The neuronal plasticity and its abnormality through epigenetics of a stress-regulated protein, M6a

2014 Fiscal Year Final Research Report

• Project/Area Number: 24700319
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neuroscience in general
• Research Institution: Niigata University
• Principal Investigator: HONDA Atsuko 新潟大学, 研究推進機構 超域学術院, 特別研究員 (40467072)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 神経科学 / 神経発生 / 神経極性 / 神経成長円錐 / 脳回路形成 / RNAi

Outline of Final Research Achievements

We found that the stress-regulated protein M6a is one of the most abundant membrane protein in the axonal growth cone during the neuronal development, and it regulates the extracellular matrix-dependent determination of neuronal polarity through its interaction with intra-, extracellular signal transduction molecules. M6a was expressed in the cortices as well as hippocampi, and regulates the neuronal polarity determination in both neurons.
shRNA knockdown experiment of M6a in the embryonic mice brain showed that acute suppression of M6a in the cerebral cortex delayed morphological transition of migrating cortical neurons from multipolar to mono- (bi-) polar in the intermediate zone and their axon formation.
Our data suggest that epigenetic depression of M6a delay the determination of neuronal polarity essential for neuronal network in the brain.

Free Research Field

神経科学