Figures & data
GABAergic interneurons function to modulate the output of pyramidal and other neurons. We propose that reduced expression of glutamate decarboxylase 1 and other GABAergic markers (SST, NPY, CCK, CB1, PV, GAT1 and reelin) along with reduced levels of NR1 and NR2A (shown by a sphere) containing glutamate receptors contributes to reduced GABA release (shown by a down arrow). This GABA hypofunction causes decreased pyramidal neuron synchronization. The model proposes that the reduced signaling at NMDA-selective glutamate receptors present on GABAergic interneurons causes the glutmatergic hypofunction, which then facilitates reduced GABA release onto the main output neurons (pyramidal neurons).
CB: Calbindin; CCK: Cholecystokinin; GAT: GABA transporter; NPY: Neuropeptide Y; NR: NMDA receptor; PV: Parvalbumin; SST: Somatostatin.
![Figure 1. Phenotypically distinct neurons reside in different cortical layers.GABAergic interneurons function to modulate the output of pyramidal and other neurons. We propose that reduced expression of glutamate decarboxylase 1 and other GABAergic markers (SST, NPY, CCK, CB1, PV, GAT1 and reelin) along with reduced levels of NR1 and NR2A (shown by a sphere) containing glutamate receptors contributes to reduced GABA release (shown by a down arrow). This GABA hypofunction causes decreased pyramidal neuron synchronization. The model proposes that the reduced signaling at NMDA-selective glutamate receptors present on GABAergic interneurons causes the glutmatergic hypofunction, which then facilitates reduced GABA release onto the main output neurons (pyramidal neurons).CB: Calbindin; CCK: Cholecystokinin; GAT: GABA transporter; NPY: Neuropeptide Y; NR: NMDA receptor; PV: Parvalbumin; SST: Somatostatin.](/cms/asset/eac69ef8-1b80-4646-b385-9e67e34a5568/iepi_a_12324566_f0001.jpg)