Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4934947 | Schizophrenia Research | 2017 | 6 Pages |
Abstract
A goal of current schizophrenia (SZ) research is to understand how multiple risk genes work together with environmental factors to produce the disease. In schizophrenia, there is elevated delta frequency EEG power in the awake state, an elevation that can be mimicked in rodents by N-methyl-d-aspartate receptor (NMDAR) antagonist action in the thalamus. This thalamic delta can be blocked by dopamine D2 receptor antagonists, agents known to be therapeutic in SZ. Experiments suggest that these oscillations can interfere with brain function and may thus be causal in producing psychosis. Here we evaluate the question of whether well-established schizophrenia risk genes may interact to affect the delta generation process. We identify 19 risk genes that can plausibly work in a synergistic fashion to generate delta oscillations.
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Behavioral Neuroscience
Authors
Edwin A. Richard, Elizaveta Khlestova, Roshan Nanu, John E. Lisman,