ライフサイエンスコーパス: principal cell

1 dox dysregulation was targeted in excitatory principal cells.

2 rom thousands of granule cells converge onto principal cells.

3 urons with concomitantly decreased firing of principal cells.

4 zed its protein and aquaporin-2 (AQP2) in CD principal cells.

5 red mCCD and isolated primary distal nephron principal cells.

6 selective or concerted inhibitory action on principal cells.

7 e temporal patterns onto distinct domains of principal cells.

8 T2-Cre transgenic mice, evoked fast IPSCs in principal cells.

9 InsR KO) specifically in the collecting duct principal cells.

10 m Aqp2-expressing progenitor cells or mature principal cells.

11 of insulin on ENaC, we used mouse mpkCCDc14 principal cells.

12 ), influence the activity of transporters in principal cells.

13 controlled by distinct epochs of activity in principal cells.

14 ion of the postsynaptic currents of cortical principal cells.

15 ential position for regulating the firing of principal cells.

16 ion and depression at excitatory synapses on principal cells.

17 glycerol (2-AG), albeit at lower levels than principal cells.

18 loss of functional inhibition of excitatory principal cells.

19 and pharmacological profile as GlyRs on MNTB principal cells.

20 ion counters their excitatory influence over principal cells.

21 reduced in BLA principal cells yet not in LA principal cells.

22 hat AgAQP1 resides in stellate cells but not principal cells.

23 of Held presynaptic endings that envelop the principal cells.

24 between beta1Pix and 14-3-3beta in cultured principal cells.

25 pressing cells and in kidney collecting duct principal cells.

26 sing AQP-2 expression in the collecting duct principal cells.

27 oluted tubule, distal convoluted tubule, and principal cells.

28 the plasma membrane of renal collecting duct principal cells.

29 reciprocal dendrodendritic connections with principal cells.

30 stellate cells but not in the other types of principal cells.

31 of polarized murine cortical collecting duct principal cells.

32 many different synaptic contacts formed with principal cells.

33 This deletion of Dot1l in principal cells abolished histone H3 K79 methylation in

34 Knockdown of betaPix in native principal cells abolished the ET-1-induced decrease in E

35 e NMDARs in all dentate gyrus and dorsal CA1 principal cells, acquired the spatial reference memory w

36 While the differences between principal cells across layers have been extensively stud

37 se spatiotemporal coordination of excitatory principal cell activity by a relatively small population

38 lain how GABAergic neurotransmission sculpts principal cell activity in a relevant fashion.

39 -existing neuronal circuitry, or the role of principal cell activity in these processes.

40 Principal cell activity induces directional growth of sp

41 tuned feedforward sensory input to modulate principal cell activity selectively.

42 highlight a critical period during which the principal cells' activity influences filopodia formation

43 Cadherins, the principal cell adhesion molecules in animal tissues, com

44 tically labeled adult kidney collecting duct principal cells after Hes1 inactivation or lithium treat

45 ing limb, late distal convoluted tubule, and principal cells all adopt a gene expression signature co

46 In the hippocampus, principal cells also establish electrical synapses with

47 Remarkably, 30%-40% of the PCNA-positive principal cells also expressed pHistone-H3, a late G2/M

48 h a common excitatory source drives both the principal cell and an interneuron, is a typical mechanis

49 hippocampus, at excitatory synapses between principal cell and oriens/alveus (O/A) interneurons, a p

50 that these mice had approximately 20% fewer principal cells and 13%-16% more intercalated cells than

51 oupled with a complete blockade of firing in principal cells and burst discharges in putative interne

52 SOM cells inhibit both principal cells and fast-spiking interneurons, indicatin

53 eurons control the activity of glutamatergic principal cells and GABAergic interneurons.

54 nephron is composed of two main cell types: principal cells and intercalated cells.

55 dles than theta; (2) the spiking of putative principal cells and interneurons in the CA1, CA3, and de

56 lationship with the translation machinery in principal cells and interneurons of the adult rat hippoc

57 les neurexin-1,2,3 are commonly expressed in principal cells and interneurons of the mouse hippocampu

58 These findings demonstrate that hippocampal principal cells and interneurons produce endocannabinoid

59 lular and intracellular recordings from both principal cells and interneurons were performed in the m

60 LTP and LTD of parallel fiber inputs to DCN principal cells and interneurons, respectively, broaden

61 tructural changes in GABAergic inhibition of principal cells and long-term plasticity of glutamateric

62 Mean activity of both putative principal cells and parvalbumin-positive interneurons (P

63 pical membrane expression in collecting duct principal cells and reduced urine volume by 45% after 5

64 ce between AnkG function in interneurons and principal cells and resultant excessive circuit sensitiv

65 st-evoked EPSPs were cell-type dependent: in principal cells and somatostatin-containing (SOM), but n

66 al circuitry, such as inhibitory synapses on principal cells and the synapses recruiting interneurons

67 ted thalamic and cortical neurons, including principal cells and two subtypes of inhibitory interneur

68 AQP2 and pAQP2 in the renal inner medullary principal cells appeared more dispersed, and the intensi

69 erns of responses in piriform cortex layer 2 principal cells: Approximately 15% of cells are excited

70 t subthreshold synaptic events from a single principal cell are sufficient to drive spikes in coupled

71 fiber inputs from the dentate gyrus onto CA3 principal cells are affected in an AD mouse model before

72 Morphological evidence suggests that CN principal cells are also contacted by inhibitory interne

73 g rates observed in aged perirhinal cortical principal cells are associated with weaker interneuron a

74 Basolateral amygdala (BLA) principal cells are capable of driving and antagonizing

75 take and aldosterone levels, collecting duct principal cells are exposed to large variations in Na(+)

76 Aergic inputs to specific spatial domains of principal cells are known to play key roles in network o

77 At a microcircuit level, these glutamatergic principal cells are reciprocally connected to GABAergic

78 omical, molecular and functional properties, principal cells are usually assumed to constitute homoge

79 modulin-dependent protein kinase II-positive principal cells as well as of parvalbumin- or somatostat

80 tive neuronal network model, randomly driven principal cell assemblies are strongly synchronized by t

81 ergic interneurons to bind and entrain large principal cell assemblies for network synchronization an

82 interneurons, strengthening and stabilising principal cell assemblies.

83 utative interneurons were discriminated from principal cells based on the autocorrelogram, waveform p

84 mpens excitability markedly in wild-type BLA principal cells but fails to do so in alpha3KO BLA cells

85 da epididymidis showed expression of CFTR in principal cells but not in other epithelial cells.

86 f mTORC1 is well characterized in excitatory principal cells but remains largely unaddressed in inhib

87 m treatment initiates proliferation of renal principal cells but that a significant percentage of the

88 receptors for GABA have been well studied in principal cells, but INs also express GABA receptors, in

89 DA-mediated synaptic currents, evoked in CA1 principal cells by Schaffer collateral stimulation, were

90 Such subpopulations of principal cells can have different local connection prop

91 ven within a single layer, subpopulations of principal cells can often be differentiated by their dis

92 o interneuron subtypes and, even more so, of principal cells can reliably shorten or abolish seizures

93 aR is almost exclusively expressed in tubule principal cells; cell-specific targeted capaR RNAi signi

94 ecovered key epithelial cell types including principal cells, clear cells, and basal cells, along wit

95 Moreover, principal cells coherent to each rhythm differentially r

96 It is unclear whether downstream activity in principal cells controls the excitability of such inhibi

97 Principal cell-derived glutamate and BDNF regulate SHF m

98 Ectopic calbindin-expressing principal cells develop relatively normal morphological

99 e how synaptic input and output of these two principal cells develop.

100 find that parvalbumin (PV) interneurons and principal cells differentially express ANK3 first exon s

101 ory processing by reducing the similarity of principal cells discharge in response to the same incomi

102 In contrast to the canonical view that principal cell discharges dominate ictal events, the ict

103 D EPSPs more reliably encode the duration of principal cell discharges than DD EPSPs, enabling GCs to

104 atures of an animal's physiological state to principal cell entrainment through the inhibitory networ

105 absorption in the CCD and indirectly reduces principal cell epithelial sodium channel abundance and f

106 e first time, between selective increases in principal cell excitability and declines in a molecularl

107 Cultured principal cells exhibited an HIF1alpha-dependent increas

108 Interneurons and principal cells exhibited unique engagement in each of t

109 forms containing exon 1b, whereas excitatory principal cells express exon 1e alone or both 1e and 1b.

110 While all BLA principal cells expressed a robust GABAergic tonic curre

111 in SIVE lesions, with macrophages being the principal cell expressing NK1-R.

112 ures of NDI and an increase in the number of principal cells expressing PCNA in the papilla.

113 kidney development for nephron formation and principal cell fate selection within the collecting duct

114 n types of the amygdala cooperate to control principal cell firing during fear-related and other beha

115 ory synaptic actions, GCs appear to modulate principal cell firing to enhance olfactory discriminatio

116 ny, exerting fast and powerful inhibition on principal cell firing, whereas the inhibitory effect of

117 sulin receptors expressed in collecting duct principal cells for ENaC activity.

118 as a significant source of inhibition to CN principal cells, forming contacts molecularly distinct f

119 ritic synaptic properties prevent individual principal cells from strongly depolarizing granule cells

120 nd the receptor's effect on intercalated and principal cell function in the cortical collecting duct

121 indles and theta; (4) individual hippocampal principal cells generally do not fire in a rhythmic mann

122 shold glutamatergic synaptic potentials in a principal cell generate an excitatory-->inhibitory synap

123 res induced by the optogenetic activation of principal cells had a hypersynchronous onset pattern wit

124 in vivo during natural behavior, relates to principal cell heterogeneity.

125 Our data indicate that in addition to principal cells, ICs are also critical in maintaining so

126 -mediated GABA/glutamate cotransmission onto principal cells in adult mice using paired recording and

127 Principal cells in all layers of MEC show signs of direc

128 stribution of AQP2 to the apical membrane of principal cells in cortical collecting ducts and connect

129 cancer subtype that is thought to arise from principal cells in distal parts of the collecting ducts.

130 Principal cells in layer V of the medial entorhinal cort

131 indicated that POR projections target mainly principal cells in MEC, including neurons that project t

132 l cell lines and in cortical collecting duct principal cells in mouse kidney tissue.

133 define a unique population of glutamatergic principal cells in mouse PFC that largely lack expressio

134 in O-GlcNAc dampens GABAergic currents onto principal cells in rodent hippocampus likely through a p

135 volved in the regulation of ATP release from principal cells in the cauda epididymidis.

136 ar-best-frequency feed-forward inhibition to principal cells in the DCN and various cells in the ante

137 ched the highest firing probability phase of principal cells in the DG and CA3.

138 KA catalytic subunit Calpha into CA1 and CA3 principal cells in the hippocampus of Prnp(0/0) mice cau

139 Fate tracing revealed mature principal cells in the inner stripe of the outer medulla

140 In principal cells in the kidney, TWIK1 gene inactivation l

141 lmodulin-dependent, protein kinase-positive, principal cells in the mouse entorhinal cortex in the in

142 glion cells that provide input to individual principal cells in the mouse lateral geniculate nucleus

143 ning whole-cell recording from identified L6 principal cells in the mouse primary visual cortex (V1)

144 Principal cells in the olfactory bulb (OB), mitral and t

145 identify a second synaptic pathway by which principal cells in the rat (both sexes) OB excite GCs by

146 Here, we show in gerbil MSO principal cells in vitro that feedforward inhibition pre

147 cifications at the level of the postsynaptic principal cell, including input-specific differences in

148 DIalpha in cultured cortical collecting duct principal cells increased ENaC subunits expression and E

149 ased plasma membrane localization of AQP2 in principal cells independent of AVP.

150 ed levels of GATAe gene expression in tubule principal cells induce uncontrolled cell proliferation,

151 teral stimulation with depolarization of CA1 principal cells induced LTP, known to be PKA dependent.

152 4(+) T cells rather than macrophages are the principal cells infected by human immunodeficiency virus

153 in mouse dorsal cochlear nucleus (DCN) where principal cells integrate primary, auditory nerve input

154 Principal cells interact with granule cells through reci

155 nterneurons such as granule cells can affect principal cells is a critical step toward understanding

156 interneurons to target calbindin-expressing principal cells is diminished.

157 -2 channels in the luminal membrane of renal principal cells is essential for urine concentration.

158 nature of the granule cell synapses with the principal cells is essential.

159 lease was detected from the mouse epididymal principal cell line (DC2) and increased by adrenaline an

160 es in two different cortical collecting duct principal cell lines and in cortical collecting duct pri

161 These findings provide evidence that DG principal cells may contribute to early AD hippocampal n

162 epithelial sodium channel activity, despite principal cell mineralocorticoid receptor expression in

163 e physiology of this structure's constituent principal cells mirrors the complexity of its anatomy.

164 The olfactory bulb contains excitatory principal cells (mitral and tufted cells) that project t

165 reponderant involvement of interneuronal and principal cell networks, respectively.

166 acks laminar or columnar organization of its principal cells; nevertheless, functional data suggest t

167 of the MEC, but in only 1.5% of nonstellate principal cells (NSPCs) and in no stellate cells.

168 itory interneurons that feedback on the same principal cells, occurs ubiquitously in the brain.

169 evealed increased basolateral Na-K-ATPase in principal cells of all potassium-adapted mice, but expre

170 P at synaptic and extrasynaptic receptors in principal cells of four different brain regions by slice

171 DHHC 3 was expressed in aquaporin 2-positive principal cells of mouse aldosterone-sensitive distal ne

172 n spine density and size was detected in CA1 principal cells of Pin1(-/-) or in Thy-1GFP mice treated

173 Whole-cell recordings from principal cells of rat cortical collecting ducts reveale

174 was confirmed in patch clamp experiments of principal cells of split open collecting ducts, where EN

175 control of Na(+), K(+), and water balance by principal cells of the collecting duct and the regulatio

176 on of aquaporin 2 (Aqp2), which localizes to principal cells of the collecting duct, we developed mic

177 adenylyl cyclase type VI specifically in the principal cells of the collecting duct.

178 Increased renin formation by principal cells of the collecting ducts forms Ang I from

179 the aquaporin-2 water channel present in the principal cells of the collecting ducts of the kidneys t

180 in descending limb of the loop of Henle, and principal cells of the collecting system.

181 t, whereas BK channel abundance increased in principal cells of the connecting tubule/collecting duct

182 selective activation characteristics of the principal cells of the DG, dentate granule cells (DGCs).

183 s intermediaries in aldosterone signaling in principal cells of the distal kidney nephron.

184 ved PON-2 expression in aquaporin 2-positive principal cells of the distal nephron of adult human kid

185 The pattern of action potential output from principal cells of the mammalian hippocampus encodes spa

186 ld nerve terminal activates CP-AMPARs in the principal cells of the medial nucleus of the trapezoid b

187 Principal cells of the medial superior olive (MSO) in th

188 s in the posteroventral cochlear nucleus and principal cells of the medial superior olive (MSO), extr

189 In the principal cells of the renal collecting duct, arginine v

190 d made local inhibitory synaptic contacts on principal cells of the VCN.

191 Notably, RSCs do not replenish principal cells or stellate cells in the upper tubules.

192 Either optogenetic inhibition of excitatory principal cells, or activation of a subpopulation of GAB

193 ory parvalbumin (PV) cells strongly regulate principal cell output and plasticity and modulate experi

194 t to play a unique role in the modulation of principal cell output.

195 In layer 2/3 principal cells, outputs from IB cells associated with I

196 etwork gamma (PING) type, with the firing of principal cells paced by recurrent perisomal IPSCs.

197 nsferase Dot1l, which is highly expressed in principal cells, participates in this process.

198 Hippocampal principal cell (PC) assemblies provide the brain with a

199 sion in the timing, extent, and synchrony of principal cell (PC) firing that is largely enforced by p

200 II output synapses is hyperpolarizing in CA1 principal cells (PCs) but depolarizing in dentate gyrus

201 While co-activation of excitatory principal cells (PCs) during ongoing activity has been e

202 n in the percentage of aquaporin 2 (Aqp2)(+) principal cells (PCs) in the collecting ducts that was a

203 With principal cells (PCs) they form complex networks.

204 RSCs respond only to loss of nearby principal cells (PCs), cells critical for maintaining io

205 the apical (luminal)/subapical region of the principal cells (PCs), the dominant cell type, with more

206 nnervate the axon initial segments (AISs) of principal cells (PCs), where the action potentials are g

207 rcalated cells (PP-ICs) and ENaC subunits in principal cells (PCs).

208 uct consists of intercalated cells (ICs) and principal cells (PCs).

209 We found that layer2 is composed of two principal cell populations (calbindin-positive and calbi

210 uminate extensive regional specialization of principal cell populations across the length of the epid

211 lance between GABAergic interneurons and the principal cell populations in distinct regions of the te

212 inhibitory circuits regulate the activity of principal cells precisely to drive olfactory-guided beha

213 These changes streamline flow across the principal cells, producing gradients more favorable for

214 Here, we studied how lithium-induced principal cell proliferation can lead to a reduced ratio

215 ipal/intercalated cells, yet lithium induces principal cell proliferation.

216 response to spiking in large populations of principal cells rather than a small group of highly acti

217 ollowed the patterns observed in neocortical principal cells rather than the hippocampal principal ce

218 OB principal cells receive their primary excitatory input f

219 ory or inhibitory synaptic potentiation onto principal cells, respectively.

220 ze in the control of the input and output of principal cells, respectively.

221 Thus, our results indicate that principal cells respond to acid by producing SDF1, which

222 Knockdown of cortactin in mpkCCD(c14) principal cells results in an increase in ENaC activity

223 Thus, the interaction between a principal cell's synaptic and voltage-gated channels may

224 bust GABAergic tonic current, only 70% of LA principal cells showed a tonic current.

225 Principal cells showed layer-specific unique membrane pr

226 In vitro single-cell recordings from principal cells showed only excitatory responses upon PO

227 iscrimination via transient disinhibition of principal cells.SIGNIFICANCE STATEMENT For the encoding

228 nd increased spontaneous IPSCs recorded from principal cells significantly more than spontaneous EPSC

229 Basket cells, whose axon terminals surround principal cell somata and proximal dendrites, have a pri

230 e strong and reliable synaptic inhibition at principal cell somata.

231 Principal cell-specific neurexin splice isoforms depend

232 by the PIIs, leading to higher precision in principal cell spike times than in a network with unifor

233 0 Hz, interregional phase-synchronization of principal cell spikes occurred mostly for LFPs in the ax

234 this period of silence was longer following principal cell stimulation compared with parvalbumin- or

235 reduced the occurrence of ictal discharges, principal cell stimulation resulted in a more prolonged

236 principal cells rather than the hippocampal principal cells, suggestive of long-range interactions.

237 h interactions between the Fc region and two principal cell surface receptors FcepsilonRI and CD23.

238 acilitated association of toxin bound to its principal cell-surface receptor, CMG2, with higher-order

239 ng them distinct from AMPA receptors at most principal cell synapses.

240 tively innervated distinct subpopulations of principal cells, targeting only those with particular lo

241 ces in long-range projection patterns of the principal cell targets, also enhance the distinct networ

242 enhancing the reliability of inhibition onto principal cell targets.

243 h layer is populated by distinct subtypes of principal cells that are born at different times during

244 e potential hyperpolarization in hippocampal principal cells that is independent of CB1Rs.

245 eads to a reduced maximal firing rate of DCN principal cells that is overcome when additional multise

246 rs through aquaporin-2 (AQP2) water pores in principal cells that line the kidney-collecting duct.

247 ic inhibitory control specifically of bulbar principal cells that respond to that odor.

248 Its principal cell, the granule cell, has spatially selectiv

249 ferents do trigger feedforward inhibition in principal cells, the present study aimed to determine wh

250 In CA1 principal cells, this subunit occupies mostly extrasynap

251 We find that odor-tuned SOM cells regulate principal cells through a purely subtractive operation t

252 ic, biasing electrical transmission from the principal cell to the interneuron.

253 How interneurons interact with principal cells to affect bulbar processing is not known

254 m can trigger transdifferentiation of mature principal cells to intercalated cells in adult kidneys.

255 whether loss of Notch signaling can trigger principal cells to lose their identity, we genetically i

256 ateral exit via Na,K-ATPase, which may allow principal cells to maintain intracellular Na(+) concentr

257 may differ significantly from those found on principal cells to open the prospect of developing IN-sp

258 not advanced age affects the ability of PRC principal cells to support these dual roles, however, is

259 By increasing excitation of principal cells together with SOM-mediated, distally dir

260 In addition, we found that human principal cells tracked fine temporal features, conveyed

261 l diversity, or whether its loss can trigger principal cell transdifferentiation (which could explain

262 We conclude that restoring appropriate principal cell tuning via circuit-based therapies, irres

263 While basophils are the principal cell type in the blood that is activated by Ig

264 dentate gyrus constitute a major excitatory principal cell type in the mammalian hippocampus; howeve

265 Goblet cells are the principal cell type involved in exocytosis of mucin gran

266 We show that the principal cell type mediating chimeric partner eliminati

267 is study, we report that basal cells are the principal cell type producing RNase 7 in cultured primar

268 progenitor cells (pOPCs) are considered the principal cell type responsible for oligodendrogenesis a

269 ogical conditions in dopaminergic neurons, a principal cell type that degenerates in Parkinson diseas

270 Here we show that the other principal cell type, intrinsic interneurons, has a multi

271 is known about the development of the other principal cell type, intrinsic interneurons.

272 Upon foraging initiation, most principal cells (Type-1) reduced their firing rate, whil

273 ray analyses of miRNA expression in the four principal cell types of the CNS (neurons, astrocytes, ol

274 The seven principal cell types of the neural retina derive from a

275 ogically and electrophysiologically distinct principal cell types that carry hippocampal output.

276 Taste buds consist of at least three principal cell types that have different functions in pr

277 onstration of distinct contributions made by principal cell types to memory-guided perceptual decisio

278 We determined the contribution of the two principal cell types to these processes by classifying n

279 rectly enhances the excitability of fusiform principal cells via activation of two distinct 5-HT rece

280 rconnections to suppress plasticity in other principal cells via the recruitment of inhibitory intern

281 ddition to region-specific specialization of principal cells, we find evidence for functionally speci

282 ry synaptic potentials (IPSPs) recorded from principal cells were more rhythmic and coherent, and sig

283 EC2 principal cells were most strongly phase modulated by EC

284 that 90% of seizure-like events recorded in principal cells were preceded by outward currents couple

285 heir duration and amplitude were higher when principal cells were targeted.

286 s of the adult rat hippocampus consisting of principal cells where the nodes are glutamatergic synaps

287 us of adult rats of either sex consisting of principal cells where the nodes are interregional glutam

288 c cation transport is known to reside in the principal cells, whereas stellate cells control the anio

289 mutation at thalamic projections contacting principal cells, whereas the same afferents on interneur

290 d C terminals contacted CAMKIIalpha-positive principal cells, whereas type B synapses contacted presu

291 etory cell types: active cation-transporting principal cells, wherein the aquaglyceroporins localize

292 We identify calbindin-expressing principal cells which are mispositioned under cellular h

293 eads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing

294 ortical collecting duct (CCD) is composed of principal cells, which mediate Na, K, and water transpor

295 rization of PVINs and synaptic inhibition of principal cells, which provide the major output of the B

296 ric analysis found elevated renin content in principal cells, which was prevented by Aliskiren.

297 hniques, we have distinguished two groups of principal cells, which we have termed type 1 and type 2.

298 using intracellular recordings from pairs of principal cells with different intersomatic spacing.

299 ivity between olfactory receptor neurons and principal cells within the olfactory bulb is not well un

300 ic currents are significantly reduced in BLA principal cells yet not in LA principal cells.