Papers

Basic information

Name OZAWA Hitoshi

Title

The single-prolonged stress paradigm alters both the morphology and stress response of magnocellular vasopressin neurons

Author

T. Yoshii,H. Sakamoto,M. Kawasaki,H. Ozawa,Y. Ueta,T. Onaka,K. Fukui,M. Kawata

Sole or Joint Author

 

Journal

Neuroscience

Publisher

 

All Volumes

 

All Pages

 

Volume

156

Number

3

Starting Page

466

Ending Page

474

Publication Date

2008-10

Referee Paper

Refereed

Invited Paper

Not invited

Language

English

MISC Class

 

Publishing Type

Research paper (scientific journal)

ISSN

 

ID:DOI

10.1016/j.neuroscience.2008.07.049

ID:NAID

 

ID:PMID

 

URL

Description

Vasopressin (AVP) plays an important role in anxiety-related and social behaviors. Single-prolonged stress (SPS) has been established as an animal acute severe stress model and has been shown to induce a lower adrenocorticotropic hormone (ACTH) response upon cortisol challenge. Here, we show results from immunoassays for AVP, ACTH, and corticosterone (CORT), and in situ hybridizations for AVP mRNA performed 7 days after SPS exposure. Immunofluorescence for AVP was also performed during the 7-day period following SPS exposure and after an additional forced swimming stress paradigm. We observed that the plasma concentrations of AVP, ACTH, and CORT were not altered by SPS
 ACTH content in the pituitary and AVP mRNA expression in the supraoptic nucleus (SON) were significantly reduced by SPS. During the 7-day period following SPS, the intensity of immunoreactivity, the size of the soma, and the immunoreactive optical density of the dendrites of AVP neurons in the SON all increased. An apparent reduction in the intensity of AVP immunoreactivity was observed in the SON at 4 h after additional stress. Additional forced swimming led to a rapid increase in the dendritic AVP content only in the controls and not in the SPS-treated rats. These findings suggest that AVP is a potential biomarker for past exposure to severe stress and that alterations in AVP may affect the development of pathogenesis in stress-related disorders. © 2008 IBRO.

ID:JGlobalID

 

arXiv ID

 

Put Code of ORCID

 

DBLP ID

 

WekoID of OpenDepo