Dlg4 and Vamp2 are involved in comorbid epilepsy and attention-deficit hyperactivity disorder: A microarray data study.

OBJECTIVE: Children with epilepsy exhibit a significantly higher risk for attention-deficit hyperactivity disorder (ADHD), which is often associated with lower quality of life. In this study, we aimed to identify molecular mechanisms associated with both epilepsy and ADHD. MATERIALS AND METHODS: Gene expression profiles of GSE12457 and GSE47752 were downloaded from the gene expression omnibus (GEO) database. Differentially expressed genes (DEGs) were separately screened in epilepsy and ADHD samples and compared with controls. Weighted gene coexpression network analysis (WGCNA) was used to identify candidate modules associated with the two disorders. Functional annotation and analysis of hub genes and molecular complex detection (MCODE) was also performed. RESULTS: Three modules closely related to epilepsy and ADHD were screened using WGCNA; DEGs in this module were involved in the synaptic vesicle cycle, axon and neuron regeneration, and neurotransmission. The Dlg4 and Vamp2 genes were selected as common candidate factors in epilepsy and ADHD pathogenesis. CONCLUSION: Dlg4 and Vamp2 could play essential roles in comorbidity between epilepsy and ADHD.

Rapid identification of the short-lived intermediates in alternating-current electrolysis by mass spectrometry.

Herein, we report the rapid mass spectrometric identification of the short-lived intermediates generated under AC electrolysis via combining bipolar electrochemistry with nanoelectrospray ionization in a hybrid ultramicroelectrode/ion emitter. The key reactive intermediates involved in the C-O/O-H cross-metathesis between 4-alkoxy anilines and alcohols were successfully captured and identified for the first time, providing direct evidence for the previously proposed mechanism.

Recurrent seizures cause immature brain injury and changes in GABA a receptor α1 and γ2 subunits.

OBJECTIVE: Recurrent seizures can cause brain damage and affect the cognitive outcome, particularly in developing children. We aimed to determine the effects of recurrent seizures on the expression of gamma-aminobutyric acid A receptor (GABAAR) α1 and γ2 subunit and neurodevelopment in immature rats. The role of the GABAAR agonist clonazepam and antagonist/partial agonist flumazenil in seizure-induced brain injury was also studied. METHODS: Recurrent seizures (RS) were induced by flurothyl inhalation in immature rats. Clonazepam (CZP) and flumazenil (FMZ) were administered to modulate GABAAR subunit expression in different experimental groups. Neurobehavioral changes and GABAAR α1 and γ2 subunit expression were studied. RESULTS: Inhalation of flurothyl for five days triggered RS and caused reflex delay, inability to adapt to new environments in adulthood, and deficits in long-term learning and memory ability in rats. Down-regulation of GABAAR α1 and γ2 subunits occurred after seizure onset and persisted for a long time. CZP treatment decreased the expression of GABAAR α1 and γ2 subunits and delayed neurodevelopment of the immature rats, whereas FMZ did not show any significant effects. CONCLUSIONS: Changes in GABAAR α1 and γ2 subunit expression and neurodevelopment were related to recurrent seizures and administration of CZP. Thus, GABAAR α1 and γ2 subunits likely play a significant role in the development of immature rats with RS and provide a novel target for therapeutic intervention.