ライフサイエンスコーパス: hyperexcitability

1 l segment (AIS) plasticity, causing neuronal hyperexcitability.

2 d cortical networks exhibit lasting abnormal hyperexcitability.

3 in GABAergic signaling and neuronal network hyperexcitability.

4 receptor hyperactivity, hyperplasticity, and hyperexcitability.

5 elds that can be associated with hippocampal hyperexcitability.

6 hemokines in the process leading to neuronal hyperexcitability.

7 and reduced membrane channel density causes hyperexcitability.

8 racortical facilitation, indicating cortical hyperexcitability.

9 cortical neurons, and resulting in neuronal hyperexcitability.

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

11 uromuscular transmission and skeletal muscle hyperexcitability.

12 o underlie or support development of network hyperexcitability.

13 ls and alleviated multiple signs of neuronal hyperexcitability.

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

15 xhibits neural circuit hyperconnectivity and hyperexcitability.

16 ng O-GlcNAcylation will depress pathological hyperexcitability.

17 rising and multiple mechanisms contribute to hyperexcitability.

18 itory circuits that results in a generalized hyperexcitability.

19 t link peripheral inflammation with neuronal hyperexcitability.

20 erized by recurrent seizures due to neuronal hyperexcitability.

21 the generation of inflammation-evoked spinal hyperexcitability.

22 rks that bias activity towards and away from hyperexcitability.

23 -existing pathologies associate with circuit hyperexcitability.

24 e cardiac myoycte and parasympathetic neuron hyperexcitability.

25 that IIS are possibly the earliest stage of hyperexcitability.

26 eurologic disorders associated with neuronal hyperexcitability.

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

28 uggesting a potential mechanism for neuronal hyperexcitability.

29 weeks of life and brain slices show neuronal hyperexcitability.

30 rocyte -: neuronal interactions and neuronal hyperexcitability.

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

32 prevents resultant agonist-induced neuronal hyperexcitability.

33 prevented both Kv4.2 depletion and dendritic hyperexcitability.

34 e tumours, and GPC3 drives gliomagenesis and hyperexcitability.

35 d anxiety disorders are characterized by BLA hyperexcitability.

36 gence of burst discharges reflecting network hyperexcitability.

37 fast potassium currents correlated with this hyperexcitability.

38 Tau reduction prevented BIN1-induced network hyperexcitability.

39 microglial dynamics prevent neuronal network hyperexcitability.

40 d GABAergic synaptic impairment and neuronal hyperexcitability.

41 ic potassium channel blockers diminished the hyperexcitability.

42 ains and transgenic AD mouse models manifest hyperexcitability.

43 al segments consistent with compensation for hyperexcitability.

44 v1.8 disease mutations induce sensory neuron hyperexcitability.

45 (42)-induced spine degeneration and neuronal hyperexcitability.

46 he synaptic perturbations underlying circuit hyperexcitability.

47 contributing to, neuronal depolarization and hyperexcitability.

48 rovide mechanistic insight into the observed hyperexcitability.

49 iseases of dysregulated K(+) homeostasis and hyperexcitability.

50 t is causally linked to neuronal and circuit hyperexcitability.

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

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

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

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

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

56 ode recordings of neuronal networks revealed hyperexcitability and altered bursting and synchronicity

57 use model of AD, IF reduces neuronal network hyperexcitability and ameliorates deficits in hippocampa

58 model mice exhibited CA1 excitatory ensemble hyperexcitability and concomitant behavioral deficits in

59 /2 muscle may help compensate for the muscle hyperexcitability and contribute to motor impersistence.

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

61 downstream of C-Raf also blocks SCI-induced hyperexcitability and depolarization, without direct eff

62 BAergic synapses resulting in pyramidal cell hyperexcitability and disruptions in network synchroniza

63 campal function with strong implications for hyperexcitability and epilepsy.SIGNIFICANCE STATEMENT At

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

65 the neurovascular unit and triggers neuronal hyperexcitability and epileptogenesis.

66 tion (E-I) ratio in cerebral cortex, causing hyperexcitability and excess spiking.

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

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

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

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

71 These results show for the first time that hyperexcitability and hyperplasticity disrupt signal tra

72 This was associated with LH(GABA) neuron hyperexcitability and impaired hippocampal long-term pot

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

74 effects on the target proteins, resulting in hyperexcitability and impairment of synaptic function an

75 mechanism to persistently promote nociceptor hyperexcitability and limit the therapeutic effectivenes

76 at blocks TREK channels, leading to neuronal hyperexcitability and migraine in rodents.

77 Cortical hyperexcitability and mislocalization of the RNA-binding

78 Given the paucity of compounds that reduce hyperexcitability and neuron loss, have anti-inflammator

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

80 Proteases sustain hyperexcitability and pain by cleaving protease-activate

81 av1.7 underlie dorsal root ganglion neuronal hyperexcitability and pain in a subset of patients with

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

83 ts reproduced the experimental phenotypes of hyperexcitability and physiological instability.

84 eated lesioned monkeys exhibited significant hyperexcitability and predominance of inhibitory synapti

85 nd that RhoA inhibition prevents both D1-MSN hyperexcitability and reduced excitatory input to D1-MSN

86 s may be useful for screening drugs to treat hyperexcitability and related synaptic damage in AD.

87 at manifest in selective initiation of brain hyperexcitability and remodelling of the synaptic consti

88 sociated with amelioration of injury-related hyperexcitability and restoration of excitatory-inhibito

89 how that EV treatment dampens injury-related hyperexcitability and restores excitatory:inhibitory bal

90 and motor dysfunctions, as well as cortical hyperexcitability and seizures.

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

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

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

94 These data demonstrate that hyperexcitability and the associated changes in GABAergi

95 Hyperexcitability and the imbalance of excitation/inhibi

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

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

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

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

100 ied by excessive glutamatergic transmission, hyperexcitability, and increased levels of postsynaptic

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

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

103 , describe a disease-relevant consequence in hyperexcitability, and provide preliminary evidence that

104 lular fluid accumulation in nerves, neuronal hyperexcitability, and seizures.

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

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

107 Cellular and circuit hyperexcitability are core features of fragile X syndrom

108 ommon mechanisms underlying the pathological hyperexcitability are largely unknown.

109 n1-dependent XLID, but the cellular bases of hyperexcitability are poorly understood.

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

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

112 turbed AIS morphological plastic response to hyperexcitability arising from proteasome inhibition, a

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

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

115 ppocampal neurons lacking APP family exhibit hyperexcitability, as evidenced by increased neuronal sp

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

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

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

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

120 hown to disrupt neuronal function and induce hyperexcitability, but it is unclear what effects Abeta-

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

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

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

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

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

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

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

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

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

130 man Alzheimer's disease (AD) brains manifest hyperexcitability, contributing to subsequent extensive

131 l activity, specifically the SK channels, in hyperexcitability defects in FXS.

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

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

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

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

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

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

138 for genes contributing to the development of hyperexcitability during epileptogenesis.

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

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

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

142 get for pathologies characterized by network hyperexcitability dysfunction, such as epilepsy.

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

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

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

146 in the prolonged response latencies, sudden hyperexcitability, enhanced cortical synchrony, elevated

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

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

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

150 Circuit hyperexcitability has been implicated in neuropathology

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

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

153 ver, the cellular and synaptic bases of this hyperexcitability have proved elusive.

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

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

156 gest that it may contribute to Tau-dependent hyperexcitability in AD.

157 n GABAergic networks and dampen pathological hyperexcitability in adults with XLID.

158 Characterisation of cortical hyperexcitability in amyotrophic lateral sclerosis and a

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

160 f synaptic drive rather than driving network hyperexcitability in autism.

161 n-of-function in Slack K(Na) channels causes hyperexcitability in both isolated neurons and in neural

162 Furthermore, recreating granule cell hyperexcitability in control mice via excitatory chemoge

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

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

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

166 was used because higher frequencies elicited hyperexcitability in females.

167 hannels is the primary cause of CA3 neuronal hyperexcitability in Fmr1 KO mice and support the critic

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

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

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

171 (i)-dependent microglia dynamics may prevent hyperexcitability in neurological diseases.

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

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

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

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

176 synaptic changes that eventually build up to hyperexcitability in the amygdala.

177 to impaired neuronal plasticity and network hyperexcitability in the auditory cortex.

178 o implicated in establishing lasting network hyperexcitability in the brain by acting upon independen

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

180 hannel dysfunction causes hippocampal neuron hyperexcitability in the FXS mouse model.

181 ative effect of these pathologies is massive hyperexcitability in the granule cells, generating both

182 expression and total Kv current, attenuated hyperexcitability in the injured DRG neurons, and allevi

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

184 ntributors to network disinhibition, but how hyperexcitability in the peritumoral microenvironment ev

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

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

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

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

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

190 (FXS) exhibit signs of neuronal and circuit hyperexcitability, including anxiety and hyperactive beh

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

192 dium channel Na(v)1.8 that induce nociceptor hyperexcitability increase resurgent currents.

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

194 Dendritic hyperexcitability induced by Kv4.2 deficiency exacerbate

195 ibuting to bladder overactivity and afferent hyperexcitability induced by prostatic inflammation.

196 Here we show that chronic neuronal hyperexcitability, induced by M-type potassium channel i

197 The hyperexcitability is aggravated by reactive oxygen speci

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

199 Neuronal and network-level hyperexcitability is commonly associated with increased

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

201 : we clearly demonstrate here that in vitro, hyperexcitability is detrimental to islets whereas under

202 these two pathways to decrease neurological hyperexcitability is discussed.

203 The hyperexcitability is mediated by excessive activity of v

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

205 Therefore, hyperexcitability is one early endophenotype of bipolar

206 Neuronal hyperexcitability is one of the major characteristics of

207 Cortical hyperexcitability is potentially an important pathophysi

208 sprouted mossy fiber synapses on hippocampal hyperexcitability is unclear.

209 Neuronal hyperexcitability is widely considered one of the hallma

210 ely following demyelination, neurons exhibit hyperexcitability, learning is impaired and behavioral i

211 ulated models of inflammatory or neuropathic hyperexcitability led to a change in the temporal patter

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

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

214 it is unclear what effects Abeta-associated hyperexcitability may have on tauopathy pathogenesis or

215 lateral hypothalamus (LH)-projecting D1-MSN hyperexcitability mediated by decreased inwardly rectify

216 ), an mRNA binding protein, and the neuronal hyperexcitability observed in the absence of FMRP likely

217 Long-term lithium treatment decreased the hyperexcitability observed in the CA3 neurons derived fr

218 Neuronal hyperexcitability occurs early in the pathogenesis of Al

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

220 rritable bowel syndrome) are associated with hyperexcitability of afferent nerves innervating the uri

221 The hyperexcitability of BD neurons is neuronal type specifi

222 ell as changes in ion channel expression and hyperexcitability of bladder afferent neurons.

223 dent potassium (K(+))-channel dysfunction in hyperexcitability of CA3 pyramidal neurons in Fmr1 knock

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

225 For example, hyperexcitability of cortical neurons is associated with

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

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

228 lts provide new molecular clues for treating hyperexcitability of hippocampal circuits associated wit

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

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

231 .6 channels was sufficient to counteract the hyperexcitability of Kcnq2-null neurons.

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

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

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

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

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

237 iated proteolysis of Nav and KCC2 drives the hyperexcitability of motoneurons which leads to spastici

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

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

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

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

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

243 id development of spontaneous activities and hyperexcitability of nociceptive neurons in the adjacent

244 Nav1.8, can make major contributions to the hyperexcitability of nociceptive neurons, likely leading

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

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

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

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

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

250 Hyperexcitability of the anterior cingulate cortex (ACC)

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

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

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

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

255 urrent density decreased in association with hyperexcitability of these neurons.

256 Lgmn caused PAR(2)-dependent hyperexcitability of trigeminal neurons from WT female m

257 t that peripheral axotomy may quickly induce hyperexcitability of uninjured nociceptors in the adjace

258 Higher BIN1 induced network hyperexcitability on multielectrode arrays, increased fr

259 Consistent with a contribution to network hyperexcitability, optogenetic activation of sprouted mo

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

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

262 ary K(+) is the main determinant of afferent hyperexcitability, organ hyperactivity and pain.

263 We recently reported a hyperexcitability phenotype displayed in dentate gyrus g

264 This hyperexcitability phenotype of young neurons in bipolar

265 lly simulated BD dentate gyrus neurons had a hyperexcitability phenotype similar to the experimental

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

267 The mechanisms for hyperexcitability range from alterations in the expressi

268 Here, we showed that hyperexcitability recapitulates TDP43 pathology by upreg

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

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

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

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

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

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

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

276 to the significantly higher neural activity (hyperexcitability) seen in the J20-hAPP mice.

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

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

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

280 ents with bipolar disorder (BD) as well as a hyperexcitability that appeared only in CA3 pyramidal hi

281 of FMRP leads to neuronal and circuit-level hyperexcitability that is thought to arise from the aber

282 les driving neuroinflammation and increasing hyperexcitability, the slower-acting metabotropic P2Y re

283 optogenetic stimulation normalized cortical hyperexcitability through changing neuronal membrane pro

284 g, revealing a reproducible progression from hyperexcitability to convulsive seizures.

285 st that enhanced NMDAR signaling and circuit hyperexcitability underlie autistic-like features in mou

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

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

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

289 e demonstrate that UBE3A suppresses neuronal hyperexcitability via ubiquitin-mediated degradation of

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

291 As this hyperexcitability was only seen in adult males, and not

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

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

294 amplified, they promote paradoxical network hyperexcitability which may be relevant to disorders inv

295 how this increased potassium current induces hyperexcitability, which could be the underlining factor

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

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

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

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

300 normalizing epilepsy-associated granule cell hyperexcitability-without correcting the underlying stru