Abstract:
:Human genetic data on psychiatric disorders repeatedly demonstrate the involvement of various genes that are associated with neural development and neurogenesis. Neurogenesis is a biological process that is critical in brain development and continues throughout life. Neurogenesis is a multi-step process starting from the division of neural stem cells/progenitor cells, leading to self-renewal and simultaneously to the production of lineage-committed cells, including neurons and glial cells. Minor defects in the neurogenesis process, such as production of fewer new neurons and malformation of neural circuits, could represent phenotypes of psychiatric disorders at molecular and cellular levels in animal models (here termed as "microphenotypes"). However, microphenotypes are not easily used as biomarkers. We have focused on a physiological condition, sensorimotor gating deficits, that can be scored by a prepulse inhibition (PPI) test. Impaired PPI is considered to be one of the compelling endophenotypes (biological markers) of mental disorders such as schizophrenia, autism, and other neurodevelopmental disorders. Because the neural circuit for PPI involves the hippocampus, a unique brain region where neurogenesis occurs postnatally, we hypothesize that an impairment of preadolescent neurogenesis is critical for the onset of sensorimotor gating defects. To test this hypothesis, we investigated a critical period of neurogenesis that can affect PPI. In this paradigm, we introduced an enriched environment to restore neurogenesis, thereby recovering PPI deficits in mice. We noted impairments in the maturation of newborn neurons in the hippocampal dentate gyrus (DG) and GABAergic neurons in the hippocampus, which could be considered as microphenotypes associated with PPI defects. More precise genetically controlled neurogenesis models (with precise time points or periods) are needed to be studied in further investigation to support our hypothesis.
journal_name
Curr Mol Medjournal_title
Current molecular medicineauthors
Osumi N,Guo N,Matsumata M,Yoshizaki Kdoi
10.2174/1566524015666150303002834subject
Has Abstractpub_date
2015-01-01 00:00:00pages
129-37issue
2eissn
1566-5240issn
1875-5666pii
CMM-EPUB-65608journal_volume
15pub_type
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更新日期:2012-12-01 00:00:00
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更新日期:2005-03-01 00:00:00
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更新日期:2009-08-01 00:00:00
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更新日期:2013-05-01 00:00:00
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更新日期:2008-09-01 00:00:00
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更新日期:2014-01-01 00:00:00
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更新日期:2019-01-01 00:00:00
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更新日期:2019-01-01 00:00:00
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更新日期:2009-09-01 00:00:00