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Full-Text Articles in Medicine and Health Sciences
Alterations Of Mglur5 And Its Endogenous Regulators Norbin, Tamalin And Preso1 In Schizophrenia: Towards A Model Of Mglur5 Dysregulation, Natalie Matosin, Francesca Fernandez-Enright, Samantha J. Fung, Jeremy S. Lum, Martin Engel, Jessica L. Andrews, Xu-Feng Huang, Cynthia S. Weickert, Kelly A. Newell
Alterations Of Mglur5 And Its Endogenous Regulators Norbin, Tamalin And Preso1 In Schizophrenia: Towards A Model Of Mglur5 Dysregulation, Natalie Matosin, Francesca Fernandez-Enright, Samantha J. Fung, Jeremy S. Lum, Martin Engel, Jessica L. Andrews, Xu-Feng Huang, Cynthia S. Weickert, Kelly A. Newell
Illawarra Health and Medical Research Institute
Knockout of genes encoding metabotropic glutamate receptor 5 (mGluR5) or its endogenous regulators, such as Norbin, induce a schizophrenia-like phenotype in rodents, suggesting dysregulation of mGluR5 in schizophrenia. Human genetic and pharmacological animal studies support this hypothesis, but no studies have explored mGluR5 dysfunction at the molecular level in the postmortem schizophrenia brain. We assessed mGluR5 mRNA and protein levels in the dorsolateral prefrontal cortex (DLPFC) using a large cohort of schizophrenia and control subjects (n = 37/group), and additionally measured protein levels of recently discovered mGluR5 endogenous regulators, Norbin (neurochondrin), Tamalin (GRASP-1), and Preso1 (FRMPD4), which regulate mGluR5 localization, …
Neuregulin 1 Prevents Phencyclidine-Induced Behavioral Impairments And Disruptions To Gabaergic Signaling In Mice, Martin Engel, Peta Snikeris, Andrew M. Jenner, Tim Karl, Xu-Feng Huang, Elisabeth T. Frank
Neuregulin 1 Prevents Phencyclidine-Induced Behavioral Impairments And Disruptions To Gabaergic Signaling In Mice, Martin Engel, Peta Snikeris, Andrew M. Jenner, Tim Karl, Xu-Feng Huang, Elisabeth T. Frank
Illawarra Health and Medical Research Institute
Background: Substantial evidence from human post-mortem and genetic studies has linked the neurotrophic factor neuregulin 1 (NRG1) to the pathophysiology of schizophrenia. Genetic animal models and in vitro experiments have suggested that altered NRG1 signaling, rather than protein changes, contributes to the symptomatology of schizophrenia. However, little is known about the effect of NRG1 on schizophrenia-relevant behavior and neurotransmission (particularly GABAergic and glutamatergic) in adult animals. Method: To address this question, we treated adult mice with the extracellular signaling domain of NRG1 and assessed spontaneous locomotor activity and acoustic startle response, as well as extracellular GABA, glutamate, and …