[1] |
Darrah SD,Miller MA,Ren D, et al. Genetic variability in glutamic acid decarboxylase genes: associations with post-traumatic seizures after severe TBI[J]. Epilepsy Res, 2013, 103(2-3): 180-194.
|
[2] |
Rao VR,Parko KL. Clinical approach to posttraumatic epilepsy[J]. Semin Neurol, 2015, 35(1): 57-63.
|
[3] |
Irimia A,Van Horn JD. Epileptogenic focus localization in treatment-resistant post-traumatic epilepsy[J]. J Clin Neurosci, 2015, 22(4): 627-631.
|
[4] |
Talos DM,Sun H,Kosaras B, et al. Altered inhibition in tuberous sclerosis and type IIb cortical dysplasia[J]. Ann Neurol, 2012, 71(4): 539-551.
|
[5] |
Kim JY,Liu CY,Zhang F, et al. Interplay between DISC1 and GABA signaling regulates neurogenesis in mice and risk for schizophrenia[J]. Cell, 2012, 148(5): 1051-1064.
|
[6] |
Hunt RF,Boychuk JA,Smith BN. Neural circuit mechanisms of post-traumatic epilepsy[J]. Front Cell Neurosci, 2013, 7: 89.
|
[7] |
Berdichevsky Y,Dryer AM,Saponjian Y, et al. PI3K-Akt signaling activates mTOR-mediated epileptogenesis in organotypic hippocampal culture model of post-traumatic epilepsy[J]. J Neurosci, 2013, 33(21): 9056-9067.
|
[8] |
Orlova KA,Tsai V,Baybis M, et al. Early progenitor cell marker expression distinguishes type II from type I focal cortical dysplasias[J]. J Neuropathol Exp Neurol, 2010, 69(8): 850-863.
|
[9] |
Wu C,Sun D. GABA receptors in brain development, function, and injury[J]. Metab Brain Dis, 2015, 30(2): 367-379.
|
[10] |
Rice A,Rafiq A,Shapiro SM, et al. Long-lasting reduction of inhibitory function and GABA A subunit mRNA expression in a model of temporal lobe epilepsy[J]. Proc Natl Acad Sci USA, 1996, 93(18): 9665-9669.
|
[11] |
Lakhani R,Vogel K R,Till A, et al. Defects in GABA metabolism affect selective autophagy pathways and are alleviated by mTOR inhibition[J]. EMBO Mol Med, 2014, 6(4): 551-566.
|
[12] |
Kalkman HO. Alterations in the expression of neuronal chloride transporters may contribute to schizophrenia[J]. Prog Neuropsycho- pharmacol Biol Psychiatry, 2011, 35(2): 410-414
|
[13] |
Hyde TM,Lipska BK,Ali T, et al. Expression of GABA signaling molecules KCC2, NKCC1, and GAD1 in cortical development and schizophrenia[J]. J Neurosci, 2011, 31(30): 11088-11095.
|
[14] |
Loscher W,Puskarjov M,Kaila K. Cation-chloride cotransporters NKCC1 and KCC2 as potential targets for novel antiepileptic and antiepileptogenic treatments[J]. Neuropharmacology, 2013, 69: 62-74.
|
[15] |
Wang F,Wang X,Shapiro LA, et al. NKCC1 up-regulation contributes to early post-traumatic seizures and increased post-traumatic seizure susceptibility[J]. Brain Struct Funct, 2016, 222(3): 1543-1556.
|
[16] |
Schwarzbach E,Bonislawski DP,Xiong G, et al. Mechanisms underlying the inability to induce area CA1 LTP in the mouse after traumatic brain injury[J]. Hippocampus, 2006, 16(6): 541-550.
|
[17] |
Wu H,Shao A,Zhao M, et al. Melatonin attenuates neuronal apoptosis through up-regulation of K(+) -Cl(-) cotransporter KCC2 expression following traumatic brain injury in rats[J]. J Pineal Res, 2016, 61(2): 241-250.
|
[18] |
Butler CR,Boychuk JA,Smith BN. Differential effects of rapamycin treatment on tonic and phasic GABAergic inhibition in dentate granule cells after focal brain injury in mice[J]. Exp Neurol, 2016, 280: 30-40.
|
[19] |
Zeng LH,Rensing NR,Wong M. The mammalian target of rapamycin (mTOR) signaling pathway mediates epileptogenesis in a model of temporal lobe epilepsy[J]. J Neurosci, 2009, 29(21): 6964-6972.
|