ライフサイエンスコーパス: hyperexcitability

1 and reduced membrane channel density causes hyperexcitability.

2 that IIS are possibly the earliest stage of hyperexcitability.

3 eurologic disorders associated with neuronal hyperexcitability.

4 TNF-alpha and IL-6 induce a state of spinal hyperexcitability.

5 weeks of life and brain slices show neuronal hyperexcitability.

6 rocyte -: neuronal interactions and neuronal hyperexcitability.

7 ceptor, suppresses the M-current and induces hyperexcitability.

8 prevents resultant agonist-induced neuronal hyperexcitability.

9 that results in long-term changes in network hyperexcitability.

10 prevented both Kv4.2 depletion and dendritic hyperexcitability.

11 d anxiety disorders are characterized by BLA hyperexcitability.

12 and glutamate to white matter anomalies and hyperexcitability.

13 uromuscular transmission and skeletal muscle hyperexcitability.

14 sing, particularly in determining peripheral hyperexcitability.

15 neurons, primarily responsible for neuronal hyperexcitability.

16 overactivation of NMDARs and drives neuronal hyperexcitability.

17 and a GluN2C/D antagonist reduces paroxysmal hyperexcitability.

18 ion of tau in mouse and Drosophila models of hyperexcitability.

19 ynaptic transmission, leading to hippocampal hyperexcitability.

20 cornu ammonis 3 (CA3)-CA1 subcircuit toward hyperexcitability.

21 ntervals, thereby contributing to DRG neuron hyperexcitability.

22 o underlie or support development of network hyperexcitability.

23 illary tangle formation and neuronal network hyperexcitability.

24 ls and alleviated multiple signs of neuronal hyperexcitability.

25 eletion may contribute to the development of hyperexcitability.

26 orders associated with tau-mediated neuronal hyperexcitability.

27 w spontaneous bursting and other evidence of hyperexcitability.

28 hite matter heterotopias displaying neuronal hyperexcitability.

29 annels underlying action potentials produces hyperexcitability.

30 f Scn1b may contribute to the development of hyperexcitability.

31 e been implicated in injury-induced neuronal hyperexcitability.

32 nervous system also shows ethanol-withdrawal hyperexcitability.

33 ifference is likely to predispose the VHC to hyperexcitability.

34 erse mode Na/Ca exchange in the mechanism of hyperexcitability.

35 necessary and sufficient to explain cellular hyperexcitability.

36 symptoms were consistent with sensory nerve hyperexcitability.

37 er of diseases associated with smooth muscle hyperexcitability.

38 racortical facilitation, indicating cortical hyperexcitability.

39 xhibits neural circuit hyperconnectivity and hyperexcitability.

40 ng O-GlcNAcylation will depress pathological hyperexcitability.

41 cortical neurons, and resulting in neuronal hyperexcitability.

42 rising and multiple mechanisms contribute to hyperexcitability.

43 itory circuits that results in a generalized hyperexcitability.

44 t link peripheral inflammation with neuronal hyperexcitability.

45 erized by recurrent seizures due to neuronal hyperexcitability.

46 the generation of inflammation-evoked spinal hyperexcitability.

47 rks that bias activity towards and away from hyperexcitability.

48 -existing pathologies associate with circuit hyperexcitability.

49 e cardiac myoycte and parasympathetic neuron hyperexcitability.

50 c lateral sclerosis (ALS) and to neocortical hyperexcitability, a prominent feature of both inherited

51 Slack channel endocytosis, and DRG neuronal hyperexcitability after PKA activation.

52 tors (mGluRs) and NMDA, in 5-HT(2A)R-induced hyperexcitability after spinal nerve ligation (SNL) in r

53 itis characterized by central nervous system hyperexcitability (agitation, myoclonus, tremor, seizure

54 However, it is unknown whether hyperexcitability also occurs in MNs that are resistant

55 finitely autoimmune, 3 with peripheral nerve hyperexcitability and 1 with a thymoma; 3 were given imm

56 uggest both a mechanism for mutation-induced hyperexcitability and a novel role for the beta3 subunit

57 normally be important in area CA3 to prevent hyperexcitability and aberrant axon outgrowth but limit

58 type appears to be the result of hippocampal hyperexcitability and aberrant fear circuit activation.

59 Decreasing tau in Kcna1(-/-) mice reduced hyperexcitability and alleviated seizure-related comorbi

60 amination of the mPFC revealed both neuronal hyperexcitability and alterations in short-term synaptic

61 ant in rare conditions with peripheral nerve hyperexcitability and appeared to associate with tumours

62 /2 muscle may help compensate for the muscle hyperexcitability and contribute to motor impersistence.

63 oligodendrocytes induce WT motor neuron (MN) hyperexcitability and death.

64 duced changes were accompanied by WDR neuron hyperexcitability and decreased pain thresholds at 4 wee

65 PA receptor GluR1 subunit and later neuronal hyperexcitability and epilepsy, suggesting that seizure-

66 P) has been implicated in the development of hyperexcitability and epileptic seizures following traum

67 the neurovascular unit and triggers neuronal hyperexcitability and epileptogenesis.

68 c excitatory input and evoked sensory neuron hyperexcitability and excitatory synaptogenesis, which t

69 ty during AD.SIGNIFICANCE STATEMENT Neuronal hyperexcitability and excitotoxicity are increasingly re

70 all degrees of membrane depolarization cause hyperexcitability and familial episodic pain disorder or

71 o-hippocampal pathway of Fmr1 KO mice causes hyperexcitability and feed-forward circuit defects, whic

72 zed by recurrent spontaneous seizures due to hyperexcitability and hypersynchrony of brain neurons.

73 we propose that SMN reduction results in MN hyperexcitability and impaired neurotransmission, the la

74 ritically evaluates the role of glia-induced hyperexcitability and inflammation in epilepsy.

75 verexpressing amyloid-beta (Abeta) decreases hyperexcitability and normalizes the excitation/inhibiti

76 that the increased contractility was due to hyperexcitability and not disinhibition of the circuitry

77 ysiology may shed light on neuronal membrane hyperexcitability and pathophysiology of myoclonus and r

78 protein kinase A signaling axis in promoting hyperexcitability and persistent firing in pyramidal neu

79 so induced PKC-dependent nociceptive C-fiber hyperexcitability and PKC translocation.

80 ory neurons; its activation induces neuronal hyperexcitability and scratching by unknown mechanisms.

81 ion overrides impaired activation to produce hyperexcitability and spontaneous firing in DRG neurons.

82 ion of A1632T in sensory neurons resulted in hyperexcitability and spontaneous firing of dorsal root

83 depolarizing shift of activation, to produce hyperexcitability and spontaneous firing of nociceptive

84 sector CA1/subiculum is sufficient to induce hyperexcitability and spontaneous recurrent seizures in

85 al that sleep loss exacerbates Abeta-induced hyperexcitability and suggest that defects in specific K

86 ling hypothesis for the generalized neuronal hyperexcitability and the anatomical alterations seen in

87 Hyperexcitability and the imbalance of excitation/inhibi

88 tic, and circuit-level mechanisms underlying hyperexcitability and their contributions to the FXS phe

89 Bladder afferent nerve hyperexcitability and urothelial ATP release with CYP-in

90 otransmission deficit in DLPFC could lead to hyperexcitability and, potentially neuronal dysfunction

91 ologies are individually sufficient to cause hyperexcitability, and because several such pathologies

92 ed glutamatergic neurotransmission, cerebral hyperexcitability, and enhanced susceptibility to cortic

93 neurons results in increased mTOR signaling, hyperexcitability, and neuronal structure deficits.

94 l neurons in the pathogenesis of neocortical hyperexcitability, and perhaps epilepsy, in AS model mic

95 t neuromuscular junction defects, motoneuron hyperexcitability, and progressive motoneuron cell loss,

96 altered cortical physiology consistent with hyperexcitability, and that this abnormality is specific

97 Patients with this indicator of network hyperexcitability are at risk for accelerated cognitive

98 ommon mechanisms underlying the pathological hyperexcitability are largely unknown.

99 umerous changes predicted to produce dentate hyperexcitability are seen in epileptic patients and ani

100 native more selective treatments to suppress hyperexcitability are therefore required.

101 ent studies have identified peripheral nerve hyperexcitability as a driver of persistent pain signali

102 This study establishes cortical hyperexcitability as an intrinsic feature of symptomatic

103 uitry especially under conditions of central hyperexcitability, as may occur in chronic pain conditio

104 (into the ACC or S1) triggered both neuronal hyperexcitability, as shown by elevated long-term potent

105 ute to the cognitive dysfunction and circuit hyperexcitability associated with Fragile X syndrome, in

106 diators could contribute to sensory neuronal hyperexcitability associated with inflammatory pain.

107 uggesting that a component of the underlying hyperexcitability associated with persistent firing refl

108 ot ganglion (DRG) neurons contributes to the hyperexcitability associated with persistent pain induce

109 the hippocampal circuitry triggered network hyperexcitability associated with the progressive loss o

110 ) is associated with development of neuronal hyperexcitability at several points along the pain pathw

111 otein synthesis-independent LTD, neocortical hyperexcitability, audiogenic seizures, and altered beha

112 Thus, our data suggest that neuronal hyperexcitability, brought about in part by reduced A-ty

113 Astrocytes are a primary defense against hyperexcitability, but their functional phenotype during

114 nociceptive neurons, and stimulated neuronal hyperexcitability by adenylyl cyclase and protein kinase

115 mpound etanercept inhibited the induction of hyperexcitability by IL-6 plus sIL-6R.

116 lpha and the inhibition of TNF-alpha-induced hyperexcitability by minocycline was overcome by coadmin

117 operties may be responsible for the neuronal hyperexcitability by these gain-of-function mutations.

118 ty, but it is now becoming clear that spinal hyperexcitability can be regulated by descending pathway

119 This hyperexcitability can be reproduced by the NMDAR antagon

120 milial neonatal seizures or peripheral nerve hyperexcitability caused by mutations in neuronal K(v)7.

121 fects in specific K(+) currents underlie the hyperexcitability caused by sleep loss and Abeta express

122 The resulting muscle hyperexcitability causes involuntary and prolonged contr

123 with a gain-of-function causing the observed hyperexcitability characteristic of this unique myoclonu

124 campus has direct implications in many brain hyperexcitability conditions, such as seizures, epilepto

125 It has been suggested that neuronal hyperexcitability contributes to Alzheimer's disease (AD

126 neurons, which, due to a transient window of hyperexcitability, could allow for preferential encoding

127 as a negative feedback to suppress neuronal hyperexcitability, demonstrated by profoundly upregulate

128 ct of TNF-alpha on the development of spinal hyperexcitability depends on IL-6 trans-signaling acting

129 to Alzheimer's disease (AD), so we asked how hyperexcitability develops in a common mouse model of be

130 current view of the pathogenesis of neuronal hyperexcitability diseases.

131 fication of autoimmune brainstem/spinal cord hyperexcitability disorders and may extend to the glycin

132 ant in ALS, we conclude that early intrinsic hyperexcitability does not contribute to motoneuron dege

133 Patients with myotonia congenita have muscle hyperexcitability due to loss-of-function mutations in t

134 Patients with myotonia congenita have muscle hyperexcitability due to loss-of-function mutations in t

135 lts suggest that astrocyte activation drives hyperexcitability during AD through a mechanism involvin

136 mpening effect was also observed on cortical hyperexcitability during in vivo EEG recordings in awake

137 e rather than terminate pathological network hyperexcitability during the clonic phase of seizures.

138 tributes, in part, to bladder afferent nerve hyperexcitability during urinary bladder inflammation or

139 In other disorders with neuronal hyperexcitability, dysfunction in the dendrites often co

140 ould monitor pathological conditions such as hyperexcitability, e.g., those seen in epilepsy, they do

141 The major pro-inflammatory and hyperexcitability effects of microRNA-22 silencing were

142 ns are less impaired, so the direct cause of hyperexcitability, epilepsy, and premature death has rem

143 ic lateral sclerosis, including motor neuron hyperexcitability, fasciculation, and differential vulne

144 independent of genotype, display an initial hyperexcitability followed by progressive loss of action

145 ons is subject to both CDI and CDF, and that hyperexcitability following injury-induced loss of CDF m

146 to be offsetting each other, but eventually hyperexcitability gives rise to dark cell degeneration a

147 Circuit hyperexcitability has been implicated in neuropathology

148 his large body of data, the theme of circuit hyperexcitability has emerged as a potential explanation

149 certain classes of AEDs that reduce network hyperexcitability have disease-modifying properties.

150 hetics and anti-epileptic drugs can suppress hyperexcitability; however, these drugs are complicated

151 de VIVIT reduced signs of glutamate-mediated hyperexcitability in 5xFAD mice, measured in vivo with m

152 atic steatosis, dyslipidemia, and behavioral hyperexcitability in Acot7(N-/-) mice.

153 enetic ablation of tau substantially reduces hyperexcitability in AD mouse lines, induced seizure mod

154 nous tau is integral for regulating neuronal hyperexcitability in adult animals and suggest that an a

155 Ube3a loss as the principal cause of circuit hyperexcitability in AS mice, lending insight into ictog

156 g peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, w

157 t on the emergence of spontaneous and evoked hyperexcitability in damaged nerves.

158 e in pain by facilitating ectopic firing and hyperexcitability in DRG neurons, however little is know

159 or anti-epileptic drugs controlling neuronal hyperexcitability in epilepsy.

160 litate the epileptogenic process or cortical hyperexcitability in experimental animal studies or thos

161 was used because higher frequencies elicited hyperexcitability in females.

162 WT) animals, replicating the early stages of hyperexcitability in Fmr1(-/y).

163 terminal that may compensate for the muscle hyperexcitability in HD.

164 tes aberrant high frequency oscillations and hyperexcitability in hippocampal networks of chronic epi

165 e for Kv1.1 loss and reverse the spontaneous hyperexcitability in Kv1.1-deficient A-axons.

166 aparanodal Kv1.1-deficiency causes intrinsic hyperexcitability in large myelinated axons in vagus ner

167 sting aberrant excitatory synaptogenesis and hyperexcitability in memory-related circuits.

168 ion leads to spontaneous and evoked neuronal hyperexcitability in myelinated fibers, coupled with dev

169 specific sodium channel isoforms that drive hyperexcitability in pain-signalling neurons, thereby pr

170 Clinical trials targeting network hyperexcitability in patients with Alzheimer's disease w

171 ea implicated in development of OCD, display hyperexcitability in PGRN knockout mice.

172 e GABAergic function is sufficient to elicit hyperexcitability in pyramidal neurons and working memor

173 is mounting evidence of neuronal and circuit hyperexcitability in several brain regions, which could

174 MN rescue also corrects hyperexcitability in SMA motor neurons and prevents sens

175 We demonstrate hyperexcitability in stg thalamic slices and further cha

176 ve and pathological aging has been linked to hyperexcitability in the aged CA3 subregion of the hippo

177 n of adult-born granule cells to hippocampal hyperexcitability in the epileptic hippocampus.SIGNIFICA

178 DG neurons, chronic Li treatment reduced the hyperexcitability in the lymphoblast-derived LR group bu

179 ex vivo hearts, implicating parasympathetic hyperexcitability in the Scn8a(N1768D/+) animals.

180 apses in the ventral thalamus, which lead to hyperexcitability in the thalamocortical circuits and ob

181 hat CA1 pyramidal neurons lacking CDKL5 show hyperexcitability in their dendritic domain that is cons

182 channel properties that underlie DRG neuron hyperexcitability in these patients.

183 ive blockade of T-currents reversed neuronal hyperexcitability in vitro and in vivo.

184 as normalized Kcna1(-/-) hippocampal network hyperexcitability in vitro.

185 We surmise that while hyperexcitability in young HSA(LR) mice can be readily e

186 t 6 weeks of age is associated with synaptic hyperexcitability, including increased frequency of spon

187 enetics of disorders characterized by neural hyperexcitability, including substance use disorders (SU

188 in cortical GABAergic neurons causes circuit hyperexcitability, increased seizure severity, and EEG a

189 ole in regulating intrinsic neuronal network hyperexcitability independently of Abeta overexpression

190 Dendritic hyperexcitability induced by Kv4.2 deficiency exacerbate

191 The hyperexcitability is aggravated by reactive oxygen speci

192 cumulation and further suggest that neuronal hyperexcitability is an important mediator of Abeta toxi

193 ll described, but it remains unclear whether hyperexcitability is attributable to disruptions in neur

194 Motoneuron (MN) hyperexcitability is commonly observed in ALS and is sug

195 Hippocampal network hyperexcitability is considered an early indicator of Al

196 these two pathways to decrease neurological hyperexcitability is discussed.

197 Our results show that hyperexcitability is not a global change among all the M

198 Therefore, hyperexcitability is one early endophenotype of bipolar

199 Cortical hyperexcitability is potentially an important pathophysi

200 etworks promote abnormal neuronal firing and hyperexcitability, it has yet to be established whether

201 al neonatal seizures and/or peripheral nerve hyperexcitability; K(v)7.4 channels, highly related to K

202 axons signal back to the cell body to induce hyperexcitability, loss of inhibition and enhanced presy

203 oneurons of mSDO1 mice did display intrinsic hyperexcitability (lower rheobase, hyperpolarized spikin

204 hich early development of occult hippocampal hyperexcitability may contribute to the pathogenesis of

205 e for its mammalian orthologue, Kv1.1, cause hyperexcitability near axon branch points and nerve term

206 on the degree and spatiotemporal features of hyperexcitability, not only IESs or FRs are generated bu

207 duced [Mg2+]o in WT phenocopied the thalamic hyperexcitability observed in stg, whereas changing [Mg2

208 Neuronal hyperexcitability occurs early in the pathogenesis of Al

209 nnels with alpha-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanos

210 results suggest that noise exposure induces hyperexcitability of AC presumably by increasing the pos

211 The hyperexcitability of Cacna1a(S218L) Purkinje cells was c

212 ted mating behavior decline due to premature hyperexcitability of cholinergic circuits used for intro

213 tractive mechanisms to explain the sustained hyperexcitability of chronic epilepsy.

214 reduced extinction, accompanied by intrinsic hyperexcitability of DG granule neurons.

215 mmortalized B-lymphocytes to verify that the hyperexcitability of DG-like neurons is reproduced in th

216 e acids and a TGR5-selective agonist induced hyperexcitability of dorsal root ganglia neurons and sti

217 ar level, where carbamazepine normalized the hyperexcitability of dorsal root ganglion neurons expres

218 that downregulation of NEDD4-2 leads to the hyperexcitability of DRG neurons and contributes to the

219 Intrinsic hyperexcitability of F-type motoneurons during early pos

220 unctional effect of NaV1.1 FHM mutations and hyperexcitability of GABAergic neurons as the pathomecha

221 y input to the hippocampus and contribute to hyperexcitability of hippocampal neurons in this model o

222 transporter levels likely contributes to the hyperexcitability of injured nerves.

223 .6 channels was sufficient to counteract the hyperexcitability of Kcnq2-null neurons.

224 nteracts the increased L2/3 pyramidal neuron hyperexcitability of Kcnq2-null neurons.

225 ation of Kcnq2 from mouse neocortex leads to hyperexcitability of layer 2/3 (L2/3) pyramidal neurons,

226 ed TNFalpha signaling, which in turn lead to hyperexcitability of medium spiny neurons and OCD-like b

227 d excessive self-grooming and the associated hyperexcitability of medium spiny neurons of the nucleus

228 ic motor dysfunction has been related to the hyperexcitability of motoneurons and to changes in spina

229 Thus, the hyperexcitability of MRGPRA3+ and MRGPRD+ neurons, broug

230 sents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follo

231 of the neurons in this circuitry, including hyperexcitability of neurons at the afferent end of the

232 ether, these data show that the induction of hyperexcitability of nociceptive deep dorsal horn neuron

233 or the full development of TNF-alpha-induced hyperexcitability of nociceptive deep horsal horn neuron

234 ary sensory neurons and cause cold-resistant hyperexcitability of nociceptors, suggesting a mechanist

235 ted elastase-induced activation of TRPV4 and hyperexcitability of nociceptors.

236 g conduction velocity, but also for limiting hyperexcitability of pyramidal neurons.

237 liplatin-induced TRPV1-sensitization and the hyperexcitability of sensory neurons and thereby to redu

238 Prior microsympathectomy greatly reduced hyperexcitability of sensory neurons induced by local DR

239 hindpaw, Na(v)1.7 currents contribute to the hyperexcitability of sensory neurons, their communicatio

240 tion at the channel level, thereby producing hyperexcitability of small dorsal root ganglion (DRG) ne

241 li, indicating that the mutation resulted in hyperexcitability of TG neurons.

242 nction of the sodium channel responsible for hyperexcitability of the fascicular-Purkinje system.

243 lformation of these spinal circuits leads to hyperexcitability of the monosynaptic reflex.

244 y 5) removal of descending systems, inducing hyperexcitability of the monosynaptic reflex.

245 Central sensitization and network hyperexcitability of the nociceptive system is a basic m

246 alographic response has been associated with hyperexcitability of the visuo-motor system.

247 lay important underlying roles in persistent hyperexcitability of these superficial dorsal horn neuro

248 t these pro-excitatory gating changes confer hyperexcitability on peripheral sensory neurons, which m

249 ay be characterized by extrastriate cortical hyperexcitability or differential attentional deployment

250 two different mechanisms, predicting either hyperexcitability or electrical silencing of KV1.2-expre

251 By contrast, no hyperexcitability or interneuron loss was observed in th

252 dings in patients supported peripheral nerve hyperexcitability over destructive axonal loss.

253 report that zebrafish kif5Aa mutants exhibit hyperexcitability, peripheral polyneuropathy, and axonal

254 This hyperexcitability phenotype of young neurons in bipolar

255 Peripheral nerve hyperexcitability (PNH) is one of the distal peripheral

256 Congenital peripheral nerve hyperexcitability (PNH) is usually associated with impai

257 ion combined with glial Env-induced neuronal hyperexcitability precipitates disease.

258 ing therapy for disorders with a detrimental hyperexcitability profile in adult animals, we identifie

259 The mechanisms for hyperexcitability range from alterations in the expressi

260 wn-regulation has been implicated in several hyperexcitability-related disorders, including epilepsy,

261 l activators is crucial for the treatment of hyperexcitability-related disorders.

262 fy the cellular mechanisms that underlie the hyperexcitability reported in the CA3 region.

263 Many silent nociceptors exhibit hyperexcitability resembling that in small-fiber neuropa

264 Spasticity is associated with the DH hyperexcitability resulting from an increase in excitati

265 Here we discuss studies that include hyperexcitability resulting from impaired supply of astr

266 eurological condition in which a basal brain hyperexcitability results in paroxysmal hypersynchronous

267 Thus, in addition to central neuron hyperexcitability, Scn8a(N1768D/+) mice have cardiac myo

268 L-6R, but not of IL-6 alone, enhanced spinal hyperexcitability similar to TNF-alpha and the inhibitio

269 neuronal circuits resulting in a persistent hyperexcitability state and other migraine-relevant mech

270 disorders that are characterized by neuronal hyperexcitability, such as epilepsy and tinnitus.

271 Administration of AOAA also reduced neuronal hyperexcitability, suppressed the sodium current density

272 straction is associated with spinal neuronal hyperexcitability that can be induced by transmitter/rec

273 BAA receptor clusters, resulting in neuronal hyperexcitability that causes dendrite shrinkage.

274 Aergic interneurons overcome the spinal cord hyperexcitability that is a hallmark of nerve injury-ind

275 In this study, an in vitro model of central hyperexcitability that uses the potassium channel blocke

276 elective TrkB antagonist) prevented neuronal hyperexcitability, the emergence of cold hypersensitivit

277 optogenetic stimulation normalized cortical hyperexcitability through changing neuronal membrane pro

278 The resulting hippocampal hyperexcitability underlies the enhanced fear memories,

279 Neuronal network hyperexcitability underlies the pathogenesis of seizures

280 We hypothesize that development of cortical hyperexcitability underlying neuropathic pain may involv

281 y contribute to early AD hippocampal network hyperexcitability via a presynaptic mechanism, and that

282 spinal synaptic plasticity and DRG neuronal hyperexcitability via TGF-beta receptor 1-mediated nonca

283 mitochondrial dysfunction caused nociceptor hyperexcitability via the translocation and activation o

284 This dendritic hyperexcitability was associated with depletion of Kv4.2

285 Antimycin A-induced hyperexcitability was dependent on mitochondrial ROS and

286 Peripheral motor hyperexcitability was found in 21% of patients with CASP

287 Antimycin A-induced nociceptor hyperexcitability was independent of TRP ankyrin 1 or TR

288 Antimycin A-induced hyperexcitability was inhibited by the PKC inhibitor bis

289 These signs of neuronal hyperexcitability were associated with a significant inc

290 These signs of neuronal hyperexcitability were associated with a significant red

291 ane, reduces IKNa, and produces DRG neuronal hyperexcitability when activated in cultured primary DRG

292 that the G856D mutation produces DRG neuron hyperexcitability which underlies pain in this kindred,

293 causes multisystem disinhibition and network hyperexcitability, which can well explain the occurrence

294 a "second line of defense" against intrinsic hyperexcitability, which may play a role in multiple con

295 TbetaR-1 inhibition decreased afferent nerve hyperexcitability with a concomitant decrease in urothel

296 lls (iPSCs), we found that SMA MNs displayed hyperexcitability with increased membrane input resistan

297 haracterized by periods of hypersynchronous, hyperexcitability within brain networks.

298 iatal-thalamic-cortical circuit dysfunction, hyperexcitability within cortical motor areas, and alter

299 rgic neurons, focusing on the development of hyperexcitability within L2/3 neocortex and in broader c

300 vating muscle are more effective at inducing hyperexcitability within spinal cord circuits compared w