Topic: gamma-aminobutyric acid

Absence seizures are classified as genetic generalized seizures. They arise from abnormalities in corticothalamic networks evident as spike-wave discharges on electroencephalograms. Altered gamma-aminobutyric acid (GABA) neurotransmission is commonly reported in rodent models for absence seizures. However, the underlying causative mechanism for seizures at the cellular and molecular level is debated and appears multifactorial, which may account for the variable efficacy of antiepileptic drugs. Current drugs fail to suppress seizures in over 30% of children with absence epilepsy. Previously, we

【Aims】Epilepsy, a recurrent neurological disease with abnormal neurotransmitter kinetics in the brain, has emerged as a global health concern. The mechanism of epileptic seizures is thought to involve a relative imbalance between excitatory and inhibitory neurotransmitters. Despite the recent advances in clinical and basic research on the pathogenesis of epilepsy, the complex relationship between the neurotransmitter dynamics and behavior with and without antiepileptic drugs (AEDs) during seizures remains unclear. We aimed to investigate the dynamics of neurotransmitters during convulsive seiz

Although the neurobiological mechanisms underlying major depressive disorder (MDD) are not fully understood, accumulating evidence suggests an association between MDD and reduced levels of gamma-aminobutyric acid (GABA) in the brain. The present study used proton magnetic resonance spectroscopy (1H-MRS) with the Mescher-Garwood point-resolved spectroscopy sequence (MEGA-PRESS) to measure GABA levels in the pregenual anterior cingulate cortex (pgACC)/medial prefrontal cortex (MPFC). We also assessed resting-state functional connectivity using functional magnetic resonance imaging (rs-fMRI). Ana

Studies in animals and humans have shown that cortical neuroplasticity can be modulated by increasing serotonin levels by administering selective serotonin reuptake inhibitors (SSRI). However, little is known about the mechanistic background, especially the contribution of intracortical inhibition and facilitation, which depend on gamma-aminobutyric acid (GABA) and glutamate. We aimed to explore the relevance of drivers of plasticity (glutamate- and GABA-dependent processes) for the effects of serotonin enhancement on tDCS-induced plasticity in healthy humans. A crossover, partially double-bli

Vaccinia-related kinase 2 (VRK2) VRK2 is one of the serine/threonine kinases that was originally identified in highly proliferative cells such as thymocytes and fetal liver cells. GWAS studies were reported that VRK2 was related molecule with neuropsychiatric diseases. And in vitro studies reported that VRK2 plays an important role in cell division and cell cycle regulation. However, little is known about the molecular mechanism and physiological function of VRK2 on the central nervous systems in vivo. In this study, we established vrk2 deficient (VRK2 KO) zebrafish and found that VRK2 KO body