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In this issue
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- Article
- Abstract
- Introduction
- Genomic Variants in GRM5 and mGlu5 Receptor Hypofunction Are Associated with Schizophrenia
- mGlu5 Potentiators Reduce Behavioral Disruptions That Are Relevant for Schizophrenia in Rodent Models
- Biased mGlu5 Receptor PAMs That Do Not Potentiate Coupling of mGlu5 Receptors to NMDA Receptors or Exert Allosteric Agonist Activity Do Not Induce Observable Adverse Effects
- mGlu1 Receptor PAMs May Have Potential Antipsychotic Effects
- The mGlu1 Receptor Ligands Display Antipsychotic-Like Effects in Rodents
- Group II (mGlu2/3) Receptor Agonists Show Efficacy for Treating Behavioral Correlates of Schizophrenia
- Clinical Trials Using mGlu2/3 Receptor Agonists Yielded Inconclusive Results
- mGlu2 Receptor PAMs May Have Potential Antipsychotic Activity
- Genetic Variants in GRM3 Are Associated with Schizophrenia
- mGlu3 Receptor Is a Promising Target for Enhancing Cognition in Schizophrenia
- mGlu4 Receptor Ligands Have the Potential To Treat Positive Symptoms of Schizophrenia
- Potential Utility of mGlu2-mGlu4 Receptor Heterodimers As Novel Antipsychotics
- Deletion or Blockade of mGlu7 Receptor Impairs Cognition
- mGlu7 Receptor NAMs Can Rescue Schizophrenia-Like Symptoms in Rodents
- Deletion of GRM8 Does Not Induce Consistent Endophenotypes of Schizophrenia
- Concluding Remarks
- Authorship Contributions
- Footnotes
- Abbreviations
- References
- Info & Metrics
- eLetters
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