Topic: GABAB receptor

The G-protein coupled receptor GABAB is an important regulator of presynaptic neurotransmitter release and postsynaptic excitability. In anti-GABABR autoimmune encephalitis pathogenic autoantibodies (aAB) target the GABAB receptor, leading to various symptoms, including epilepsy, cognitive disorders, and short-term memory loss. Here we aimed at evaluating the influence of these aAB on hippocampal-dependent cognitive and epileptic pathways. We used purified patient-derived antibodies (control- and anti-GABABR-IgG) in a chronic mouse model of the disease to evaluate the memory formation via Nove

GABAB receptor (GBR) activation inhibits neurotransmitter release in axon terminals in the brain, except in medial habenula (MHb) terminals, which show robust potentiation. However, mechanisms underlying this enigmatic potentiation remain elusive. Here, we report that GBR activation on MHb terminals induces an activity-dependent transition from a facilitating, tonic to a depressing, phasic neurotransmitter release mode. This transition is accompanied by a 4.1-fold increase in readily releasable vesicle pool (RRP) size and a 3.5-fold increase of docked synaptic vesicles at the presynaptic activ

In the dentate gyrus (DG), granule cells (GCs) and local interneurons transform dense cortical neuron ensemble theta/gamma band activity into sparse DG output to generate contextual representations. GABAB receptor-mediated inhibition contributes to sparse DG activity, but it is unclear how it contributes to frequency-dependent synaptic integration and spike output. We recorded perforant-path excitatory postsynaptic potentials from GCs in ventral horizontal slices from adult male and female mice and found GABAB-receptor dependent inhibition of action potential firing during gamma frequency trai