Skip to main content

Neuronal Cell Death and Inflammation

  • Reference work entry
  • First Online:
Encyclopedia of Neuroscience

Synonyms

Excitotoxicity; Apoptosis; Necrosis; Virotexias; Encephalitis; Chemokines; Cytokines; Chemtaxis; Blood brain barrier; Matrix metallo Proteinases

Definition

Exitotoxicity is a mechanism which often leads to Neuronal cell damage or death. Excitotoxicity occurs when glutamate receptors on neurons are overactivated. Neuronophagia occurs when nerve cells are phagocytosed or internalized by macrophages. This often happens to clear debris after the neurons have undergone apoptosis, but in some neuroinflammatory or neurodegenerative conditions, the neurons may be killed as the macrophages digest them. Necrosis is a process of cell death whereby cells swell, rupture, and release their contents, causing inflammationand damage to neighboring cells. In the nervous system, this usually happens in response to stroke or trauma. In contrast to necrosis, apoptosis is a form of cell death which does not cause inflammation, but, rather, is frequently the result of inflammatory processes....

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Institutional subscriptions

References

  1. Merrill JE, Benveniste EN (1996) Cytokines in inflammatory brain lesions: helpful and harmful. Trends Neurosci 19:331–338

    Article  CAS  PubMed  Google Scholar 

  2. Kruman I, Nath A, Mattson MP (1998) HIV protein Tat induces apoptosis by a mechanism involving mitochondrial calcium overload and caspase activation. Expt Neurol 154:276–288

    Article  CAS  Google Scholar 

  3. Briscoe DM, Cotran RS, Pober JS (1992) Effects of tumor necrosis factor, lipopolysaccharide, and IL-4 on the expression of vascular cell adhesion molecule-1 in vivo. Correlation with CD3+ T cell infiltration. J Immunol 149:2954–2960

    Article  CAS  PubMed  Google Scholar 

  4. Nath A (1999) Pathobiology of HIV dementia. Sem Neurol 19:113–128

    Article  CAS  Google Scholar 

  5. Nath A, Conant K, Chen P, Scott C, Major EO (1999) Transient exposure to HIV-1 Tat protein results in cytokine production in macrophages and astrocytes: a hit and run phenomenon. J Biol Chem 274:17098–17102

    Article  CAS  PubMed  Google Scholar 

  6. Libby RT, Lavallee CR, Balkema GW, Brunken WJ, Hunter DD (1999) Disruption of laminin beta2 chain production causes alterations in morphology and function in the CNS. J Neurosci 19:9399–9411

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Gu Z, Kaul M, Yan B, Kridel SJ, Cui J, Strongin A et al. (2002) S-nitrosylation of matrix metalloproteinases: signaling pathway to neuronal cell death. Science 297:1186–1190

    Article  CAS  PubMed  Google Scholar 

  8. McQuibban GA, Gong JH, Tam EM, McCulloch CA, Clark-Lewis I, Overall CM (2000) Inflammation dampened by gelatinase A cleavage of monocyte chemoattractant protein-3. Science 289:1202–1206

    Article  CAS  PubMed  Google Scholar 

  9. Rumbaugh J, Turchan-Cholewo J, Galey D, St Hillaire C, Anderson C, Conant K et al. (2006) Interaction of HIV Tat and matrix metalloproteinase in HIV neuropathogenesis: a new host defense mechanism. FASEB J 20:1736–1738

    Article  CAS  PubMed  Google Scholar 

  10. Masliah E, Ge N, Achim CL, Hansen LA, Wiley CA (1996) Selective neuronal vulnerability in HIV encephalitis. J Neuropathol Exp Neurol 51:585–593

    Article  Google Scholar 

Download references

Acknowledgement

This work was supported by National Institutes of Health grants to JR and AN.

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2009 Springer-Verlag GmbH Berlin Heidelberg

About this entry

Check for updates. Verify currency and authenticity via CrossMark

Cite this entry

Rumbaugh, J.A., Nath, A. (2009). Neuronal Cell Death and Inflammation. In: Binder, M.D., Hirokawa, N., Windhorst, U. (eds) Encyclopedia of Neuroscience. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-29678-2_3910

Download citation

Publish with us

Policies and ethics