Topic: excitatory postsynaptic currents

Autism Spectrum Disorder (ASD) is characterized mainly by social and sensory-motor abnormal and repetitive behavior patterns. Over hundreds of genes and thousands of genetic variants were reported to be highly penetrant and causative of ASD. Many of these mutations cause comorbidities such as epilepsy and intellectual disabilities (ID). In this study, we measured cortical neurons derived from induced pluripotent stem cells (iPSCs) of patients with four mutations in the genes GRIN2B, SHANK3, UBTF, as well as chromosomal duplication in the 7q11.23 region and compared them to neurons derived from

N-methyl-D-aspartate receptor (NMDAR) is a glutamate-gated ion channel permeable to calcium that plays critical roles in synaptic transmission, synaptogenesis, and plasticity. Recent sequencing data in neurological and psychiatric patients reveal numerous variants in genes encoding NMDAR subunits. In our study, we have created and evaluated a transgenic mouse line carrying a frameshift variant (Grin2b L825FfsX4) resulting in the deletion of about half of the GluN2B subunit. Our methods included patch-clamp recordings from hippocampal neurons in both wild-type (Grin2bWT/WT) and transgenic (Grin

Hypoinsulinemia is a pathological consequence of diabetes mellitus that can stimulate the development of neurodegenerative processes in the brain due to dysfunction of insulin signaling cascades into neurons and impaired synaptic plasticity properties. We used the whole-cell patch-clamp recording of evoked glutamatergic excitatory postsynaptic currents (eEPSCs) with the local stimulation of presynaptic axon to investigate the insulin (100 nM) effect on the paired-pulse plasticity at cultured hippocampal neurons under hypoinsulinemia (4 days insulin-free media incubation).At control normoinsuli