Back to Search Start Over

Chronic restraint stress down-regulates amygdaloid expression of polysialylated neural cell adhesion molecule.

Authors :
Cordero MI
Rodríguez JJ
Davies HA
Peddie CJ
Sandi C
Stewart MG
Source :
Neuroscience [Neuroscience] 2005; Vol. 133 (4), pp. 903-10.
Publication Year :
2005

Abstract

The amygdala is a brain area which plays a decisive role in fear and anxiety. Since exposure to chronic stress can induce profound effects in emotion and cognition, plasticity in specific amygdaloid nuclei in response to prior stress has been hypothesized to account for stress-induced emotional alterations. In order to identify amygdala nuclei which may be affected under chronic stress conditions we evaluated the effects of 21-days chronic restraint stress on the expression of a molecule implicated crucially in alterations in structural plasticity: the polysialylated neural cell adhesion molecule. We found that polysialylated neural cell adhesion molecule-immunoreactivity within the amygdala, present in somata and neuronal processes, has a regional gradient with the central medial and medial amygdaloid nuclei showing the highest levels. Our results demonstrate that chronic restraint stress induced an overall reduction in polysialylated neural cell adhesion molecule-immunoreactivity in the amygdaloid complex, mainly due to a significant decrease in the central medial amygdaloid and medial amygdaloid nuclei. Our data suggest that polysialylated neural cell adhesion molecule in these nuclei may play a prominent role in functional and structural remodeling induced by stress, being a potential mechanism for cognitive and emotional modulation. Furthermore, these finding provide the first clear evidence that life experiences can regulate the expression of polysialylated neural cell adhesion molecule in the amygdaloid complex.

Details

Language :
English
ISSN :
0306-4522
Volume :
133
Issue :
4
Database :
MEDLINE
Journal :
Neuroscience
Publication Type :
Academic Journal
Accession number :
15927407
Full Text :
https://doi.org/10.1016/j.neuroscience.2005.03.046