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1 o seizure development and progression (i.e., epileptogenesis).
2 of these cellular deficits may help predict epileptogenesis.
3 tion-dependent neuronal plasticity including epileptogenesis.
4 astrogliosis is a cause or a consequence of epileptogenesis.
5 p, may be proposed as putative biomarkers of epileptogenesis.
6 th, in older animals may augment TBI-induced epileptogenesis.
7 signaling cascade reduces the probability of epileptogenesis.
8 and triggers neuronal hyperexcitability and epileptogenesis.
9 eptors in provoking seizures and in kindling epileptogenesis.
10 ate excitability is causally associated with epileptogenesis.
11 igger of inflammatory cascades implicated in epileptogenesis.
12 tes by serum-derived albumin, is involved in epileptogenesis.
13 le of facilitated NMDA receptor signaling in epileptogenesis.
14 hat HIF-1alpha is an important factor during epileptogenesis.
15 us, and to explore their relationship during epileptogenesis.
16 her allergic inflammation contributes toward epileptogenesis.
17 nd has also been implicated in temporal lobe epileptogenesis.
18 mpus and exhibit neuroplastic changes during epileptogenesis.
19 ences of increased protein synthesis in FXS, epileptogenesis.
20 ority of restructuring in the dentate during epileptogenesis.
21 (TrkB) is thought to be critical for limbic epileptogenesis.
22 t these excitatory synapses that may promote epileptogenesis.
23 odifying neuronal excitability and promoting epileptogenesis.
24 otentially modifiable therapeutic targets in epileptogenesis.
25 id not directly correlate with inhibition of epileptogenesis.
26 ylation, leading to impaired function during epileptogenesis.
27 pocampus in response to kainate (KA)-induced epileptogenesis.
28 mitant with inhibition of CI activity during epileptogenesis.
29 cellular bioenergetics during the process of epileptogenesis.
30 europathological alterations associated with epileptogenesis.
31 chanisms, and may be an early contributor to epileptogenesis.
32 xpression in neuropathologies that accompany epileptogenesis.
33 nule cells might contribute to temporal lobe epileptogenesis.
34 ving intact neurons alleviated posttraumatic epileptogenesis.
35 ke on group I mGluR-mediated translation and epileptogenesis.
36 bling group I mGluR-mediated translation and epileptogenesis.
37 T2 changes nor interictal activity predicted epileptogenesis.
38 S generation, contributed also to subsequent epileptogenesis.
39 ith a role for this inflammatory mediator in epileptogenesis.
40 s an important molecular mechanism of limbic epileptogenesis.
41 o neuronal hyperexcitability and possibly to epileptogenesis.
42 ciated with both ischemia-induced injury and epileptogenesis.
43 m with specific characteristics that promote epileptogenesis.
44 he inducing agonist and serves as a model of epileptogenesis.
45 be utilized to suppress seizures and perhaps epileptogenesis.
46 ity, heightened gamma band oscillations, and epileptogenesis.
47 ERAD by the mutant protein may contribute to epileptogenesis.
48 ting in artificially prolonged latencies for epileptogenesis.
49 anism associated with group I mGluR-mediated epileptogenesis.
50 ion may affect HCN channel properties during epileptogenesis.
51 for seizure suppression and modification of epileptogenesis.
52 ate to normal brain development and possibly epileptogenesis.
53 ectively enhanced during critical periods of epileptogenesis.
54 ucted status epilepticus (SE) and subsequent epileptogenesis.
55 ated with formative mechanisms of poststroke epileptogenesis.
56 e, is a potential predictor and modulator of epileptogenesis.
57 ion of phospholipase Cgamma1 is required for epileptogenesis.
58 d forebrain ADK were resistant to subsequent epileptogenesis.
59 ure), or 3 weeks after (newborn) pilocarpine-epileptogenesis.
60 no effective therapy is available to prevent epileptogenesis.
61 s of rat neocortex, a model of posttraumatic epileptogenesis.
62 ts, including alpha4, and may play a role in epileptogenesis.
63 gnaling influences neuronal excitability and epileptogenesis.
64 ition may also play an important role during epileptogenesis.
65 reased synaptic excitation and contribute to epileptogenesis.
66 le AMPARs in excitotoxic cellular injury and epileptogenesis.
67 and other Src family kinases contributes to epileptogenesis.
68 pothesized as a major factor contributing to epileptogenesis.
69 re hypothesized to be critical components of epileptogenesis.
70 d alpha2delta4, which act synergistically in epileptogenesis.
71 nt drugs, suggesting an age-specific form of epileptogenesis.
72 ay represent an early stage of posttraumatic epileptogenesis.
73 pathological cellular processes that promote epileptogenesis.
74 also highly susceptible to acutely provoked epileptogenesis.
75 -mediated activation of TrkB is required for epileptogenesis.
76 ma1) signaling induced by a seizure promotes epileptogenesis.
77 d a subset of animals to an earlier state of epileptogenesis.
78 xpression occurred in the hippocampus during epileptogenesis.
79 activation of phospholipase Cgamma1 promotes epileptogenesis.
80 the development of hyperexcitability during epileptogenesis.
81 oscillations (HFOs) are newer biomarkers for epileptogenesis.
82 imit glutamate release, thus contributing to epileptogenesis.
83 ppocampal CA3 neurons, a classical focus for epileptogenesis.
84 in the brain and blood of animals undergoing epileptogenesis.
85 rly-born DGCs that are mature at the time of epileptogenesis.
86 s, suggesting its functional significance in epileptogenesis.
87 reflect pathophysiological processes beyond epileptogenesis.
88 nst hCA II and hCA VII, isoforms involved in epileptogenesis.
89 43 in the brain and serum over the course of epileptogenesis.
90 the acute and latent phase of injury-induced epileptogenesis.
91 abolites may be able to serve as a marker of epileptogenesis.
92 ol for identifying brain inflammation during epileptogenesis.
93 es to hippocampal dendrites that may promote epileptogenesis.
94 e an epileptogenic brain insult can mitigate epileptogenesis.
95 hippocampal culture model of post-traumatic epileptogenesis.
96 nto the role of microglial activation during epileptogenesis.
97 tatory neurotransmission plays a key role in epileptogenesis.
98 e gyrus, potentially mediating temporal lobe epileptogenesis.
99 vals and a poor measure of the time frame of epileptogenesis, (2) epileptogenesis is a continuous pro
100 in mice, indicating that the drug slows down epileptogenesis, a finding deserving further investigati
101 lts suggest GAP-43 as a key factor promoting epileptogenesis, a possible therapeutic target for treat
102 riod may serve as a diagnostic biomarker for epileptogenesis, able to predict the future onset of spo
103 models, discovery of new basic mechanisms of epileptogenesis, acceleration of proof of principle stud
107 These results indicate that hippocampal epileptogenesis after convulsive status epilepticus is a
109 hese atypical astrocytes might contribute to epileptogenesis after diffuse TBI.SIGNIFICANCE STATEMENT
111 s utility to delineate mechanisms underlying epileptogenesis after pediatric brain injury, and provid
112 lp develop therapeutic strategies to prevent epileptogenesis after stroke and elucidate some of the m
113 izures develop is critical for understanding epileptogenesis, an understanding of how and why recurre
114 ion of the adenosine system is implicated in epileptogenesis and cell therapies have been developed t
115 abolism in rat plasma and hippocampus during epileptogenesis and chronic epilepsy in the kainic acid
116 nts and determine the latency to hippocampal epileptogenesis and clinical epilepsy, we developed an e
117 EGCs that develop after SE may contribute to epileptogenesis and cognitive impairments that follow SE
118 zure duration as an important determinant in epileptogenesis and defining the predictive roles of int
119 ovel insights into the mechanisms underlying epileptogenesis and discover potential preventive treatm
121 MGB1 isoforms are mechanistic biomarkers for epileptogenesis and drug-resistant epilepsy in humans, n
122 leptic brain and as a potential biomarker of epileptogenesis and epileptogenicity and for presurgical
123 chmarks is to develop reliable biomarkers of epileptogenesis and epileptogenicity that could revoluti
124 gest an important role of innate immunity in epileptogenesis and focus on glial inhibition, through p
125 k clinically relevant noninvasive markers of epileptogenesis and found that reduced amygdala T2 relax
128 Thus, novel insights into the mechanisms of epileptogenesis and identification of new drug targets c
129 BDNF expression, only a modest impairment of epileptogenesis and increased hippocampal TrkB activatio
130 ulation of the endocannabinoid system during epileptogenesis and indicates that the CB(1) receptor re
132 d may be associated with both the process of epileptogenesis and maintenance of the epileptic state.
133 for understanding the mechanisms underlying epileptogenesis and may provide insights into why sponta
134 rks in MTLE may improve the understanding of epileptogenesis and neuropsychological impairments assoc
136 ling pathways that control susceptibility to epileptogenesis and possibly persistence of an epileptic
137 in DNA methylation homeostasis may underlie epileptogenesis and reversal of these epigenetic changes
141 Here, we tested the hypothesis that during epileptogenesis and spontaneous recurrent seizures (SRS)
143 lepticus (SE) are crucial for the process of epileptogenesis and targeting seizure-induced neurogenes
144 ts receptor, TrkB, in the hippocampus during epileptogenesis and that BDNF-mediated activation of Trk
145 pathway has been implicated in mechanisms of epileptogenesis and the mTORC1 inhibitor, rapamycin, has
146 mic transcription of individual genes during epileptogenesis and thereby contribute to the developmen
147 d retest paradigm in AS model mice to assess epileptogenesis and to gain mechanistic insights owed to
148 Ca(2+)](i) remained markedly elevated during epileptogenesis and was still elevated indefinitely in t
149 urons also were altered in the brain-injury, epileptogenesis, and chronic-epilepsy phases of AE.
152 d our understanding of circuit mechanisms of epileptogenesis, and have potential implications for the
153 age (MRI) provided predictive biomarkers for epileptogenesis, and if the inflammatory mediator interl
154 ycin (mTOR) signaling pathway is involved in epileptogenesis, and mTOR inhibitors prevent epilepsy in
155 old for status epilepticus (SE), accelerated epileptogenesis, and once epilepsy was induced, depressi
156 d alpha2delta4, which act synergistically in epileptogenesis, and thereby contributes to a seizure-in
160 occurs in both neurons and astrocytes during epileptogenesis, as assessed by measuring biochemical an
161 ergic inhibition, which may be key factor in epileptogenesis, as the seizures in vivo are blocked by
163 activation as well as neuronal cell loss in epileptogenesis-associated brain regions at all investig
164 uptake and binding potential were evident in epileptogenesis-associated brain regions, such as the hi
166 this information, we propose a mechanism of epileptogenesis based on enhanced K(V) 1.2 inactivation
167 Deficits in KCC2 activity are implicated in epileptogenesis, but how increased neuronal activity lea
169 ing that peri-insult generated cells mediate epileptogenesis, but that seizures per se are initiated
170 e BDNF receptor, TrkB, is critical to limbic epileptogenesis, but the responsible downstream signalin
171 ive stress was reduced in animals undergoing epileptogenesis by a transient treatment with N-acetylcy
172 more physiologically relevant and linked to epileptogenesis, by characterizing the effects of these
175 Genes selectively regulated by NRSF during epileptogenesis coded for ion channels, receptors, and o
177 ro preparations, during early post-traumatic epileptogenesis demonstrated rapid increases in the frac
179 yer recording determined whether hippocampal epileptogenesis develops immediately or long after injur
181 these findings to the general mechanisms of epileptogenesis during development and points out gaps i
183 critical role for AMPA receptors (AMPARs) in epileptogenesis during this critical period in the devel
184 ressor genes and serially monitored cortical epileptogenesis during tumor infiltration with in vivo e
185 us epilepticus (SE), can trigger a period of epileptogenesis during which functional and structural r
186 HFOs can be used as a reliable biomarker for epileptogenesis, epileptogenicity, and the delineation o
187 r an isolated seizure limited progression of epileptogenesis, evidenced by the reduced severity and d
188 mmature granule cells exposed to pilocarpine-epileptogenesis exhibited aberrant hilar basal dendrites
189 utamate receptor (mGluR) stimulation include epileptogenesis, expressed in vitro as the conversion of
190 the effects of inhibiting TrkB signaling on epileptogenesis following an isolated seizure, we implem
191 he specific subunit Kv3.4 is affected during epileptogenesis following pilocarpine-induced status epi
193 icographic or intrahippocampal recordings of epileptogenesis (from the insult to the first spontaneou
194 addressed the role of TGF-beta signaling in epileptogenesis in 2 different rat models of vascular in
195 we studied the properties of the TBI-induced epileptogenesis in a biophysically realistic cortical ne
197 d early and late components of tumor-related epileptogenesis in a genetically tractable, immunocompet
204 expression and hippocampal apoptosis during epileptogenesis in comparison with the positive control.
213 of metabolic genes in the hippocampus during epileptogenesis in male rats in the pilocarpine model of
217 sed several forms of seizure sensitivity and epileptogenesis in rats selectively bred for vulnerabili
222 in mitigating neuronal loss and attenuating epileptogenesis in the excitatory injury model of epilep
223 oforms, exhibited an increased resistance to epileptogenesis in the hippocampus and amygdala kindling
226 e that mTOR signaling mediates mechanisms of epileptogenesis in the kainate rat model and that mTOR i
227 by Nav beta1 contributes to the mechanism of epileptogenesis in these animals as well as in patients.
229 epileptiform discharge in vitro and kindling epileptogenesis in vivo with partial gamma-aminobutyric
231 hanisms at play during epilepsy development (epileptogenesis) in animal models of TLE could enable th
233 is study was to develop an in vitro model of epileptogenesis induced by glutamate injury in organotyp
234 transiently administered for 2 weeks during epileptogenesis inhibited oxidative stress more efficien
237 re of the time frame of epileptogenesis, (2) epileptogenesis is a continuous process that extends muc
238 ical conditions, and one prominent theory of epileptogenesis is based on the assumption that mossy ce
239 Understanding molecular mechanisms mediating epileptogenesis is critical for developing more effectiv
241 me course of fluid percussion injury-induced epileptogenesis is dramatically biased by the definition
251 table to the complex alterations involved in epileptogenesis, it is likely that multitargeted approac
252 scence microscopy during the injury (acute), epileptogenesis (latency), and chronic-epilepsy phases o
256 Interneuron death and reorganization during epileptogenesis may disrupt the synchrony of hippocampal
257 s in vitro model of glutamate injury-induced epileptogenesis may help develop therapeutic strategies
260 suggests astrocyte mGluR5 expression during epileptogenesis may recapitulate earlier developmental r
261 ase in h channels during a critical phase of epileptogenesis mechanistically underlies dendritic hype
264 s recurrent seizures and could contribute to epileptogenesis or development of the epileptic state.
265 GluK1 kainate receptors are not required for epileptogenesis or seizure expression in this model.
266 er pharmacological induction of an otherwise epileptogenesis-precipitating acute brain injury, transg
268 f animals with antiinflammatory drugs during epileptogenesis prevented both disease progression and b
269 NMDARs, we conclude that astrocytes modulate epileptogenesis, recurrent spontaneous seizures, and pat
270 s, the pathophysiological mechanisms of such epileptogenesis remain unknown and no adjunctive therapy
273 n of epilepsy models to define mechanisms of epileptogenesis remains vital for future therapies.
274 mpal interneuron activity has been linked to epileptogenesis, seizures and the oscillatory synaptic a
276 erefore, our study identifies a mechanism of epileptogenesis that links MAP kinase to Eph/Ephrin and
277 ning synapses is a reversible, early step in epileptogenesis that offers a novel therapeutic target i
279 es, and survival during this period of early epileptogenesis (the development of epilepsy) following
280 d from IL-6 -: treated mice show that during epileptogenesis, the cells respond to repetitive orthodr
281 ptic plasticity (HSP) mediates posttraumatic epileptogenesis through unbalanced synaptic scaling, par
282 onal model to relate changes observed during epileptogenesis to a decreased tendency to burst in the
286 dissected the circuit mechanisms underlying epileptogenesis using a mouse model of focal cortical ma
287 ltered gene expression and thus may underlie epileptogenesis via induction of permanent changes in ne
293 lial mTOR signaling in excitatory injury and epileptogenesis, we generated mice with restrictive dele
294 addition, changes in theta band power during epileptogenesis were associated with altered locomotor a
295 s as crucial mediators in the development of epileptogenesis, which is the process whereby a normal b
296 gests that impaired autophagy contributes to epileptogenesis, which may be of interest as a potential
297 ys of understanding the molecular pathway of epileptogenesis, widening the spectrum of possible thera
298 ats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neu
299 he repeated flurothyl paradigm is a model of epileptogenesis with spontaneous seizures that remit.
301 ate the molecular and cellular mechanisms of epileptogenesis without any complication from drug-induc