Cited by 34Neuroscience and Neuropharmacology ResearchStress Responses and CortisolNeurogenesis and neuroplasticity mechanisms

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

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McCall, Trudy, Weil, Zachary M., Nacher, Juan, Bloss, Erik B., El Maarouf, Abderrahman, Rutishauser, Urs, McEwen, Bruce S.·2013·Experimental Neurology

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.

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Crossref · 10.1016/j.expneurol.2012.11.028

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  • The plasticity resulting from polysialic acid expression appears to be important for neuronal migration and for reorganization following injury.

    “The ' plasticity ' resulting from polysialic acid expression appears to be important for neuronal migration as well as reorganization following injury (546 -554).”

    From Biological roles of glycans (2017) · cites this paper as [553]

    The References (page unavailable) cite studies linking polysialic acid to neuronal migration, and the Introduction (page unavailable) describes PSA-NCAM expression changing after ischemic injury. The paper also discusses PSA-dependent structural plasticity, but these passages do not establish that it is important for reorganization following injury. (LLM, conf=0.78)

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Research works printed but not linked: 2

  1. [50]Seki T Arai Y 1999 Different polysialic acid-neural cell adhesion molecule expression patterns in distinct types of mossy fiber boutons in the adult hippocampus J Comp Neurol 410 115 125 10397399
  2. [58]Washbourne P Dityatev A Scheiffele P Biederer T Weiner JA Christopherson KS El-Husseini A 2004 Cell adhesion molecules in synapse formation J Neurosci 24 9244 9249 15496659 PMC6730099

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Authors
McCall, T., Weil, Z. M., Nacher, J., Bloss, E. B., El Maarouf, A., Rutishauser, U., & McEwen, B. S.
Affiliations
  • Rockefeller University (US)
  • The Ohio State University Wexner Medical Center (US)
  • Icahn School of Medicine at Mount Sinai (US)
Corresponding author
Weil, Zachary M.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2013-03
Volume
241
Pages
5-12
ISSN
0014-4886 (ISSN-L)
OpenAlex
W2089781305
Cited by
34
References
61
Citations by year
2023: 1 · 2022: 2 · 2021: 2 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 3 · 2016: 6 · 2015: 6 · 2014: 3 · 2013: 1
FWCI
1.32
Type
journal article
Language
en
Open access
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • NIH (MH41256)
  • Spanish Ministry of Science and Innovation (MICINN-FEDER) BFU2009-12284/BFI, MICINN-PIM2010ERN-00577/NEUCONNECT)
  • Generalitat Valenciana (ACOMP/2012/229)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
polysialic acid, CD56, chronic immobilization stress, CA3 pyramidal cells, excitotoxicity, kainic acid, dendritic plasticity, hippocampus, mossy fibers, neuropeptide Y, NR2B
MeSH terms
Analysis of Variance, Animals, Dendrites, Disease Models, Animal, Fluoresceins, Gene Expression Regulation, Kainic Acid, Male, Metalloendopeptidases, Nerve Degeneration, Organic Chemicals, Sialic Acids, Stress, Psychological, Body Mass Index, Receptors, N-Methyl-D-Aspartate, Silver Staining, Rats, Sprague-Dawley, Pyramidal Cells, Excitatory Amino Acid Agonists, Neural Cell Adhesion Molecules, Rats, CA3 Region, Hippocampal

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