gamma-aminobutyric acid has been researched along with Cerebral Cortical Dysplasia in 15 studies
gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.
gamma-aminobutyric acid : A gamma-amino acid that is butanoic acid with the amino substituent located at C-4.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Abnormalities in the gamma-aminobutyric acid (GABA)-ergic system could be responsible for seizures in cortical dysplasia (CD)." | 3.74 | Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasia. ( André, VM; Cepeda, C; Huynh, M; Levine, MS; Mathern, GW; Vinters, HV, 2008) |
| "Focal cortical dysplasia (FCD) is a major cause of drug-resistant epilepsy; however the underlying epileptogenic mechanisms of FCD metabolism in epilepsy patients remain unclear." | 1.62 | Focal corticarl dysplasia in epilepsy is associated with GABA increase. ( Chen, Y; Gong, T; Lin, L; Lin, Y; Liu, Y; Wang, G, 2021) |
| "Focal cortical dysplasias (FCDs) are frequently associated with the medical refractory epilepsy in both children and adults." | 1.42 | Increased expression of TRPC5 in cortical lesions of the focal cortical dysplasia. ( Guo, W; Shu, HF; Xu, GZ; Yang, H; Yue, HY; Zheng, DH, 2015) |
| "Gabapentin has been shown to disrupt the interaction of thrombospondin (TSP) with α2δ-1, an auxiliary calcium channel subunit." | 1.40 | Gabapentin attenuates hyperexcitability in the freeze-lesion model of developmental cortical malformation. ( Andresen, L; Dulla, CG; Hampton, D; Maguire, J; Morel, L; Taylor-Weiner, A; Yang, Y, 2014) |
| "Focal cortical dysplasia (FCD), which is characterized histologically by disorganized cortical lamination and large abnormal cells, is one of the major causes of intractable epilepsies." | 1.37 | KCC2 was downregulated in small neurons localized in epileptogenic human focal cortical dysplasia. ( Fujiwara, T; Fukuda, A; Inoue, Y; Matsuda, K; Mihara, T; Okabe, A; Sato, K; Shimizu-Okabe, C; Tanaka, M; Yagi, K, 2011) |
| "In human patients, cortical dysplasia produced by Doublecortin (DCX) mutations lead to mental retardation and intractable infantile epilepsies, but the underlying mechanisms are not known." | 1.35 | Abnormal network activity in a targeted genetic model of human double cortex. ( Ackman, JB; Aniksztejn, L; Becq, H; Ben-Ari, Y; Cardoso, C; Crépel, V; Pellegrino, C; Represa, A, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 3 (20.00) | 29.6817 |
| 2010's | 11 (73.33) | 24.3611 |
| 2020's | 1 (6.67) | 2.80 |
| Authors | Studies |
|---|---|
| Gong, T | 1 |
| Liu, Y | 1 |
| Chen, Y | 1 |
| Lin, L | 1 |
| Lin, Y | 1 |
| Wang, G | 1 |
| Blauwblomme, T | 1 |
| Dossi, E | 1 |
| Pellegrino, C | 2 |
| Goubert, E | 1 |
| Iglesias, BG | 1 |
| Sainte-Rose, C | 1 |
| Rouach, N | 1 |
| Nabbout, R | 1 |
| Huberfeld, G | 1 |
| Fukuda, A | 3 |
| Wang, T | 2 |
| Xu, GZ | 1 |
| Shu, HF | 1 |
| Yue, HY | 1 |
| Zheng, DH | 1 |
| Guo, W | 1 |
| Yang, H | 1 |
| Andresen, L | 1 |
| Hampton, D | 1 |
| Taylor-Weiner, A | 1 |
| Morel, L | 1 |
| Yang, Y | 1 |
| Maguire, J | 1 |
| Dulla, CG | 1 |
| Medici, V | 1 |
| Rossini, L | 1 |
| Deleo, F | 1 |
| Tringali, G | 1 |
| Tassi, L | 1 |
| Cardinale, F | 1 |
| Bramerio, M | 1 |
| de Curtis, M | 1 |
| Garbelli, R | 1 |
| Spreafico, R | 2 |
| André, VM | 2 |
| Cepeda, C | 2 |
| Vinters, HV | 2 |
| Huynh, M | 2 |
| Mathern, GW | 2 |
| Levine, MS | 2 |
| Ackman, JB | 1 |
| Aniksztejn, L | 1 |
| Crépel, V | 1 |
| Becq, H | 1 |
| Cardoso, C | 1 |
| Ben-Ari, Y | 1 |
| Represa, A | 1 |
| Zhou, FW | 1 |
| Roper, SN | 1 |
| Shimizu-Okabe, C | 1 |
| Tanaka, M | 1 |
| Matsuda, K | 1 |
| Mihara, T | 1 |
| Okabe, A | 1 |
| Sato, K | 1 |
| Inoue, Y | 1 |
| Fujiwara, T | 1 |
| Yagi, K | 1 |
| Mori, T | 1 |
| Mori, K | 1 |
| Fujii, E | 1 |
| Toda, Y | 1 |
| Miyazaki, M | 1 |
| Harada, M | 1 |
| Kagami, S | 1 |
| Sakakibara, T | 1 |
| Sukigara, S | 1 |
| Otsuki, T | 1 |
| Takahashi, A | 1 |
| Kaneko, Y | 1 |
| Kaido, T | 1 |
| Saito, Y | 1 |
| Sato, N | 1 |
| Nakagawa, E | 1 |
| Sugai, K | 1 |
| Sasaki, M | 1 |
| Goto, Y | 1 |
| Itoh, M | 1 |
| Kumada, T | 1 |
| Morishima, T | 1 |
| Iwata, S | 1 |
| Kaneko, T | 1 |
| Yanagawa, Y | 1 |
| Yoshida, S | 1 |
| Moroni, RF | 1 |
| Inverardi, F | 1 |
| Regondi, MC | 1 |
| Panzica, F | 1 |
| Frassoni, C | 1 |
15 other studies available for gamma-aminobutyric acid and Cerebral Cortical Dysplasia
| Article | Year |
|---|---|
Focal corticarl dysplasia in epilepsy is associated with GABA increase.
Topics: Epilepsy; Female; gamma-Aminobutyric Acid; Glutathione; Humans; Magnetic Resonance Imaging; Malforma | 2021 |
Gamma-aminobutyric acidergic transmission underlies interictal epileptogenicity in pediatric focal cortical dysplasia.
Topics: Adolescent; Cerebral Cortex; Child; Child, Preschool; Electroencephalography; Epilepsies, Partial; F | 2019 |
A perturbation of multimodal GABA functions underlying the formation of focal cortical malformations: assessments by using animal models.
Topics: Animals; Cerebral Cortex; Disease Models, Animal; gamma-Aminobutyric Acid; Malformations of Cortical | 2013 |
Increased expression of TRPC5 in cortical lesions of the focal cortical dysplasia.
Topics: Case-Control Studies; Cerebral Cortex; Child; Child, Preschool; Female; GABAergic Neurons; gamma-Ami | 2015 |
Gabapentin attenuates hyperexcitability in the freeze-lesion model of developmental cortical malformation.
Topics: Age Factors; Amines; Animals; Animals, Newborn; Anticonvulsants; Calcium Channels; Cyclohexanecarbox | 2014 |
Different parvalbumin and GABA expression in human epileptogenic focal cortical dysplasia.
Topics: Adolescent; Adult; Brain; Cell Count; Child, Preschool; Epilepsy; Female; gamma-Aminobutyric Acid; G | 2016 |
Pyramidal cell responses to gamma-aminobutyric acid differ in type I and type II cortical dysplasia.
Topics: Cells, Cultured; Child; Child, Preschool; Female; Fluorescent Antibody Technique; GABA Agonists; gam | 2008 |
Abnormal network activity in a targeted genetic model of human double cortex.
Topics: Analysis of Variance; Animals; Animals, Genetically Modified; Animals, Newborn; Bicuculline; Cerebra | 2009 |
Densities of glutamatergic and GABAergic presynaptic terminals are altered in experimental cortical dysplasia.
Topics: Analysis of Variance; Animals; Animals, Newborn; Cerebral Cortex; Disease Models, Animal; Embryo, Ma | 2010 |
Interneurons, GABAA currents, and subunit composition of the GABAA receptor in type I and type II cortical dysplasia.
Topics: Child; gamma-Aminobutyric Acid; Humans; Interneurons; Malformations of Cortical Development; Neocort | 2010 |
KCC2 was downregulated in small neurons localized in epileptogenic human focal cortical dysplasia.
Topics: Adult; Child; Chlorides; Down-Regulation; Drug Resistance; Epilepsy; Female; gamma-Aminobutyric Acid | 2011 |
Neuroradiological and neurofunctional examinations for patients with 22q11.2 deletion.
Topics: Case-Control Studies; Child; Child, Preschool; DiGeorge Syndrome; Electroencephalography; Epilepsy; | 2011 |
Imbalance of interneuron distribution between neocortex and basal ganglia: consideration of epileptogenesis of focal cortical dysplasia.
Topics: Adolescent; Brain Diseases; Calbindin 2; Calbindins; Case-Control Studies; Caudate Nucleus; Cell Cou | 2012 |
Accumulation of GABAergic neurons, causing a focal ambient GABA gradient, and downregulation of KCC2 are induced during microgyrus formation in a mouse model of polymicrogyria.
Topics: Age Factors; Animals; Animals, Newborn; Bicuculline; Cell Count; Cerebral Cortex; Disease Models, An | 2014 |
Altered spatial distribution of PV-cortical cells and dysmorphic neurons in the somatosensory cortex of BCNU-treated rat model of cortical dysplasia.
Topics: Animals; Animals, Newborn; Antibodies; Calbindins; Carmustine; Classical Lissencephalies and Subcort | 2008 |