Abstract
Glutamatergic abnormalities are commonly observed in schizophrenia (SZ) and are hypothesized to play an important role in cognitive dysfunction. While the contribution of postsynaptic glutamate receptors to SZ psychopathology has been extensively examined, less is known about the role played by enzymes involved in glutamate metabolism and homeostasis. We examined mice with a brain-wide deficit in the glutamate metabolizing enzyme glutamate dehydrogenase (GDH), encoded by Glud1, which leads to glutamate excess due to reduced glutamate metabolism in astrocytes.
| Original language | English |
|---|---|
| Pages (from-to) | S124 |
| Number of pages | 1 |
| Journal | Schizophrenia Bulletin |
| Volume | 45 |
| Issue number | Suppl 2 |
| DOIs | |
| State | Published - Apr 2019 |
Bibliographical note
Congress of the Schizophrenia-International-Research-Society (SRIS), Orlando, FL, APR 10-14, 2019Fingerprint
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