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. 2022:1400:15-33.
doi: 10.1007/978-3-030-97182-3_2.

What Can We Learn from Animal Models to Study Schizophrenia?

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What Can We Learn from Animal Models to Study Schizophrenia?

Fernanda Crunfli et al. Adv Exp Med Biol. 2022.

Abstract

Schizophrenia is a complex and heterogeneous neurodevelopmental psychiatric disorder characterized by a variety of symptoms classically grouped into three main domains: positive (hallucinations, delusions, and thought disorder) and negative symptoms (social withdrawal, lack of affect) and cognitive dysfunction (attention, working and episodic memory functions, and processing speed). This disorder places an immense emotional and economic pressure on the individual and society-at-large. Although the etiology of schizophrenia is not completely known, it is proposed to involve abnormalities in neurodevelopmental processes and dysregulation in the signaling mediated by several neurotransmitters, such as dopamine, glutamate, and GABA. Preclinical research using animal models are essential in our understanding of disease development and pathology as well as the discovery and advance of novel treatment choices. Here we describe rodent models for studying schizophrenia, including those based on the effects of drugs (pharmacological models), neurodevelopmental disruption, demyelination, and genetic alterations. The advantages and limitations of such models are highlighted. We also discussed the great potential of proteomic technologies in unraveling the molecular mechanism of schizophrenia through animal models.

Keywords: Animal models; Dopamine; Glutamate; Proteomic; Psychosis; Schizophrenia.

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References

    1. Ackenheil, M., & Weber, K. (2004). Differing response to antipsychotic therapy in schizophrenia: pharmacogenomic aspects. Dialogues in Clinical Neuroscience, 6(1), 71–77. - PubMed - PMC - DOI
    1. Ackerman, C. M., & Chang, C. J. (2018). Copper signaling in the brain and beyond. The Journal of Biological Chemistry, 293(13), 4628–4635. - PubMed - DOI
    1. Aguilar-Valles, A., Rodrigue, B., & Matta-Camacho, E. (2020 August). Maternal immune activation and the development of dopaminergic neurotransmission of the offspring: relevance for schizophrenia and other psychoses. Frontiers in Psychiatry / Frontiers Research Foundation, 11, 852. - DOI
    1. Andreini, C., Banci, L., Bertini, I., & Rosato, A. (2008). Occurrence of copper proteins through the three domains of life: a bioinformatic approach. Journal of Proteome Research, 7(1), 209–216. - PubMed - DOI
    1. Arsenault, D., St-Amour, I., Cisbani, G., Rousseau, L.-S., & Cicchetti, F. (2014). The different effects of LPS and poly I:C prenatal immune challenges on the behavior, development and inflammatory responses in pregnant mice and their offspring. Brain, Behavior, and Immunity, 38(May), 77–90. - PubMed - DOI

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