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

6533b7d0fe1ef96bd125af3f

RESEARCH PRODUCT

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

Abderrahman El Maarouf Bruce S. Mcewen Zachary M. Weil Erik B. Bloss Urs Rutishauser Juan Nacher Trudy J. Mccall

subject

Male Silver Staining Kainic acid Excitotoxicity Hippocampus Biology Hippocampal formation medicine.disease_cause Receptors N-Methyl-D-Aspartate Article Body Mass Index Rats Sprague-Dawley Synapse chemistry.chemical_compound Developmental Neuroscience Excitatory Amino Acid Agonists medicine Animals Organic Chemicals Receptor Neural Cell Adhesion Molecules Analysis of Variance Kainic Acid Polysialic acid Pyramidal Cells Metalloendopeptidases Dendrites Fluoresceins CA3 Region Hippocampal Rats Cell biology Disease Models Animal Gene Expression Regulation nervous system Neurology chemistry Nerve Degeneration Sialic Acids Neural cell adhesion molecule Neuroscience Stress Psychological

description

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.

year	journal	country	edition	language
2012-09-12	Experimental Neurology

https://doi.org/10.1016/j.expneurol.2012.11.028