Sharma Ajaykumar N, Fries Gabriel R, Galvez Juan F, Valvassori Samira S, Soares Jair C, Carvalho André F, Quevedo Joao
Center for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston, Houston, TX 77054, USA; Center of Excellence on Mood Disorders, Department of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston, Houston, TX 77054, USA.
Center for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston, Houston, TX 77054, USA.
Prog Neuropsychopharmacol Biol Psychiatry. 2016 Apr 3;66:22-34. doi: 10.1016/j.pnpbp.2015.11.001. Epub 2015 Nov 4.
The current pathophysiological understanding of mechanisms leading to onset and progression of bipolar manic episodes remains limited. At the same time, available animal models for mania have limited face, construct, and predictive validities. Additionally, these models fail to encompass recent pathophysiological frameworks of bipolar disorder (BD), e.g. neuroprogression. Therefore, there is a need to search for novel preclinical models for mania that could comprehensively address these limitations. Herein we review the history, validity, and caveats of currently available animal models for mania. We also review new genetic models for mania, namely knockout mice for genes involved in neurotransmission, synapse formation, and intracellular signaling pathways. Furthermore, we review recent trends in preclinical models for mania that may aid in the comprehension of mechanisms underlying the neuroprogressive and recurring nature of BD. In conclusion, the validity of animal models for mania remains limited. Nevertheless, novel (e.g. genetic) animal models as well as adaptation of existing paradigms hold promise.
目前对于导致双相躁狂发作及其进展的机制的病理生理学理解仍然有限。与此同时,现有的躁狂症动物模型在表面效度、结构效度和预测效度方面都存在局限性。此外,这些模型未能涵盖双相情感障碍(BD)最近的病理生理框架,如神经进展。因此,需要寻找能够全面解决这些局限性的新型躁狂症临床前模型。在此,我们回顾了目前可用的躁狂症动物模型的历史、效度和注意事项。我们还回顾了新型躁狂症基因模型,即参与神经传递、突触形成和细胞内信号通路的基因敲除小鼠。此外,我们回顾了躁狂症临床前模型的最新趋势,这些趋势可能有助于理解BD神经进展和复发性质背后的机制。总之,躁狂症动物模型的效度仍然有限。然而,新型(如基因)动物模型以及对现有范式的调整具有前景。