Depletion of polysialic acid from neural cell adhesion molecule (PSA-NCAM) increases CA3 dendritic arborization and increases vulnerability to excitotoxicity Journal Article

   

Authors:	McCall, T.; Weil, Z. M.; Nacher, J.; Bloss, E. B.; El-Maarouf, A. ; Rutishauser, U.; McEwen, B. S.
Article Title:	Depletion of polysialic acid from neural cell adhesion molecule (PSA-NCAM) increases CA3 dendritic arborization and increases vulnerability to excitotoxicity
Abstract:	Chronic immobilization stress (CIS) shortens apical dendritic trees of CA3 pyramidal neurons in the hippocampus of the male rat, and dendritic length may be a determinant of vulnerability to stress. Expression of the polysialylated form of neural cell adhesion molecule (PSA-NCAM) in the hippocampal formation is increased by stress, while PSA removal by Endo-neuraminidase-N (endo-N) is known to cause the mossy fibers to defasciculate and synapse ectopically in their CA3 target area. We show here that enzymatic removal of PSA produced a remarkable expansion of dendritic arbors of CA3 pyramidal neurons, with a lesser effect in CA1. This expansion eclipsed the CIS-induced shortening of CA3 dendrites, with the expanded dendrites of both no-stress-endo-N and CIS-endo-N rats being longer than those in no-stress-control rats and much longer than those in CIS-control rats. As predicted by the hypothesis that endo-N-induced dendritic expansion might increase vulnerability to excitotoxic challenge, systemic injection with kainic acid, showed markedly increased neuronal degeneration, as assessed by fluorojade B histochemistry, in rats that had been treated with endo-N compared to vehicle-treated rats throughout the entire hippocampal formation. PSA removal also exacerbated the CIS-induced reduction in body weight and abolished effects of CIS on NPY and NR2B mRNA levels. These findings support the hypothesis that CA3 arbor plasticity plays a protective role during prolonged stress and clarify the role of PSA-NCAM in stress-induced dendritic plasticity. © 2012 Elsevier Inc.
Keywords:	cell death; stress; plasticity; psa-ncam; dendritic branching; excitotoxicity
Journal Title:	Experimental Neurology
Volume:	241
Issue:	1
ISSN:	0014-4886
Publisher:	Elsevier Inc.
Date Published:	2012-12-07
Start Page:	5
End Page:	12
Language:	English
DOI:	10.1016/j.expneurol.2012.11.028
PROVIDER:	scopus
PUBMED:	23219884
PMCID:	PMC3570583
DOI/URL:	http://www.scopus.com/inward/record.url?eid=2-s2.0-84872022087&partnerID=40&md5=23bf1e9209975e67facbea05f287a301
Notes:	--- - "Export Date: 1 February 2013" - "CODEN: EXNEA" - "Source: Scopus"

https://synapse.mskcc.org/synapse/works/has_related_data_chk/38137