ライフサイエンスコーパス: pyramidal cell

1 g endosomes to transport Akt1 in hippocampal pyramidal cells.

2 a synchrony code at long time scales for CA3 pyramidal cells.

3 impairment in feedforward inhibition in CA3 pyramidal cells.

4 of LTP at Schaffer collateral synapses onto pyramidal cells.

5 ease inhibitory postsynaptic currents on CA1 pyramidal cells.

6 d hilar mossy cells, and is amplified in CA3 pyramidal cells.

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

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

9 nels are significantly higher in ventral CA1 pyramidal cells.

10 etection window for excitatory inputs to CA1 pyramidal cells.

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

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

13 tributes to persistent firing in neocortical pyramidal cells.

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

15 put patterns in perisomatic dendrites of CA1 pyramidal cells.

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

17 tic integration along the dendritic arbor of pyramidal cells.

18 ation and maintenance of axonal terminals on pyramidal cells.

19 ailable knowledge regarding the structure of pyramidal cells.

20 A1 interneurons but caused depolarization in pyramidal cells.

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

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

23 tatin interneurons, which themselves inhibit pyramidal cells.

24 reconstructions of Lucifer yellow-filled CA1 pyramidal cells.

25 er attentional rate modulation than putative pyramidal cells.

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

27 rization required for associative LTP in CA3 pyramidal cells.

28 aired mitochondrial function in both PVI and pyramidal cells.

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

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

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

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

33 pulations and the resulting disinhibition of pyramidal cells.

34 synaptic plasticity between interneurons and pyramidal cells.

35 firing rate changes of interneurons but not pyramidal cells.

36 ptic ratio is thus specific for the types of pyramidal cells.

37 imate the membrane potential perturbation in pyramidal cells.

38 distinctive subcellular localization within pyramidal cells.

39 ven as they flip from exciting to inhibiting pyramidal cells.

40 ld larger for L2 than L3 and L5 thick-tufted pyramidal cells.

41 tic responses and somatic spike rates within pyramidal cells.

42 in interneurons and GluN1/2A/2B receptors in pyramidal cells.

43 eurons, which target the distal dendrites of pyramidal cells.

44 CD may lead to paradoxical depolarization of pyramidal cells.

45 ng pericellular baskets contacting somata of pyramidal cells.

46 frequency-tuned activity of layer 2/3 (L2/3) pyramidal cells.

47 suggesting delayed functional-maturation of pyramidal-cells.

48 Patch-clamp recordings of ventral CA1 pyramidal cells 24 h after a single systemic administrat

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

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

51 In hippocampal pyramidal cells, a small subset of dendritic spines cont

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

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

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

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

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

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

58 ng interneurons mediate distinct features of pyramidal cell activity(4-6), the SCG2-dependent reorgan

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

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

61 havior in rats by optogenetically inhibiting pyramidal cell and interneuron subpopulations.

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

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

64 exerted a GABA-A mediated inhibition of host pyramidal cells and blocked gabapentin preference (i.e.

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

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

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

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

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

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

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

72 all membrane time constants observed in both pyramidal cells and interneuron cell bodies, the low-fre

73 Pyramidal cells and interneurons expressing parvalbumin

74 llular recordings of somatosensory layer 2/3 pyramidal cells and interneurons in awake male and femal

75 ion strength from layer 2/3 cells to layer 5 pyramidal cells and interneurons was stronger during wak

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

77 act on intrinsic membrane properties in both pyramidal cells and interneurons.

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

79 late phase of spike-frequency adaptation in pyramidal cells and is recruited later than both SK and

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

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

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

83 ium to characterize the activity profiles of pyramidal cells and parvalbumin- and somatostatin-expres

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

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

86 H and EM to reconstruct hundreds of cortical pyramidal cells and show that more superficial cells rec

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

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

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

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

91 tive/nitrosative stress of prefrontal cortex pyramidal cells, and ultimately improved the behavior of

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

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

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

95 levels in murine cortex, and increases both pyramidal cell arborization and PSD-95 expression in the

96 Reduced pyramidal cell arborization occurs with stress and MDD,

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

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

99 onal assemblies composed of interneurons and pyramidal cells are prominent in the somatosensory corte

100 ver, many neuronal classes, such as cortical pyramidal cells, are electrically extended objects.

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

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

103 be connectomic principles for the control of pyramidal cells at their apical dendrites and support di

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

105 Intriguingly, CA3 pyramidal cell backprojections that specifically target

106 is well described in principal glutamatergic pyramidal cells but poorly understood in GABAergic inhib

107 The mPFC contains multiple types of pyramidal cells, but it is unclear whether a particular

108 inal cortex layer 2, putative CA1-projecting pyramidal cells, but not putative dentate gyrus/CA3-proj

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

110 mes in primary cultures of mouse hippocampal pyramidal cells by live-cell imaging and showed that the

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

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

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

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

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 erage the precise targeting of chandelier-to-pyramidal cell connectivity to understand how homeostati

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

119 is prediction, hippocampal gamma rhythms and pyramidal cell coupling to theta phase are significantly

120 Their inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumi

121 We imaged calcium signals in pyramidal cell dendrites in the motor cortex of mice per

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

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

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

125 a-aminobutyric acid interneurons that target pyramidal cell dendrites, has been reported in several b

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

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

128 In addition, we identified changes in pyramidal cell dendritic spines and axon initial segment

129 gamma power is increased with pyramidal cell disinhibition and with remission from MDD

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

131 Hippocampal pyramidal cells encode memory engrams, which guide adapt

132 M rapidly activated biophysically unique PFC pyramidal cell ensembles.

133 ion of GABA release and synaptic inputs onto pyramidal cells erode the emergence of functional topogr

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

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

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

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

138 These pyramidal cells express specialized nicotinic acetylchol

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

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

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

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

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

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

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

146 whether and how burst propensity relates to pyramidal cell heterogeneity.

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

148 in forebrain GABAergic synapses resulting in pyramidal cell hyperexcitability and disruptions in netw

149 nappreciated role for MRs in controlling CA2 pyramidal cell identity and in facilitating CA2-dependen

150 r identified multiple classes of isocortical pyramidal cell in a pattern matching their known organiz

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

152 nses of granule cells, mossy cells, and pCA3 pyramidal cells in a local/global cue mismatch task.

153 innervation of apical dendrites of cortical pyramidal cells in a region between layers (L) 1 and 2 u

154 excitability and are mislocalized within CA1 pyramidal cells in a rodent model of TLE.

155 We recorded from CA3 pyramidal cells in a slice preparation from 6-month-old

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

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

158 onal properties of L2, L3 and subtypes of L5 pyramidal cells in cortex.

159 Pyramidal cells in cortical Layers 5 and 6 are the only

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

161 ing electrophysiological recordings from CA1 pyramidal cells in freely moving mice, we report that a

162 was used to examine the role of neocortical pyramidal cells in generating spasms.

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

164 We recorded EPSCs from CA1 pyramidal cells in hippocampal slices from adult rats an

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

166 input by inhibiting the apical dendrites of pyramidal cells in layers 2/3 and 5, but it is unknown w

167 hat was tested on basolateral amygdala (BLa) pyramidal cells in mouse brain slices.

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

169 iGluSnFR variants in vitro, transfection of pyramidal cells in organotypic hippocampal cultures, and

170 e derived from dual whole-cell recordings of pyramidal cells in organotypic hippocampal slice culture

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

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

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

174 NKA transport activity in single hippocampal pyramidal cells in situ We have found that neuronal NKA

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

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

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

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

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 ns and found that activating Drd1 expressing pyramidal cells in the mPFC produces rapid and long-last

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

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

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

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

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

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

189 A-evoked) firing rate of rat CA1 hippocampal pyramidal cells, in vivo.

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

191 GABA, excess PNN deposition likely increases pyramidal cell inhibition.

192 easuring spike transmission probabilities in pyramidal cell-interneuron spike cross-correlations that

193 grouping of similarly tuned interneurons and pyramidal cells into cliques may ensure that ensembles o

194 By genetically converting superficial IT pyramidal cells into PT-like deep-layer pyramidal cells,

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

196 dendrites, soma, or axon initial segment of pyramidal cells is determined by synaptic molecules that

197 Moreover, mEPSC frequency in mutant CA1 pyramidal cells is elevated, consistent with a higher de

198 tic inhibition onto dendrites of hippocampal pyramidal cells is increased.

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

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

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

202 ppocampal neuropil layers and weakly stained pyramidal cell layers.

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

204 utamatergic input to mouse prefrontal cortex pyramidal cells, leading to antidepressant-relevant acti

205 ults indicate that progenitor cells generate pyramidal cell lineages with a wide range of sizes and l

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

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

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

209 The pyramidal cell model explicitly incorporated the cotrans

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

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

212 ctional synaptic connections before emerging pyramidal cell networks.

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

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

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

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

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

218 n to reduce spine density in hippocampal CA1 pyramidal cells of rodents, and this reduction is revers

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

220 ngth and the lack of dendritic spines in the pyramidal cells of the prefrontal cortex (PFC) are preva

221 We found that, in pyramidal cells of visual and prefrontal cortices and hi

222 und that increases in the activity of either pyramidal cells or individual ChCs during this temporal

223 Our models explain how the activation of pyramidal cells or PV(+) cells can trigger SWRs, as show

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

225 a type of GABAergic interneuron that control pyramidal cell output through axo-axonic synapses that t

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

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

228 These interneuron-pyramidal cell partnerships may represent a fundamental

229 Here, we show how the interactions between pyramidal cells, parvalbumin-positive (PV(+)) basket cel

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

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

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

233 crossed with mouse lines labeling excitatory pyramidal cells (PCs) and inhibitory PV cells.

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

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

236 , it contains the distal "tuft" dendrites of pyramidal cells (PCs) located in deeper layers.

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

238 kes initiated in the distal trunk of layer 5 pyramidal cells (PCs) underlie nonlinear dynamic changes

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

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

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

242 ion, brain estrogen content, and hippocampal pyramidal cell physiology.

243 ng and related reorganization of hippocampal pyramidal cell population dynamics.

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

245 Among putative pyramidal cells, preferred phase tiles phase space, but

246 distal dendritic regions respectively of CA1 pyramidal cells, PV-iLTD and SST-iLTP coordinate a repri

247 ng cortical microcircuits, namely excitatory pyramidal cells (PYCs) and inhibitory gamma-aminobutyric

248 Hippocampal pyramidal cells (PYRs) of the mammalian brain provide mn

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

250 ensure that ensembles of functionally alike pyramidal cells recruited during perceptual tasks and sp

251 FICANCE STATEMENT A minimal model of layer 5 pyramidal cells replicates all known features crucial fo

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

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

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

255 Only L3 pyramidal cells showed homogeneous inhibitory input frac

256 iggers as well as converging effects on Drd1-pyramidal cell signaling that underlie the antidepressan

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

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

259 echanism linking local neurotrophic support, pyramidal cell structure, dendritic inhibition, and mood

260 Remarkably, acute chemogenetic inhibition of pyramidal cells successfully corrected memory deficits a

261 Chemogenetic activation of neocortical pyramidal cells supported these observations, as it incr

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

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

264 HT(4)R acutely in the mPFC or targeting mPFC pyramidal cell terminals in the DRN might constitute a s

265 nput was at least about 2-fold larger for L5 pyramidal cells than for all others.

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

267 ndrite-targeting interneurons, which inhibit pyramidal cells that are not required for memory formati

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

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

270 Similarly tuned pyramidal cells that preferentially target each other ma

271 dentate gyrus granule cells (DGGCs) and CA1 pyramidal cells, the effects of G(q/11)-coupled muscarin

272 CA3 pyramidal cells, the targets of DGC-derived mossy fibers

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

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

275 l IT pyramidal cells into PT-like deep-layer pyramidal cells, they alter the position, connectivity,

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

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

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

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

280 ce that the classical CA3, CA1 and subiculum pyramidal cell types all exhibit prominent and spatially

281 Rat pyramidal cells typically lack these channels, while the

282 ivation of interneurons suppressed firing of pyramidal cells, unexpectedly the majority of interneuro

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

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

285 ontrast, photostimulation of Drd2 expressing pyramidal cells was ineffective across anxiety-like and

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

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

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

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

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

291 ng primarily the extrasynaptic domain of CA1 pyramidal cells, where it mediates tonic inhibitory cond

292 ection window of direct excitatory inputs to pyramidal cells whereas increasing [GABA] through GABA u

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

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

295 tors in hippocampal interneurons but not CA1 pyramidal cells, which is consistent with the expression

296 s pathological hyperactivity of motor cortex pyramidal cells, while concurrently activating somatosta

297 tential small-world cliques, we searched for pyramidal cells whose calcium events had a consistent te

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

299 ied rabies virus identified these neurons as pyramidal cells with apical dendrites extending into sup

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