Skip to main content
. Author manuscript; available in PMC: 2019 Dec 14.
Published in final edited form as: Mol Psychiatry. 2019 Apr 12;25(1):131–147. doi: 10.1038/s41380-019-0414-4

Figure 3: Simplified Model of the Putative Psychosis-Inducing Effects of Kynurenic Acid.

Figure 3:

Cortical GABAergic interneurons normally exert an inhibitory tone on glutamatergic pyramidal neurons that project to the ventral tegmental area (VTA) and modulate dopaminergic neurotransmission. Excess kynurenic acid production by astrocytes may cause NMDA receptor hypofunction on cortical GABA interneurons leading to reductions in GABAergic neurotransmission and the disinhibition of cortical glutamate projections. Theoretically, this abnormally increased glutamatergic activity causes overactivation of the mesolimbic DA pathway and the excessive release of dopamine in the ventral striatum, ultimately leading to the development of psychosis.