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Editorial

Schizophrenia and the Epigenetic Hypothesis

Pages 341-344 | Published online: 02 Jun 2010

Figures & data

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.

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.

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