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mGlu potentiation enhances prelimbic somatostatin interneuron activity to rescue schizophrenia-like physiological and cognitive deficits.
Cell Rep
November 2021
Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA; Warren Center for Neuroscience Drug Discovery, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Kennedy Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Institute for Chemical Biology, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37232, USA. Electronic address:
Evidence for prefrontal cortical (PFC) GABAergic dysfunction is one of the most consistent findings in schizophrenia and may contribute to cognitive deficits. Recent studies suggest that the mGlu subtype of metabotropic glutamate receptor regulates cortical inhibition; however, understanding the mechanisms through which mGlu positive allosteric modulators (PAMs) regulate PFC microcircuit function and cognition is essential for advancing these potential therapeutics toward the clinic. We report a series of electrophysiology, optogenetic, pharmacological magnetic resonance imaging, and animal behavior studies demonstrating that activation of mGlu receptors increases inhibitory transmission in the prelimbic PFC by selective excitation of somatostatin-expressing interneurons (SST-INs).
View Article and Find Full Text PDFEffortful goal-directed behavior in schizophrenia: Computational subtypes and associations with cognition.
J Abnorm Psychol
October 2019
Department of Psychology.
Schizophrenia is associated with amotivation and reduced goal-directed behavior, which have been linked to poor functional outcomes. Motivational deficits in schizophrenia are often measured using effort-based decision-making (EBDM) paradigms, revealing consistent alterations in effort expenditure relative to controls. Although these results have generally been interpreted in terms of decreased motivation, the ability to use trial-by-trial changes in reward magnitude or probability of receipt to guide effort allocation may also be affected by cognitive deficits.
View Article and Find Full Text PDFPick Your Model Wisely: Understanding the Negative Symptoms of Schizophrenia in Rodent Models.
ACS Chem Neurosci
January 2019
Department of Pharmacology , Vanderbilt University, Nashville , Tennessee 37232 , United States.
While the negative symptoms comprise one of the cardinal symptom domains of schizophrenia, there are numerous deficits that are included in this category of symptoms. Therefore, when modeling negative symptoms preclinically, it is important to consider which symptom is being modeled by a specific assay and to try to gain an understanding of the translational value of the findings. It is hoped that enhancing the translational value of animal models will allow for better treatment outcomes for the negative symptoms of schizophrenia in the future.
View Article and Find Full Text PDFAssociation of schizophrenia polygenic risk score with manic and depressive psychosis in bipolar disorder.
Transl Psychiatry
September 2018
Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA.
Bipolar disorder (BD) is highly heterogeneous in symptomatology. Narrowing the clinical phenotype may increase the power to identify risk genes that contribute to particular BD subtypes. This study was designed to test the hypothesis that genetic overlap between schizophrenia (SZ) and BD is higher for BD with a history of manic psychosis.
View Article and Find Full Text PDFEvidence that COMT genotype and proline interact on negative-symptom outcomes in schizophrenia and bipolar disorder.
Transl Psychiatry
September 2016
Department of Psychiatry, New York University School of Medicine, New York, NY, USA.
Elevated peripheral proline is associated with psychiatric disorders, and there is evidence that proline is a neuromodulator. The proline dehydrogenase (PRODH) gene, which encodes the enzyme that catalyzes proline catabolism, maps to human chromosome 22q11.2, a region conferring risk of schizophrenia.
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