Format

Send to

Choose Destination
See comment in PubMed Commons below
CNS Neurosci Ther. 2014 Feb;20(2):172-81. doi: 10.1111/cns.12202. Epub 2013 Nov 27.

Increased activation of synapsin 1 and mitogen-activated protein kinases/extracellular signal-regulated kinase in the amygdala of maternal separation rats.

Author information

  • 1Kohwang Medical Research Institute, School of Medicine, Kyung Hee University, Seoul, Republic of Korea.

Abstract

BACKGROUND:

Early life stress (ELS) causes alterations in emotionality and anxiety levels as a significant risk factor for psychiatric problems, and these alterations have been associated with amygdala activity.

AIMS:

To elucidate the molecular mechanism on the development of psychiatric problems following ELS, we identified the alteration of molecules in the amygdala using maternal separation (MS; pnd 14-21) rats through gene expression and DNA methylation microarray analysis, and studied the involvement of candidate genes using a Western blot and immunohistochemistry analysis.

RESULTS:

Through a microarray analysis, in the amygdala of MS rats, we found a downregulation of mRNA expression of synapsin 1 (Syn1) gene with hypermethylation of its transcription start site (TSS), and the alterations of mRNA expressions of Syn1 activation-related kinase genes including mitogen-activated protein kinases (Mapks) with change of their TSS methylation. In addition, MS increased not only Syn1 phosphorylation at the phosphorylation sites by Mapk/extracellular signal-regulated kinase (Erk), but also Mapk/Erk phosphorylation in the amygdala. Furthermore, double immunofluorescence staining showed that MS could elevate phospho-Mapk/Erk immunoreactivity (IR) in Syn1-expression puncta.

CONCLUSION:

These findings indicated that the activation of Mapk/Erk and Syn1 may be a key mechanism modulating synaptic neurotransmition in the amygdala of MS rats.

KEYWORDS:

Amygdala; Early life stress; Maternal separation; Mitogen-activated protein kinase; Synapsin 1

PMID:
24279756
DOI:
10.1111/cns.12202
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center