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1 er than the underlying disease process (i.e. epileptogenesis).
2 otentially modifiable therapeutic targets in epileptogenesis.
3 id not directly correlate with inhibition of epileptogenesis.
4 ylation, leading to impaired function during epileptogenesis.
5 pocampus in response to kainate (KA)-induced epileptogenesis.
6 mitant with inhibition of CI activity during epileptogenesis.
7 cellular bioenergetics during the process of epileptogenesis.
8 europathological alterations associated with epileptogenesis.
9 chanisms, and may be an early contributor to epileptogenesis.
10 xpression in neuropathologies that accompany epileptogenesis.
11 nule cells might contribute to temporal lobe epileptogenesis.
12 ving intact neurons alleviated posttraumatic epileptogenesis.
13 ke on group I mGluR-mediated translation and epileptogenesis.
14 bling group I mGluR-mediated translation and epileptogenesis.
15 T2 changes nor interictal activity predicted epileptogenesis.
16 in the brain and blood of animals undergoing epileptogenesis.
17 S generation, contributed also to subsequent epileptogenesis.
18 ith a role for this inflammatory mediator in epileptogenesis.
19 s an important molecular mechanism of limbic epileptogenesis.
20 o neuronal hyperexcitability and possibly to epileptogenesis.
21 ciated with both ischemia-induced injury and epileptogenesis.
22 m with specific characteristics that promote epileptogenesis.
23 he inducing agonist and serves as a model of epileptogenesis.
24 be utilized to suppress seizures and perhaps epileptogenesis.
25 ity, heightened gamma band oscillations, and epileptogenesis.
26 ERAD by the mutant protein may contribute to epileptogenesis.
27 ting in artificially prolonged latencies for epileptogenesis.
28 anism associated with group I mGluR-mediated epileptogenesis.
29 rly-born DGCs that are mature at the time of epileptogenesis.
30 for seizure suppression and modification of epileptogenesis.
31 ate to normal brain development and possibly epileptogenesis.
32 ectively enhanced during critical periods of epileptogenesis.
33 ucted status epilepticus (SE) and subsequent epileptogenesis.
34 ated with formative mechanisms of poststroke epileptogenesis.
35 imit glutamate release, thus contributing to epileptogenesis.
36 e, is a potential predictor and modulator of epileptogenesis.
37 d forebrain ADK were resistant to subsequent epileptogenesis.
38 ure), or 3 weeks after (newborn) pilocarpine-epileptogenesis.
39 no effective therapy is available to prevent epileptogenesis.
40 s of rat neocortex, a model of posttraumatic epileptogenesis.
41 ts, including alpha4, and may play a role in epileptogenesis.
42 gnaling influences neuronal excitability and epileptogenesis.
43 ition may also play an important role during epileptogenesis.
44 reased synaptic excitation and contribute to epileptogenesis.
45 le AMPARs in excitotoxic cellular injury and epileptogenesis.
46 and other Src family kinases contributes to epileptogenesis.
47 pothesized as a major factor contributing to epileptogenesis.
48 re hypothesized to be critical components of epileptogenesis.
49 nt drugs, suggesting an age-specific form of epileptogenesis.
50 ay represent an early stage of posttraumatic epileptogenesis.
51 pathological cellular processes that promote epileptogenesis.
52 also highly susceptible to acutely provoked epileptogenesis.
53 s, suggesting its functional significance in epileptogenesis.
54 -mediated activation of TrkB is required for epileptogenesis.
55 nts, suggesting that FRs are associated with epileptogenesis.
56 e neocortical and hippocampal post-traumatic epileptogenesis.
57 atterns of regulation during development and epileptogenesis.
58 vous system development and certain forms of epileptogenesis.
59 ticus following specific insults may prevent epileptogenesis.
60 atum oriens of the hippocampus during limbic epileptogenesis.
61 h) in controlling dendritic excitability and epileptogenesis.
62 reflect pathophysiological processes beyond epileptogenesis.
63 al for interrupting the processes underlying epileptogenesis.
64 ect localized pathological events related to epileptogenesis.
65 nst hCA II and hCA VII, isoforms involved in epileptogenesis.
66 t no detectable regulatory effects on limbic epileptogenesis.
67 one mechanism by which BDNF promotes limbic epileptogenesis.
68 persist for up to 1 year after induction of epileptogenesis.
69 ent of the given pathology in the process of epileptogenesis.
70 ersisted up to 1 year after the induction of epileptogenesis.
71 43 in the brain and serum over the course of epileptogenesis.
72 the acute and latent phase of injury-induced epileptogenesis.
73 abolites may be able to serve as a marker of epileptogenesis.
74 ol for identifying brain inflammation during epileptogenesis.
75 es to hippocampal dendrites that may promote epileptogenesis.
76 e an epileptogenic brain insult can mitigate epileptogenesis.
77 hippocampal culture model of post-traumatic epileptogenesis.
78 nto the role of microglial activation during epileptogenesis.
79 tatory neurotransmission plays a key role in epileptogenesis.
80 e gyrus, potentially mediating temporal lobe epileptogenesis.
81 tion-dependent neuronal plasticity including epileptogenesis.
82 astrogliosis is a cause or a consequence of epileptogenesis.
83 p, may be proposed as putative biomarkers of epileptogenesis.
84 th, in older animals may augment TBI-induced epileptogenesis.
85 signaling cascade reduces the probability of epileptogenesis.
86 and triggers neuronal hyperexcitability and epileptogenesis.
87 ppocampal CA3 neurons, a classical focus for epileptogenesis.
88 eptors in provoking seizures and in kindling epileptogenesis.
89 igger of inflammatory cascades implicated in epileptogenesis.
90 tes by serum-derived albumin, is involved in epileptogenesis.
91 le of facilitated NMDA receptor signaling in epileptogenesis.
92 hat HIF-1alpha is an important factor during epileptogenesis.
93 us, and to explore their relationship during epileptogenesis.
94 her allergic inflammation contributes toward epileptogenesis.
95 nd has also been implicated in temporal lobe epileptogenesis.
96 mpus and exhibit neuroplastic changes during epileptogenesis.
97 ences of increased protein synthesis in FXS, epileptogenesis.
98 ority of restructuring in the dentate during epileptogenesis.
99 (TrkB) is thought to be critical for limbic epileptogenesis.
100 t these excitatory synapses that may promote epileptogenesis.
101 vals and a poor measure of the time frame of epileptogenesis, (2) epileptogenesis is a continuous pro
102 in mice, indicating that the drug slows down epileptogenesis, a finding deserving further investigati
103 lts suggest GAP-43 as a key factor promoting epileptogenesis, a possible therapeutic target for treat
104 riod may serve as a diagnostic biomarker for epileptogenesis, able to predict the future onset of spo
105 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
108 bitory synapses, and the critical period for epileptogenesis after head injury has been better define
110 s utility to delineate mechanisms underlying epileptogenesis after pediatric brain injury, and provid
111 lp develop therapeutic strategies to prevent epileptogenesis after stroke and elucidate some of the m
112 izures develop is critical for understanding epileptogenesis, an understanding of how and why recurre
113 ion of the adenosine system is implicated in epileptogenesis and cell therapies have been developed t
114 abolism in rat plasma and hippocampus during epileptogenesis and chronic epilepsy in the kainic acid
115 nts and determine the latency to hippocampal epileptogenesis and clinical epilepsy, we developed an e
116 EGCs that develop after SE may contribute to epileptogenesis and cognitive impairments that follow SE
117 zure duration as an important determinant in epileptogenesis and defining the predictive roles of int
118 ovel insights into the mechanisms underlying epileptogenesis and discover potential preventive treatm
120 MGB1 isoforms are mechanistic biomarkers for epileptogenesis and drug-resistant epilepsy in humans, n
121 leptic brain and as a potential biomarker of epileptogenesis and epileptogenicity and for presurgical
122 chmarks is to develop reliable biomarkers of epileptogenesis and epileptogenicity that could revoluti
123 gest an important role of innate immunity in epileptogenesis and focus on glial inhibition, through p
124 l studies of basic mechanisms of spontaneous epileptogenesis and for preclinical screening of effecti
125 k clinically relevant noninvasive markers of epileptogenesis and found that reduced amygdala T2 relax
128 BDNF expression, only a modest impairment of epileptogenesis and increased hippocampal TrkB activatio
129 ulation of the endocannabinoid system during epileptogenesis and indicates that the CB(1) receptor re
130 d may be associated with both the process of epileptogenesis and maintenance of the epileptic state.
131 for understanding the mechanisms underlying epileptogenesis and may provide insights into why sponta
132 rks in MTLE may improve the understanding of epileptogenesis and neuropsychological impairments assoc
133 has in turn enriched our knowledge of human epileptogenesis and normal brain development and functio
135 ibute to network alterations associated with epileptogenesis and offers a useful strategy for identif
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 ts receptor, TrkB, in the hippocampus during epileptogenesis and that BDNF-mediated activation of Trk
142 he data that support the concepts underlying epileptogenesis and the model systems that are presumed
143 pathway has been implicated in mechanisms of epileptogenesis and the mTORC1 inhibitor, rapamycin, has
144 Ca(2+)](i) remained markedly elevated during epileptogenesis and was still elevated indefinitely in t
145 ver 600 were regulated during development or epileptogenesis, and 37 of these were either upregulated
146 urons also were altered in the brain-injury, epileptogenesis, and chronic-epilepsy phases of AE.
149 s in synaptic function and formation play in epileptogenesis, and further illustrate just how closely
150 d our understanding of circuit mechanisms of epileptogenesis, and have potential implications for the
151 age (MRI) provided predictive biomarkers for epileptogenesis, and if the inflammatory mediator interl
152 ycin (mTOR) signaling pathway is involved in epileptogenesis, and mTOR inhibitors prevent epilepsy in
153 old for status epilepticus (SE), accelerated epileptogenesis, and once epilepsy was induced, depressi
155 leptic drugs are not effective in preventing epileptogenesis; antiepileptic drugs were, however, not
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 Deficits in KCC2 activity are implicated in epileptogenesis, but how increased neuronal activity lea
168 ing that peri-insult generated cells mediate epileptogenesis, but that seizures per se are initiated
169 e BDNF receptor, TrkB, is critical to limbic epileptogenesis, but the responsible downstream signalin
170 B (trkB) receptor activation promotes limbic epileptogenesis, but whether or where trkB activation oc
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
176 ro preparations, during early post-traumatic epileptogenesis demonstrated rapid increases in the frac
178 yer recording determined whether hippocampal epileptogenesis develops immediately or long after injur
180 these findings to the general mechanisms of epileptogenesis during development and points out gaps i
182 critical role for AMPA receptors (AMPARs) in epileptogenesis during this critical period in the devel
183 HFOs can be used as a reliable biomarker for epileptogenesis, epileptogenicity, and the delineation o
184 mmature granule cells exposed to pilocarpine-epileptogenesis exhibited aberrant hilar basal dendrites
185 utamate receptor (mGluR) stimulation include epileptogenesis, expressed in vitro as the conversion of
186 he specific subunit Kv3.4 is affected during epileptogenesis following pilocarpine-induced status epi
187 icographic or intrahippocampal recordings of epileptogenesis (from the insult to the first spontaneou
189 addressed the role of TGF-beta signaling in epileptogenesis in 2 different rat models of vascular in
190 we studied the properties of the TBI-induced epileptogenesis in a biophysically realistic cortical ne
193 se oscillations occur in the early stages of epileptogenesis in areas adjacent to the brain lesion an
196 expression and hippocampal apoptosis during epileptogenesis in comparison with the positive control.
206 of metabolic genes in the hippocampus during epileptogenesis in male rats in the pilocarpine model of
210 sed several forms of seizure sensitivity and epileptogenesis in rats selectively bred for vulnerabili
217 oforms, exhibited an increased resistance to epileptogenesis in the hippocampus and amygdala kindling
220 e that mTOR signaling mediates mechanisms of epileptogenesis in the kainate rat model and that mTOR i
222 by Nav beta1 contributes to the mechanism of epileptogenesis in these animals as well as in patients.
223 n intact model of epilepsy and indicate that epileptogenesis in this model produced long-lasting alte
225 nabling even short RE cell bursts to promote epileptogenesis in two ways: first, by activating GABA(B
228 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
236 re of the time frame of epileptogenesis, (2) epileptogenesis is a continuous process that extends muc
237 ical conditions, and one prominent theory of epileptogenesis is based on the assumption that mossy ce
238 Understanding molecular mechanisms mediating epileptogenesis is critical for developing more effectiv
240 me course of fluid percussion injury-induced epileptogenesis is dramatically biased by the definition
252 table to the complex alterations involved in epileptogenesis, it is likely that multitargeted approac
253 scence microscopy during the injury (acute), epileptogenesis (latency), and chronic-epilepsy phases o
257 s in vitro model of glutamate injury-induced epileptogenesis may help develop therapeutic strategies
260 ase in h channels during a critical phase of epileptogenesis mechanistically underlies dendritic hype
263 s recurrent seizures and could contribute to epileptogenesis or development of the epileptic state.
264 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
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
278 d from IL-6 -: treated mice show that during epileptogenesis, the cells respond to repetitive orthodr
279 ptic plasticity (HSP) mediates posttraumatic epileptogenesis through unbalanced synaptic scaling, par
280 onal model to relate changes observed during epileptogenesis to a decreased tendency to burst in the
284 ltered gene expression and thus may underlie epileptogenesis via induction of permanent changes in ne
289 addition, changes in theta band power during epileptogenesis were associated with altered locomotor a
291 s as crucial mediators in the development of epileptogenesis, which is the process whereby a normal b
292 gests that impaired autophagy contributes to epileptogenesis, which may be of interest as a potential
293 ys of understanding the molecular pathway of epileptogenesis, widening the spectrum of possible thera
294 ats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neu
295 he repeated flurothyl paradigm is a model of epileptogenesis with spontaneous seizures that remit.
296 tic animals at 1 year after the induction of epileptogenesis with two different fluorescent dyes (Fur
298 ate the molecular and cellular mechanisms of epileptogenesis without any complication from drug-induc
300 synchronous burst firing is associated with epileptogenesis, yet the evidence from human studies lin
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