Neuregulin-1 signalling and antipsychotic treatment

  title={Neuregulin-1 signalling and antipsychotic treatment},
  author={Chao Deng and Bo Pan and Martin Engel and Xu-Feng Huang},
Identifying the signalling pathways underlying the pathophysiology of schizophrenia is an essential step in the rational development of new antipsychotic drugs for this devastating disease. Evidence from genetic, transgenic and post-mortem studies have strongly supported neuregulin-1 (NRG1)–ErbB4 signalling as a schizophrenia susceptibility pathway. NRG1–ErbB4 signalling plays crucial roles in regulating neurodevelopment and neurotransmission, with implications for the pathophysiology of… 
Effects of prolonged antipsychotic administration on neuregulin-1/ErbB signaling in rat prefrontal cortex and myocardium: implications for the therapeutic action and cardiac adverse effect.
Examination of NRG1/ErbB system in rat prefrontal cortex and myocardium following 4-week intraperitoneal administration of haloperidol, risperidone or clozapine showed evidence of the effect of antipsychotic exposure on myocardial NRG 1/ ErbB signaling, along with the activated NRG2/Er b system in brain, providing a potential link between the therapeutic actions and cardiotoxicity.
Neuregulin-1 and schizophrenia in the genome-wide association study era
Effects of Risperidone and Prenatal Poly I:C Exposure on GABAA Receptors and AKT-GSK3β Pathway in the Ventral Tegmental Area of Female Juvenile Rats
It is suggested that Poly I:C-elicited maternal immune activation and risperidone differentially modulate GABAergic neurotransmission and AKT-GSK3β signaling in the VTA of adolescent rats.
Schizophrenia and neurogenesis: A stem cell approach
The ANKS1B gene and its associated phenotypes: focus on CNS drug response.
Current human association evidence for ANKS1B is reviewed, showing strong plausibility for involvement in CNS drug response because it encodes a postsynaptic effector protein that mediates long-term changes to neuronal biology.


Antipsychotic treatment and neuregulin 1–ErbB4 signalling in schizophrenia
Reciprocal signalling between NR2 subunits of the NMDA receptor and neuregulin1 and their role in schizophrenia
Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia
  • D. Balu, J. Coyle
  • Psychology, Medicine
    Neuroscience & Biobehavioral Reviews
  • 2011
The neuregulin signaling pathway and schizophrenia: From genes to synapses and neural circuits
  • A. Buonanno
  • Psychology, Biology
    Brain Research Bulletin
  • 2010
Altered neuregulin 1–erbB4 signaling contributes to NMDA> receptor hypofunction in schizophrenia
It is found that NRG1 stimulation suppresses NMDA receptor activation in the human prefrontal cortex, as previously reported in the rodent cortex, and this findings suggest that enhancedNRG1 signaling may contribute to NMDA hypofunction in schizophrenia.
Schizophrenia susceptibility pathway neuregulin 1–ErbB4 suppresses Src upregulation of NMDA receptors
NRG1β-ErbB4 signaling prevented induction of long-term potentiation at hippocampal Schaffer collateral–CA1 synapses and suppressed Src-dependent enhancement of NMDAR responses during theta-burst stimulation, and was proposed to participate in cognitive dysfunction in schizophrenia by aberrantly suppressing SRC-mediated enhancement of synaptic N MDAR function.
Neuregulin 1 and susceptibility to schizophrenia.
The results of a genomewide scan of schizophrenia families in Iceland show that schizophrenia maps to chromosome 8p, and extensive fine-mapping of the 8p locus and haplotype-association analysis identifies neuregulin 1 (NRG1) as a candidate gene for schizophrenia.
ErbB4 Localization to Interneurons: Clearer Insights into Schizophrenia Pathology
Signaling pathways in schizophrenia: emerging targets and therapeutic strategies.
Neuregulin links dopaminergic and glutamatergic neurotransmission to control hippocampal synaptic plasticity
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.