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• W2048045992 abstract "Neuregulin-1 (NRG-1) and its receptor ErbB4 are genetically linked with schizophrenia, a complex developmental disorder of high heritability but unknown etiology that has been proposed to result from deficits in functional connectivity and synaptic plasticity. Based on pharmacological evidence, disbalances in dopaminergic and glutamatergic transmission systems are believed to contribute to its pathophysiology, but genetic data supporting a causative role for either are sparse. Stimulation of NRG-1/ErbB4 signaling inhibits or reverts hippocampal long-term potentiation at glutamatergic synapses between Schaeffer collateral afferents and CA1 pyramidal neurons (SC->CA1). We have recently demonstrated that NRG-1 regulates glutamatergic plasticity by rapidly increasing extracellular hippocampal dopamine levels and activation of D4 dopamine receptors (D4R). These new findings position NRG-1/ErbB4 signaling pathway at the crossroads between dopaminergic and glutamatergic neurotransmission and offer novel ways to consolidate genetic, functional and pharmacological data toward a better understanding of the etiological processes underlying schizophrenia, and the role of NRG-1 for normal synaptic function and plasticity. The currently available data suggest that hippocampal interneurons might play a crucial role in mediating NRG-1 induced depotentiation. This interpretation is in line with other evidence pointing towards an involvement of GABAergic cells in the etiology of schizophrenia." @default.
• W2048045992 created "2016-06-24" @default.
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• W2048045992 date "2009-05-01" @default.
• W2048045992 modified "2023-10-16" @default.
• W2048045992 title "Neuregulin links dopaminergic and glutamatergic neurotransmission to control hippocampal synaptic plasticity" @default.
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• W2048045992 doi "https://doi.org/10.4161/cib.2.3.7825" @default.
• W2048045992 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2717536" @default.
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