Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia.

By John E. Lisman, J. Coyle, R. W. Green, Daniel C. Javitt, F. Benes, Stephan Heckers, Anthony A. Grace. Trends in Neurosciences, 2008

1,044 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f1721eb92609fbc1a945e7a249c1fd4944f0d11f

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Citations in the corpus

Common circuit defect of excitatory-inhibitory balance in mouse models of autism (2009, neutral): “Decreased GABA signaling is now well-established in schizophrenia [66], which is seen not only as a reduction of GABA concentration and GAD67 in postmortem brain, but also as a restricted deficit of PV staining [67, 68].”
Computational psychiatry as a bridge from neuroscience to clinical applications (2016, background): “Reducing NMDA receptor density on inhibitory interneurons as found in schizophrenia 89 led to weaker and broader attractor states ( Fig.”
Interneuron dysfunction in psychiatric disorders (2012, background): “As the PV + interneuron class comprises basket and chandelier cells, this defect might reflect a perturbation of both perisomatic and axo-axonic inhibition of pyramidal neurons, as well as impairment of synchronization in the gamma rang”
Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, background): “However, there is substantial therapeutic potential in augmentation of NMDA receptor activity (Lisman et al., 2008).”
The Computational Anatomy of Psychosis (2013, background): “Stephan et al. (2009), Morrison (2012), Carlsson et al. (1999), Lisman et al. (2008), Simpson et al. (2010). other in numerous ways (Cepeda and Levine, 2006).”
Neurophysiological and Computational Principles of Cortical Rhythms in Cognition (2010, background): “Fourth, NMDA hypofunction leads to a selective reduction of the excitatory drive for a subpopulation of interneurons (72, 389, 582, 1024); one of the consequences could be abnormal inhibition-dependent synchronous oscillations (593, 633, 818).”
Beyond classical benzodiazepines: Novel therapeutic potential of GABAA receptor subtypes (2011, background): “, activates tonic firing of dopaminergic neurons in the midbrain; this circuit involves glutamatergic neurons in the hippocampus, GABAergic neurons in the nucleus accumbens and GABAergic neurons in the ventral pallidu”
Abnormal neural oscillations and synchrony in schizophrenia (2010, background): “In addition to the involvement of GABA- and NMDA-receptor mediated neurotransmission, data from animal models have suggested that alterations in the dopaminergic and cholinergic systems may contribute to abnormal oscillation”