations of TRN activity can account for abnormal electroencephalogr

155 our study provides a comprehensive atlas of TRN neurons at single-cell resolution and links molecula

156 med unusual synapses close to cell bodies of TRN neurons and had more large and efficient terminals t

157 nstructed neuron, revealed three clusters of TRN neurons that differed in cell body shape and size, d

158 gle X-ray scattering data for the complex of TRN-SR2 with truncated integrase, we propose a molecular

159 Depletion of TRN-1, which we characterized by mass spectrometry, sign

160 the TRN precede the postnatal development of TRN-to-VB inhibition.

161 mice, we found that brief selective drive of TRN switched the thalamocortical firing mode from tonic

162 des quantitative, genome-scale evaluation of TRN inference, combining ATAC-seq and RNA-seq data.

163 y we demonstrate stable complex formation of TRN-SR2 and RanGTP in solution.

164 For a significant fraction of TRN neurons, synaptic inputs or brief depolarizing curre

165 egrase interacts with the N-terminal half of TRN-SR2 principally through the HEAT repeats 4, 10, and

166 Direct optogenetic inhibition of TRN-PV neurons was ineffective in blocking spindles but

167 We have now studied the interaction of TRN-SR2 and HIV IN in molecular detail and identified th

168 was used to characterize the interaction of TRN-SR2 with a truncated variant of the HIV-1 integrase,

169 latory activity, mediated by an interplay of TRN-VB synaptic circuits that generate rhythmicity and T

170 e deletion of Cx36 affects the maturation of TRN and VB neurons, electrical coupling and GABAergic sy

171 sis supported a model wherein one monomer of TRN-SR2 is bound to one monomer of RanGTP.

172 the dLGN, we reconstructed a large number of TRN neurons that were retrogradely labeled following inj

173 Differences in the intrinsic physiology of TRN cell types, including state-dependent bursting, cont

174 tical for engaging the hydrophobic pocket of TRN-1 at position W730.

175 ompanied by a consistent phase precession of TRN spike times relative to the cortical oscillation.

176 can help study the structural properties of TRN based on connectivity and clustering tendency of mot

177 The properties of TRN-mediated inhibition in VB also depended on the Cx36

178 We find that optogenetic stimulation of TRN neurons and their axons evokes GABAergic IPSCs in TR

179 lts provide insights into how subnetworks of TRN neurons may differentially process distinct classes

180 ulate activity of the major subpopulation of TRN GABAergic neurons, which express the calcium-binding

181 suggest that there exist a subpopulation of TRN neurons that receive convergent inputs from multiple

182 s integrative approach enabled generation of TRNs with increased information content relative to R. s

183 refore needed for reliable identification of TRNs in this context.

184 ch approaches enable rapid reconstruction of TRNs, the overwhelming combinatorics of possible network

185 These experiments indicate that one TRN-SR2 molecule can specifically bind one CCD-CTD dimer

186 naptic inputs can powerfully entrain ongoing TRN neuronal activity.

187 nically relevant behavioural phenotypes onto TRN dysfunction in a human disease model, while also ide

188 Transportin 3 (TNPO3 or TRN-SR2) has been shown to be an important cellular fact

189 eus (TRN) form GABAergic synapses with other TRN neurons and that these interconnections are importan

190 proach can be used to simultaneously produce TRN models for each related organism used in the compara

191 While activity of limbic-projecting TRN neurons positively correlates with arousal, sensory-

192 strate its ability to accurately reconstruct TRNs in biological complex systems.

193 can be successfully used to help reconstruct TRNs from high-throughput data, and highlights the poten

194 and gene expression compendia to reconstruct TRNs in a genome-wide perspective.

195 nd the chaperones; this antagonism regulates TRN development, as well as synaptic functions of GABAer

196 flow and observations to build a large-scale TRN model for the alpha-Proteobacterium Rhodobacter spha

197 a novel workflow for generating large-scale TRN models that integrates comparative genomics data, gl

198 gene expression data to assemble large-scale TRN models with high-quality predictions.

199 the PFC does not directly project to sensory TRN subnetworks, the circuitry underlying this process h

200 t their properties and their role in shaping TRN neuronal activity are not well understood.

201 Although in concentrated solutions TRN-SR2 by itself was predominantly present as a dimer,

202 (HTK) at 4 degrees C (HTK group, n=5) or SOM-TRN-001 at 21 degrees C (SOM group, n=5).

203 In the somatosensory TRN we observed two groups of genetically defined neuron

204 closely resemble those of the somatosensory TRN.

205 g specializations of these two somatosensory TRN subcircuits therefore appear to be tuned to the sign

206 In the absence of Cx36, some TRN neurons express asymmetric electrical coupling media

207 ween the establishment of cell-type-specific TRNs and RT control during lineage specification.

208 tion of predictions from this R. sphaeroides TRN model showed that high precision and recall was also

209 formation content relative to R. sphaeroides TRN models built via other approaches.

210 One such factor, transportin SR2 (TRN-SR2)/transportin 3 (TNPO3), promotes infection by HI

211 The karyopherin transportin SR2 (TRN-SR2, TNPO3) is responsible for shuttling specific ca

212 Transportin-SR2 (TRN-SR2 and TNPO3) is a cellular cofactor of HIV replica

213 Transportin-SR2 (TRN-SR2, Transportin-3, TNPO3) is a cellular karyopherin

214 We refine and extend our previous Th17 TRN, using our new TRN inference methods to integrate al

215 We conclude that TRN can induce rapid modulation of local cortical state.

216 Immunohistochemical data indicate that TRN neurons express very low levels of the Cl(-) transpo

217 dramatic structural damage, indicating that TRN-1 is necessary and sufficient for uncoating in vitro

218 Here, we propose that TRN circuits are specialized to exert thalamic control a

219 Our study suggests that TRN-1 mediates the timely release of the HIV-1 genome fr

220 The TRN also facilitates quantification of population-level

221 The TRN structure and its condition-dependent activity uncov

222 The TRN, therefore, is in a strategic location to regulate t

223 Because the TRN receives bottom-up sensory input and top-down cortic

224 t except for a short period after birth, the TRN of the mouse lacks intrinsic GABAergic connections.

225 nges occur (e.g., the expression of both the TRN mRNAs and proteins) when the FLP neurons ectopically

226 We previously characterized the TRN-SR2 binding interface in IN and introduced mutations

227 How specific circuits connecting the TRN with sensory thalamic structures implement these fun

228 lf was predominantly present as a dimer, the TRN-SR2-RanGTP complex was significantly more compact.

229 tional evidence supports broad roles for the TRN in arousal, attention, and sensory selection.

230 ic trees and fewer divergent inputs from the TRN compared to WT cells.

231 IV IN in molecular detail and identified the TRN-SR2 interacting regions of IN.

232 TFs playing key roles in the TRN include well-known regulators of neural and behavior

233 We found that cellular heterogeneity in the TRN is characterized by a transcriptomic gradient of two

234 Plasticity of electrical synapses in the TRN may be a key mechanism underlying these processes.

235 profound abnormalities of PV neurons in the TRN of subjects with SZ and BD, and offer support for th

236 amine intrinsic GABAergic connections in the TRN of the mouse.

237 Electrical synapses in the TRN precede the postnatal development of TRN-to-VB inhib

238 ve for PV) and WFA/PNNs were observed in the TRN, with no effects of duration of illness or age at on

239 armacological targeting and not found in the TRN-restricted deletion mouse.

240 erm depression of electrical synapses in the TRN.

241 ponse properties in the visual sector of the TRN and measured an inhibitory relationship with the con

242 neurons arrayed across the thickness of the TRN and target their axons to both first- and higher-ord

243 elationship between the visual sector of the TRN and the dLGN, we reconstructed a large number of TRN

244 nectivity that mediates re-excitation of the TRN but preserves asynchronous firing.

245 This representation of the TRN covers 842 genes representing 76% of the variance in

246 Although the importance of the TRN has long been recognised(7-9), understanding of its

247 r gross characterizations of the role of the TRN in human behavior.

248 the somatosensory and visual circuits of the TRN in mice.

249 de causal support for the involvement of the TRN in state regulation in vivo and introduce a new mode

250 A direct involvement of the TRN in SZ and BD has not been tested thus far.

251 structural organization and function of the TRN is particularly interesting in the context of highly

252 o changes the number and organization of the TRN MTs and affects TRN axonal morphology.

253 opose that ErbB4 sets the sensitivity of the TRN to cortical inputs at levels that can support sensor

254 pagation in TRNs and the organization of the TRN topology with FFLs as building blocks.

255 A useful description of the TRN would decompose the transcriptome into targeted effe

256 Despite the importance of the TRN, its activity has been scarcely investigated in vivo

257 g functional modules within the plane of the TRN, with axons that selectively inhibit local groups of

258 Finally, we present a homology model of the TRN-SR2-RanGTP complex that is in excellent agreement wi

259 ch reside along the surrounding edges of the TRN-synapse with the posterior medial thalamic nucleus,

260 ctions are important for the function of the TRN.

261 ibute evenly throughout the thickness of the TRN.

262 iated by an enhanced cortical drive onto the TRN that promotes the TRN-mediated cortical feedback inh

263 ortical drive onto the TRN that promotes the TRN-mediated cortical feedback inhibition of thalamic ne

264 alamic nuclei across brain states, where the TRN separately controls external sensory and internal li

265 erns, and medial-lateral position within the TRN.

266 effective channel for the ensemble along the TRNs, this study integrates body mechanics and the spati

267 tween the extracellular matrix (ECM) and the TRNs but could not detect any differences in touch-induc

268 the TRNs, as well as harsh touch in both the TRNs and the PVD nociceptors.

269 By connecting TFs to genes, the TRNs suggest means to selectively regulate ILC effector

270 7 are also essential for gentle touch in the TRNs, as well as harsh touch in both the TRNs and the PV

271 ge number of 15-p MTs, normally found in the TRNs, is not essential for mechanosensation.

272 In the TRNs, we analyze process outgrowth and show that four tu

273 ith MEC-4 when MEC-4 is overexpressed in the TRNs.

274 the experimental findings, predicts that the TRNs function as a band-pass mechanical filter, and prov

275 at the insulin signaling cascade within the TRNs.

276 s contain low amounts of the mRNAs for these TRN genes, they do not have detectable proteins.

277 We put forth that these TRN abnormalities may contribute to disruptions of sleep

278 As this TRN covers the majority of the transcriptome and concise

279 ~67% of the predicted gene clusters in this TRN are enriched for functions ranging from photosynthes

280 idated the organization and activity of this TRN by applying independent component analysis to a comp

281 Transportin-SR2 (Tnpo3, TRN-SR2), a human karyopherin encoded by the TNPO3 gene,

282 es, whereas late cells fired in antiphase to TRN activity and also had higher firing rates than early

283 l domain of HIV-1 IN that mediate binding to TRN-SR2 were recently delineated.

284 ation of a major GABA/PV inhibitory input to TRN arising from basal forebrain parvalbumin neurons (BF

285 Modulation of the BF-PV input to TRN may improve these neural abnormalities.

286 The different pathways to TRN suggest distinct mechanisms of attention to external

287 rom the amygdala sends robust projections to TRN.

288 wo mechanosensory systems: the gentle-touch (TRNs) and harsh-touch (PVD) circuits.

289 The two TRN cell groups process their inputs in pathway-specific

290 The two TRN subpopulations make differential connections with th

291 Whereas the sensory dendrite of wild-type TRNs is packed with a cross-linked bundle of long, 15-pr

292 TF logics and to reconstruct the underlying TRNs.

293 The structure and function of visual TRN subcircuits closely resemble those of the somatosens

294 A model in which TRN-SR2 imports the viral preintegration complex into th

295 , HIV-1 IN is released from the complex with TRN-SR2 by RanGTP.

296 191)) retaining the ability to interact with TRN-SR2.

297 , that significantly reduce interaction with TRN-SR2.

298 in IN as important for the interaction with TRN-SR2: Phe-185/Lys-186/Arg-187/Lys-188 in the CCD and

299 arly cells generally fired in synchrony with TRN spikes, whereas late cells fired in antiphase to TRN

300 y, roles A, B and C), and contrast them with TRN nodes having high connectivity on the basis of their

301 both thalamic relay cells and neurons within TRN.