ライフサイエンスコーパス: pyramidal cell

1 y different (i.e., faster in interneurons vs pyramidal cells).

2 ents (mEPSCs) in CA1 interneurons but not in pyramidal cells.

3 tatin interneurons, which themselves inhibit pyramidal cells.

4 xert some form of divisive inhibition on the pyramidal cells.

5 reconstructions of Lucifer yellow-filled CA1 pyramidal cells.

6 er attentional rate modulation than putative pyramidal cells.

7 synaptic currents (sIPSCs) recorded from CA1 pyramidal cells.

8 rization required for associative LTP in CA3 pyramidal cells.

9 interneurons, and more than fourfold in CA1 pyramidal cells.

10 ole of NMDA spikes in associative LTP in CA3 pyramidal cells.

11 m clusters on the basal dendrites of layer 5 pyramidal cells.

12 s model on the intrinsic excitability of BLA pyramidal cells.

13 cript expression in these two populations of pyramidal cells.

14 ets belonged to interneurons and the rest to pyramidal cells.

15 e alterations were more prominent in layer 5 pyramidal cells.

16 y downregulated specifically in deep layer 3 pyramidal cells.

17 reaching the threshold for bursting in most pyramidal cells.

18 onnectivity with other interneuron types and pyramidal cells.

19 refore, HD cells are likely to be excitatory pyramidal cells.

20 nels are significantly higher in ventral CA1 pyramidal cells.

21 ess Ptf1a exclusively in developing cortical pyramidal cells.

22 a spectrum of inherent responsiveness across pyramidal cells.

23 bution and branching of neurites in cortical pyramidal cells.

24 ations of the experienced sound by layer 2/3 pyramidal cells.

25 oscillations generated at the apical tuft of pyramidal cells.

26 ong-latency feedforward GABAergic input onto pyramidal cells.

27 aintenance of dendritic spines in excitatory pyramidal cells.

28 ial and organize the phase-locked spiking of pyramidal cells.

29 ered EPSCs both on local interneurons and on pyramidal cells.

30 s indiscriminately contact most neighbouring pyramidal cells.

31 albumin-expressing cells targeting different pyramidal cells.

32 and suppress long-range amygdala-projecting pyramidal cells.

33 mulus in both tsA-201 cells and male rat CA1 pyramidal cells.

34 tributes to persistent firing in neocortical pyramidal cells.

35 n (PV) expressing interneurons and layer 2/3 pyramidal cells.

36 n transfer at synapses, is weaker in ventral pyramidal cells.

37 tic integration along the dendritic arbor of pyramidal cells.

38 e they prolong the duration of slow IPSCs in pyramidal cells.

39 ation and maintenance of axonal terminals on pyramidal cells.

40 ailable knowledge regarding the structure of pyramidal cells.

41 A1 interneurons but caused depolarization in pyramidal cells.

42 equencies in both control and Ndufs4(KO) CA1 pyramidal cells.

43 suggesting delayed functional-maturation of pyramidal-cells.

44 The LTD by single pyramidal cell 40 Hz spike bursts is specific to connect

45 In hippocampal pyramidal cells, a prominent elevation of CaV1 activity

46 We study the dendritic branching angles of pyramidal cells across layers to further shed light on t

47 e existence of patches of calbindin-positive pyramidal cells across these species, arranged periodica

48 e of fast inhibition in layers 2/3-switching pyramidal cell action potential outputs from single, spa

49 at nicotine can differentially influence PFC pyramidal cell activity by nAChR modulation of layer II/

50 duced potentiation of postsynaptic layer 2/3 pyramidal cell activity of male, but not female, mice, t

51 domains of pyramidal cells, thereby shaping pyramidal cell activity patterns.

52 ng O-GlcNAcylation decreases spontaneous CA3 pyramidal cell activity under basal and hyperexcitable c

53 y-dependent as it is disrupted by perturbing pyramidal cell activity.

54 from other DGCs as well as from CA3 and CA1 pyramidal cells after pilocarpine treatment, changes tha

55 a oscillations, implemented onto hippocampal pyramidal cells along their somato-dendritic axis, can b

56 e changes contribute to periodic bursting in pyramidal cells, an essential component in the onset of

57 dual neurons, and multineuronal sequences of pyramidal cell and interneuron spiking, were correlated

58 ncrease in the intrinsic excitability of BLA pyramidal cells and a blunting of the medium component o

59 ng from inhibitory to excitatory in affected pyramidal cells and also increase neuronal excitability.

60 synaptic inputs from SST(+) interneurons to pyramidal cells and corresponding chronic reductions in

61 ate tonic inhibition (TI) in hippocampal CA1 pyramidal cells and etomidate enhances TI, etomidate enh

62 y analysis and intracellular recordings from pyramidal cells and fast-spiking stratum pyramidale inte

63 cise synaptic communication of glutamatergic pyramidal cells and fast-spiking, parvalbumin-positive G

64 Using whole-cell recordings from CA1 pyramidal cells and field recordings in the hippocampal

65 d, as characterized by c-Fos upregulation in pyramidal cells and GABA interneurons coexpressing vasoa

66 g-term potentiation (LTP) in hippocampal CA1 pyramidal cells and hippocampal-dependent cognitive func

67 cells had the anatomical characteristics of pyramidal cells and included most recorded HD cells.

68 stant optogenetic stimulation targeting both pyramidal cells and inhibitory interneurons has recently

69 ed by a complex interplay between excitatory pyramidal cells and inhibitory interneurons.

70 We recorded from pyramidal cells and interneurons expressing parvalbumin

71 Pyramidal cells and interneurons expressing parvalbumin

72 ensity and timing of the spiking activity of pyramidal cells and interneurons was strongly correlated

73 amp and juxtacellular configuration from CA3 pyramidal cells and interneurons.

74 in laser-microdissected DLPFC layer 3 and 5 pyramidal cells and layer 3 parvalbumin interneurons, an

75 in laser-microdissected DLPFC layer 3 and 5 pyramidal cells and layer 3 parvalbumin interneurons, an

76 ing mature dentate granule cells, area CA1-3 pyramidal cells and mossy cells.

77 cell reverse transcriptase-PCR revealed that pyramidal cells and not astrocytes are the main cell typ

78 xperimentally: interconnected populations of pyramidal cells and parvalbumin-positive inhibitory cell

79 ell-attached recordings to separate putative pyramidal cells and putative stellate cells recorded ext

80 itic spines, produced spine loss in cortical pyramidal cells and striatal hyperdopaminergia in mice.

81 the hippocampus in humans and atrophy of CA3 pyramidal cells and suppression of adult neurogenesis in

82 ptations found experimentally in neocortical pyramidal cells and tectal neurons in vitro.

83 strongly tuned head-direction (HD) cells are pyramidal cells and therefore likely to provide an excit

84 lso reduced evoked monosynaptic IPSCs in CA1 pyramidal cells and, in contrast to its effect on SC-CA1

85 s, 2) in vitro recordings of hippocampal CA1 pyramidal cells, and 3) in vivo recordings of neocortica

86 n intricate circuit with granule cells, CA3c pyramidal cells, and local interneurons, but the influen

87 -clamp recordings were obtained from layer V pyramidal cells, and monosynaptic GABA(A) receptor-media

88 xon boutons, dendritic spines of ACx layer 5 pyramidal cells, and putative LA-ACx synaptic pairs afte

89 by postsynaptic AMPAR internalization in PFC pyramidal cells, and we observed a profound impairment i

90 s showed an increase in spine density on CA3 pyramidal cell apical dendrites (stratum radiatum) and a

91 tion of adult neurogenesis led to atrophy of pyramidal cell apical dendrites in dorsal CA3 and to neu

92 Mossy fiber synapses on CA3 pyramidal cells are 'conditional detonators' that reliab

93 CA1 pyramidal cells are even more strongly excited by hCSF.

94 nt multiphoton imaging, we show that layer 6 pyramidal cells are unable to sustain cholinergic excita

95 e of Halorhodopsin to load clusters of mouse pyramidal cells artificially with Cl(-).

96 Our data identify superficial layer 2/3 pyramidal cells as critical for moderation of stress in

97 prostaglandin mediating sensory-evoked NVC, pyramidal cells as their principal source and vasodilato

98 ha4betadelta GABAA receptors (GABARs) on CA1 pyramidal cells, as assessed by electron microscopic (EM

99 ns, thereby contributing to the selection of pyramidal cell assemblies at the theta trough via disinh

100 synaptic connections to and from neighboring pyramidal cells at a much higher rate than those from th

101 n microscopic (EM) reconstruction of rat CA3 pyramidal cell axon terminals revealed approximately 1.7

102 ty or optogenetic stimulation of ventral CA1 pyramidal cell axons, whereas principal neurons are inhi

103 Intriguingly, CA3 pyramidal cell backprojections that specifically target

104 eurons not only to initiate the discharge of pyramidal cells but also to control excitation in the re

105 on of glutamatergic synapses between layer 5 pyramidal cells by combining optogenetics and 2-photon c

106 Its primary output cells, CA1 pyramidal cells (CA1 PCs), vary in genetics, morphology,

107 anonical neuronal population-hippocampal CA1 pyramidal cells (CA1 PCs)-and systematically examined th

108 cular plants contain a conspicuous inverted, pyramidal cell called the apical cell (AC), which is uni

109 ld features of the membrane potential of CA1 pyramidal cells can be explained by inheritance and that

110 In the human neocortex, single excitatory pyramidal cells can elicit very large glutamatergic EPSP

111 deletion of Dag1, encoding dystroglycan, in pyramidal cells caused loss of CCK-positive basket cell

112 identifies four broad spiking (BS) putative pyramidal cell classes and three narrow spiking (NS) put

113 rogeneity within and between the neocortical pyramidal-cell classes in layers 2/3, 4, and the slender

114 tions of model neurons, for each of the four pyramidal-cell classes, that adhere to experimentally ob

115 -term plasticity of excitatory inputs to CA3 pyramidal cells combines with robust feedforward inhibit

116 lecular properties of excitatory synapses on pyramidal cells, comparatively little is known about exc

117 s) at cholecystokinin-expressing interneuron-pyramidal cell connections and imaged presynaptic [Ca(2+

118 t restoration of the chloride homeostasis in pyramidal cells could be a viable antiepileptic strategy

119 been proposed in which phasic currents from pyramidal cells could drive synchronized feedback inhibi

120 e that connectivity between interneurons and pyramidal cell dendrites is more precise and spatially s

121 arly defined inhibitory interneurons and CA1 pyramidal cell dendrites using correlative light-electro

122 (HCN1) channels are predominantly located in pyramidal cell dendrites within the cortex.

123 ts with schizophrenia show evidence of dlPFC pyramidal cell dendritic atrophy, likely reductions in c

124 ion, we show that EE significantly increased pyramidal cell dendritic branching and BDNF protein leve

125 tance and driving forces in neonatal rat CA3 pyramidal cells during GDPs.

126 e observed functional diversity of subicular pyramidal cells during sharp-wave associated ripples.

127 released to distinct dendritic zones of CA1 pyramidal cells during sleep and wakefulness to coordina

128 we measured ongoing activity of neocortical pyramidal cells during various arousal states in the rTg

129 e oligomers were introduced into neocortical pyramidal cells during whole-cell recording and, using a

130 Thus, the action of GABA on CA3 pyramidal cells dynamically changes during GDPs from exc

131 ould provide new insights into the nature of pyramidal cell dysfunction in the illness.

132 When a single cortical pyramidal cell establishes a synapse onto a somatostatin

133 e in NVC, in vivo optogenetic stimulation of pyramidal cells evoked COX-2-dependent hyperemic respons

134 ion, which contributes to an increase in BLA pyramidal cell excitability and highlights BLA SK channe

135 se phenotypes were associated with increased pyramidal cell excitability due to changes in inherent m

136 potential generation, and thus downregulate pyramidal cell excitability.

137 eurons in cortical processing (regulation of pyramidal cell excitatory input) and behavioral control

138 , when mice engage in sound-guided behavior, pyramidal cell excitatory responses to habituated sounds

139 Although dorsal and ventral CA1 pyramidal cells exhibit markedly different gene expressi

140 and endocannabinoid signaling in infralimbic pyramidal cells fails to control abnormal amygdala-drive

141 and first observed that the distribution of pyramidal cell firing rates was wide and strongly skewed

142 and chronic stress promote increases in BLA pyramidal cell firing, and decreasing BLA excitability a

143 of individually microdissected deep layer 3 pyramidal cells from a subset of the same subjects and f

144 cordings from morphologically identified CA3 pyramidal cells from control and complex IV-deficient mi

145 find that the dendritic branching angles of pyramidal cells from layers II-VI of the juvenile rat so

146 -seq reveals that Ptf1a significantly alters pyramidal cell gene expression, upregulating numerous Pt

147 Loss of dystroglycan in pyramidal cells had little influence on clustering of ot

148 enhances TI, etomidate enhancement of TI in pyramidal cells has been proposed as the underlying mech

149 Thus, in rat motor cortex, pyramidal cells have long duration action potentials, wh

150 function in young normal mice, that old CA1 pyramidal cells have reduced excitability and increased

151 ion and kinetics at excitatory synapses onto pyramidal cells; however, little is known about NMDAR ma

152 report that deletion of Wfs1 from layer 2/3 pyramidal cells impairs the ability of the mPFC to suppr

153 es a novel subclass of layer 5 glutamatergic pyramidal cell in mouse PFC (either sex).

154 proximal and distal dendrites of neocortical pyramidal cells in awake behaving mice.

155 tic brain, whereas axons of interneurons and pyramidal cells in CA1 appear to sprout across the hippo

156 we also found that optogenetic inhibition of pyramidal cells in CA1 did not significantly affect the

157 memory depends on the activity of excitatory pyramidal cells in DLPFC layer 3 and, to a lesser extent

158 Individual pyramidal cells in DLPFC layers 3 or 5 were captured by

159 nctional features that are characteristic of pyramidal cells in each cortical layer.

160 tionally segregated inputs onto dendrites of pyramidal cells in hippocampal areas CA3 and CA1.

161 BAergic interneurons providing inhibition to pyramidal cells in layer 2/3 (L2/3) of adult mouse barre

162 Here we discover that pyramidal cells in layer 2/3 of mouse primary visual cor

163 , in part, on neural circuitry that includes pyramidal cells in layer 3 (L3) and layer 5 (L5) of the

164 Intracellular recordings from layer V pyramidal cells in neocortical slices obtained from IL-6

165 age clamp recordings were then made from CA1 pyramidal cells in normal aCSF.

166 between putative inhibitory interneurons and pyramidal cells in PFC and VIP.

167 croscopy revealed more DOR-labeled spines of pyramidal cells in proestrous females than males.

168 We recorded activity from CA1 pyramidal cells in rat pups while they were trained on t

169 PGC-1alpha increases the I/E ratio onto CA1 pyramidal cells in response to Schaffer collateral stimu

170 pine deficits preferentially in deep layer 3 pyramidal cells in schizophrenia.

171 e significantly lower in DLPFC layer 3 and 5 pyramidal cells in schizophrenia.

172 For pyramidal cells in superficial mouse visual cortex (V1),

173 erlying increase in input resistance in deep pyramidal cells in temporal and prefrontal association n

174 c acidergic interneurons, some glutamatergic pyramidal cells in the brain are also surrounded by PNNs

175 ical composition of subnuclear structures of pyramidal cells in the CA2 region in mouse brain hippoca

176 ted genes specific to layer 3 and/or layer 5 pyramidal cells in the DLPFC of schizophrenia subjects.

177 Pools of L3 and L5 pyramidal cells in the DLPFC were individually captured

178 density of dendritic spines on deep layer 3 pyramidal cells in the dorsolateral prefrontal cortex (D

179 Lower dendritic spine density on layer 3 pyramidal cells in the dorsolateral prefrontal cortex (D

180 ng Channelrhodopsin-2 and Archaerhodopsin in pyramidal cells in the hippocampal CA1 region, achieving

181 atch-clamp recordings were made from layer V pyramidal cells in the infralimbic mPFC in rat brain sli

182 wed that (fast-spiking, FS) interneurons and pyramidal cells in the presubiculum can be distinguished

183 m-chloride cotransporter KCC2 in a subset of pyramidal cells in the subiculum, a key structure genera

184 slower in PV interneurons than in excitatory pyramidal cells in visual cortex.

185 holinergic-innervation of calbindin-positive pyramidal-cells in layer-2 emerged around birth while re

186 The tonic excitation of pyramidal cells, in combination with an increased respon

187 GABA-gated currents in DGGCs, but not in CA1 pyramidal cells, in NSW animals.

188 st-spiking CA1 interneurons, as well as from pyramidal cells, in the presence of human cerebrospinal

189 ted the loss of KCC2 in a critical number of pyramidal cells increased external potassium and intrace

190 show here that in the subiculum a subset of pyramidal cells is activated, whereas another subset is

191 subunit of SK-type K(+) channels in ventral pyramidal cells is associated with an enhanced activatio

192 s suggest that ErbB4 signaling in excitatory pyramidal cells is critical for the proper formation and

193 or the first time that NMDAR hypofunction in pyramidal cells is sufficient to cause electrophysiologi

194 profiles exhibited by dorsal and ventral CA1 pyramidal cells is unclear.

195 localized to dendritic shafts and spines of pyramidal cells, is uniquely expressed during cortical n

196 noreactivity (IR) was most noticeable in the pyramidal cell layer and interspersed interneurons, espe

197 d local field potentials from the dorsal CA1 pyramidal cell layer of 7- to 8-month-old wild-type and

198 d local field potentials from the dorsal CA1 pyramidal cell layer of 7-8 month old wild-type and rTg4

199 campus in the granule cell layer, hilus, and pyramidal cell layer of CA3, CA2, and CA1 subfields.

200 calcium imaging of neuronal activity, in the pyramidal cell layer of mouse hippocampal in vitro prepa

201 increased independent of adrenals in the CA1 pyramidal cell layer, dentate gyrus polymorphic layer, b

202 ocated in the superficial portion of the CA1 pyramidal cell layer, whereas it is absent from deep-lay

203 ppocampal neuropil layers and weakly stained pyramidal cell layers.

204 ronal density of large-caliber neurons only (pyramidal cells, layers 3 and 5).

205 rts a tonic enhancement of Ih selectively in pyramidal cells located in the superficial portion of th

206 tyric acid (GABA) interneurons disinhibiting pyramidal cells may be relevant to this hyperglutamaterg

207 hat molecular alterations in DLPFC L3 and L5 pyramidal cells might be characteristic of the disease p

208 The pyramidal cell model explicitly incorporated the cotrans

209 hat input to the apical tufts of neocortical pyramidal cells modulates their response to basal input.

210 s overexpression leads to defective cortical pyramidal cell morphology, synaptic plasticity deficits,

211 the induction of hippocampal LTP and on CA1 pyramidal cell morphology.

212 ctional synaptic connections before emerging pyramidal cell networks.

213 Granule and pyramidal cell neurons within the dentate gyrus and CA1

214 ls and mossy cells of the dentate gyrus, and pyramidal cells of areas CA3, CA2, and CA1.

215 bers (MFs) corelease glutamate and GABA onto pyramidal cells of CA3 during development, until the end

216 ransiently corelease glutamate and GABA onto pyramidal cells of CA3.

217 by reduced frequency of inhibitory events in pyramidal cells of dystroglycan-deficient mice and furth

218 , 4, and the slender-tufted and thick-tufted pyramidal cells of layer 5 using a combination of intrac

219 erated in apical dendritic spines of layer V pyramidal cells of medial prefrontal cortex (mPFC).

220 etabotropic KAR signaling were absent in CA3 pyramidal cells of Neto-null mice.

221 yer V cells receive an excitatory input from pyramidal cells of the basolateral amygdala (BLA), neuro

222 y tonic conductance recorded in layer II/III pyramidal cells of the mouse juvenile (postnatal day 12-

223 cillations, whereas closed-loop silencing of pyramidal cells or activation of parvalbumin- (PV) or so

224 sitive (PV(+)) neurons control the timing of pyramidal cell output in cortical neuron networks.

225 min-positive (PV(+)) neurons tightly control pyramidal cell output.

226 We demonstrate that, at connected layer 5 pyramidal cell pairs of developing mouse visual cortex,

227 , and output selectively targeted to layer 2 pyramidal cell patches of MEC).

228 We explored the presence of CP-AMPARs at pyramidal cell (PC) inputs to Martinotti cells (MCs) and

229 re during these events, but the mechanism of pyramidal cell (PC) participation remains elusive.

230 er 3 (L3) via reciprocal connections between pyramidal cells (PCs) and parvalbumin (PV)-containing in

231 Hippocampal pyramidal cells (PCs) express many GABAAR subunit types

232 streams mediated by subsets of glutamatergic pyramidal cells (PCs) that receive diverse inputs and pr

233 sence of miniature IPSCs in Cre(+) layer 2/3 pyramidal cells (PCs) with unchanged amplitudes and rise

234 excitation and inhibition of CA1 hippocampal pyramidal cells (PCs), cells known to participate in cir

235 larization, which is specific to CA3 and CA2 pyramidal cells (PCs), depends on the activation of neur

236 lar recordings of CA3 neurons in vivo In CA3 pyramidal cells (PCs), mf-CA3 synaptic responses consist

237 to conserve the distribution of stellate and pyramidal cells, periodic arrangement of calbindin patch

238 perisomatic voltage responses of the diverse pyramidal-cell populations when the class-dependent stat

239 ears to encode HD information via excitatory pyramidal cells, possibly also involving FS interneurons

240 on the dynamics and structural integrity of pyramidal cell postsynaptic structures known to guide th

241 parvalbumin-expressing interneurons (PV) and pyramidal cells (PYRs).

242 l layer 4 spiny stellate cells and layer 2/3 pyramidal cells requires the activation of NMDA receptor

243 e or value, whereas distinct hippocampal CA1 pyramidal cells responded differentially to ketamine-ind

244 Tests in CA1 hippocampal pyramidal cells reveal that a slow AHP is reduced by blo

245 Thus, the equalization of E/I ratios across pyramidal cells reveals an unexpected degree of order in

246 Contrary to the stellate cells, pyramidal cells show weaker temporal coding.

247 Putative pyramidal cells showed no repetition-related firing rate

248 In CA1 pyramidal cells, SK channels in dendritic spines were sh

249 the same subjects, suggesting that they are pyramidal cell specific.

250 ocortical complex events, observed as single pyramidal cell spike-evoked discharge of cell assemblies

251 timulus representation by gamma-synchronized pyramidal cell spikes.

252 of activation in CA1 and dramatically limits pyramidal cell spiking, reducing hippocampal output.

253 ry postsynaptic responses in the majority of pyramidal cells, spiny stellate cells, and interneurons

254 assification for dopaminergic neurons or CA1 pyramidal cell subtypes regardless of the brain states f

255 rity of Schaffer collateral to CA1 (Sch-CA1) pyramidal cell synapses following global ischemia is not

256 l established property of mossy fiber to CA3 pyramidal cell synapses is the extensive short-term faci

257 LTP was enhanced at Schaffer collateral-CA1 pyramidal cell synapses.

258 rward inhibition of spike transfer at mf-CA3 pyramidal cell synapses.

259 In turn, pyramidal cell targets of SST(+) neurons showed an incre

260 cortical microcircuit motif: populations of pyramidal cells that are densely interconnected with inh

261 nal models of developing and mature cortical pyramidal cells that express NaV1.2.

262 its enhanced excitatory synaptic strength in pyramidal cells that is induced postsynaptically and dep

263 nt to induce synaptic plasticity between CA3 pyramidal cells, thereby complementing the sparse action

264 tion at the Schaffer collateral input to CA1 pyramidal cells, thereby lowering the threshold to induc

265 rons target different subcellular domains of pyramidal cells, thereby shaping pyramidal cell activity

266 , send functional monosynaptic inputs to CA2 pyramidal cells through abundant longitudinal projection

267 sing interneurons (VIPs) disinhibit cortical pyramidal cells through inhibition of other inhibitory i

268 In pyramidal cells, TNFalpha drives the insertion of AMPA-t

269 modified an existing model of a layer 5 (L5) pyramidal cell to explore how dendritic integration in t

270 times more functional release sites in human pyramidal cell to fast-spiking interneuron connections c

271 responses of two different types of cortical pyramidal cells to patterned stimulation by two-photon g

272 In cortical pyramidal cells, tonic inhibition is regulated by age an

273 In DLPFC L3 and L5 pyramidal cells, transcriptome alterations were numerous

274 when firing in a set of spontaneously active pyramidal cells triggers a gradual, exponential buildup

275 CA1 pyramidal cell-type-specific, genome-wide profiling of r

276 Rat pyramidal cells typically lack these channels, while the

277 rved was not restricted to synapses with CA3 pyramidal cells via large mossy-fibre boutons, but rathe

278 We found pyramidal cell volumes in layers III and V in the dorsol

279 e increased excitability of interneurons and pyramidal cells was accompanied by reductions in after-h

280 ssion was mostly normal, inhibition onto CA1 pyramidal cells was altered in Cntnap2(-/-) mice.

281 A slow afterhyperpolarization in pyramidal cells was reduced by a selective block of CaV1

282 a(N1768D/+) CA1, but not CA3 or neocortical, pyramidal cells was significantly reduced compared with

283 at depolarization of a small group of nearby pyramidal cells was sufficient to induce high-frequency

284 Excitatory/inhibitory GABA actions on pyramidal cells were assessed by monitoring the alterati

285 ences in neuronal properties of the presumed pyramidal cells were found between PrL and DP, with many

286 CA1 pyramidal cells were phase-locked mainly to fast gamma (

287 lls and the inhibitory drive they exerted on pyramidal cells were reduced in conditional mice lacking

288 Spikes with features of interneurons and pyramidal cells were simultaneously acquired by multiple

289 n both species patches of calbindin-positive pyramidal cells were superimposed on scattered stellate

290 intrinsic firing and evoked NMDA currents in pyramidal cells, whereas D2 receptor function was unalte

291 had spines, suggesting that they belonged to pyramidal cells, whereas others had morphological featur

292 e alterations were more prominent in layer 3 pyramidal cells, whereas UPS-related gene alterations we

293 s to synaptic homeostasis in mature cortical pyramidal cells, which perpetuates brain dysfunction int

294 lso indicated a decrease in gain of parietal pyramidal cells, which was correlated with participants'

295 es were preferentially contributed by layer3 pyramidal cells, whose long-range axons branched within

296 le, where basket cells selectively innervate pyramidal cells with GABAergic synapses.

297 e show that HD cells in the presubiculum are pyramidal cells, with FS interneurons only showing weak

298 voltage dynamics in cultured neurons and in pyramidal cells within neocortical tissue slices.

299 pression, specifically in DLPFC layer 3 or 5 pyramidal cells, would reveal new and/or more robust sch

300 ion of intracellular chloride is impaired in pyramidal cells, yet how this dysregulation may lead to