Jan Fredrik Kismul

AMPAR α $$ \alpha $$ -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor ACC Anterior cingulate cortex AUC Area under curve EEG Electroencephalogram EEG Electroencephalogram ERP Event-related potential GABAR γ $$ \gamma $$ -aminobutyric acid IAF Integrate-and-fire MMN Mismatch negativity NMDAR N-methyl-D-aspartate receptor PFC Prefrontal cortex SCZ Schizophrenia STDP Spike-timing dependent plasticity SSA Stimulus-specific adaptation Population abbreviations ES Excitatory,...

Discussion Here, we developed a biochemically detailed model of GABABRs and their effects on neuronal excitability through their Giβγ-mediated interactions with GIRK channels and VGCCs. Our model has two important advances compared to existing models. Firstly, the model describes the GABABR and Giβγ activity in both pre- and postsynaptic terminals.

Abstract GABAB receptors (GABABRs) are an important building block in neural activity. Despite their widely hypothesized role in many basic neuronal functions and mental disorder symptomatology, there is a lack of biophysically and biochemically detailed models of these receptors and the way they mediate neuronal inhibition.