Fig. 5. Proposed mechanism of action of astrocytic GABA in regulation of PP to DG granule neuron synaptic transmission. Under normal conditions, GABA from astrocytes located in the molecular layer of DG, targets GABAB receptors on axonal terminals of hilar interneurons that project onto the proximal dendritic and the perisomatic regions of granule neurons. Activation of the interneuronal GABAB results in a decrease in transmitter release at interneuron to granule neuron synapse and hence disinhibits the granule neuron activity. In diseased DG of APP/PS1 mice, reactive astrocytes in molecular layer of DG have aberrantly elevated production and rates of release of GABA. This GABA activates GABAA receptors on PP to DG granule neuron terminals and reduces release probability in PP to granule neuron synapse, thus inhibiting PP to DG granule neuron synaptic transmission. IN, hillar interneuron; GN, granule neuron; Aβ, beta-amyloid.
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