ライフサイエンスコーパス: principal cell

1 selective or concerted inhibitory action on principal cells.

2 e temporal patterns onto distinct domains of principal cells.

3 of polarized murine cortical collecting duct principal cells.

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

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

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

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

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

9 controlled by distinct epochs of activity in principal cells.

10 ion of the postsynaptic currents of cortical principal cells.

11 ential position for regulating the firing of principal cells.

12 ion and depression at excitatory synapses on principal cells.

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

14 loss of functional inhibition of excitatory principal cells.

15 and pharmacological profile as GlyRs on MNTB principal cells.

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

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

18 of Held presynaptic endings that envelop the principal cells.

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

20 ion between VFO power and synaptic inputs to principal cells.

21 the apical surface of either intercalated or principal cells.

22 ed in the apical membrane of collecting duct principal cells.

23 water channel aquaporin-2 in collecting duct principal cells.

24 oned next to intercalated cells than next to principal cells.

25 many different synaptic contacts formed with principal cells.

26 tivity in both mouse and rat collecting duct principal cells.

27 naling underlies Hebbian postsynaptic LTP in principal cells.

28 ce of perisomatic inhibition for hippocampal principal cells.

29 eedback inhibition regulates spike timing in principal cells.

30 interneurons were the dendrites of Layer III principal cells.

31 n the apical membrane of the collecting duct principal cells.

32 dox dysregulation was targeted in excitatory principal cells.

33 rom thousands of granule cells converge onto principal cells.

34 urons with concomitantly decreased firing of principal cells.

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

36 red mCCD and isolated primary distal nephron principal cells.

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

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

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

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

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

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

43 Principal cell activity induces directional growth of sp

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

45 interneurons (even by means of non-rhythmic principal cell activity) is sufficient to generate emerg

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

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

48 Integrins are the principal cell adhesion receptors that mediate leukocyte

49 observed in cell-attached apical patches of principal cells after stimulation by forskolin/3-isobuty

50 this water channel to the apical membrane of principal cells along the collecting ducts.

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

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

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

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

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

56 likely increases synchrony among excitatory principal cells and contributes to the destabilization o

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

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

59 functional categories such as glutamatergic principal cells and inhibitory interneurons.

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

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

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

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

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

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

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

67 s of dentate gyrus granule cells target both principal cells and local circuit inhibitory interneuron

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

69 ed complex spikes, and which synapse on both principal cells and one another.

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

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

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

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

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

75 derived stellate cells intercalating between principal cells, and a paralogue, tiptop, is expressed i

76 ess RhCG and that B-type intercalated cells, principal cells, and inner medullary collecting duct cel

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

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

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

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

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

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

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

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

85 l environments, a constant proportion of CA1 principal cells are place cells, each with a spatial rec

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

87 Here, we show that rat hippocampal CA3 principal cells are significantly more active during SWR

88 uited by sensory stimuli and how they impact principal cells are unclear.

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

90 ately the cell body and dendritic regions of principal cells, are modulated similarly by cholinergic

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

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

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

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

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

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

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

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

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

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

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

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

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

104 Moreover, principal cells coherent to each rhythm differentially r

105 In the distal nephron, principal cells contain BK-alpha/beta1 channels and inte

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

107 Principal cell-derived glutamate and BDNF regulate SHF m

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

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

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

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

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

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

114 Cultured principal cells exhibited an HIF1alpha-dependent increas

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

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

117 ile encoding spatial experience, hippocampal principal cells express IEGs in a behaviorally dependent

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

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

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

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

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

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

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

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

126 ted Cl(-) channels in the apical membrane of principal cells from the cortical collecting duct obtain

127 -) channel activity was completely absent in principal cells from transgenic mice expressing the Delt

128 In principal cells, GABA(A) receptor-mediated synaptic inpu

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

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

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

132 In hippocampal principal cells, I(M) controls action potential (AP) acc

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

134 IGF-I acutely increased P(o) of ENaC in CCD principal cells in a PI3-K-sensitive manner.

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

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

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

138 ABAergic basket cells selectively innervated principal cells in layer II of the rat MEC that projecte

139 Principal cells in layer V of the medial entorhinal cort

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

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

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

143 Our results indicate NK cells are the principal cells in PBMC that kill RTX-opsonized B cells,

144 of hsc70 and AQP2 on the apical membrane of principal cells in rat kidney collecting ducts.

145 lation of AQP2 in rat kidney collecting duct principal cells in situ, and in several kidney epithelia

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

147 trafficking to the apical plasma membrane of principal cells in the collecting duct, and increased AQ

148 through and processing within the network of principal cells in the cortical circuit.

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

150 The locations of firing fields of principal cells in the hippocampal formation were genera

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

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

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

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

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

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

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

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

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

160 4(+) T cells rather than macrophages are the principal cells infected by human immunodeficiency virus

161 Thus, in contrast to principal cells, inhibitory synaptic input onto CA3 inte

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

163 Principal cells interact with granule cells through reci

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

165 -2 channels in the luminal membrane of renal principal cells is essential for urine concentration.

166 alysis revealed that LTP and LTD in layer IV principal cells is lost shortly after the eyes open, but

167 critical for determining the spike output of principal cells, is mediated by two physiologically dist

168 a mediator of epithelial cell proliferation, principal cells isolated from cystic BPK and noncystic B

169 microvascular endothelial cells (BMEC), the principal cell layer composing the blood-brain barrier (

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

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

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

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

174 crease Na(+) reabsorption across mpkCCD(c14) principal cell monolayers in a PI3-K-sensitive manner.

175 NaC abundance and function in cultured mouse principal cells (mpkCCD).

176 ession in immortalized mouse collecting duct principal cells (mpkCCDcl4).

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

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

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

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

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

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

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

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

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

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

187 Using whole-cell patch clamp of principal cells of split-open CD from Na(+)-restricted r

188 Mitral cells, the principal cells of the accessory olfactory bulb (AOB), r

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

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

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

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

193 s in a number of different tissues including principal cells of the collecting ducts in the kidney an

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

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

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

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

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

199 d AQP9 co-localize in the apical membrane of principal cells of the epididymis and the vas deferens,

200 r, rebound spikes are rarely observed in the principal cells of the hippocampus under physiological c

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

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

203 Na(+) channel (ENaC) expressed by epithelial principal cells of the renal collecting duct may be resp

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

205 Medium spiny neurons (MSNs) are the principal cells of the striatum and perform a central ro

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

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

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

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

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

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

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

213 K secretion takes place by K entering principal cells (PC) from blood side through Na+, K+ -AT

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 ynapses onto both excitatory regular-spiking principal cells (RS cells) and inhibitory fast-spiking i

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

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

234 Principal cells showed layer-specific unique membrane pr

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

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

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

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

239 Principal cell-specific neurexin splice isoforms depend

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

241 0 Hz, interregional phase-synchronization of principal cell spikes occurred mostly for LFPs in the ax

242 known to veto and regulate the synchrony of principal cell spiking.

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

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

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

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

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

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

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

250 enhancing the reliability of inhibition onto principal cell targets.

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

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

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

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

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

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

257 tive density of surrounding interneurons and principal cells through their ability to sense the combi

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

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

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

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

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

263 aling and ENaC within the apical membrane of principal cells to the physiologic control of this ion c

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

265 findings demonstrate that in collecting duct principal cells, TonEBP plays a central role in regulati

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

267 Here we identify the oenocyte as the principal cell type accumulating lipid droplets during s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 sensing dye JC-1, the apical mitochondria of principal cells were found to be selectively responsive

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

286 EC2 principal cells were most strongly phase modulated by EC

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

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

289 It can be elicited at many synapses on principal cells, where it depends on Ca(2+) influx throu

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

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

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

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 nal cord respiratory motor neuron pools, the principal cells whose dysfunction precipitates death in

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.