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Cerebrospinal fluid of brain trauma patients inhibits in vitro neuronal network function via NMDA receptors†

  1. Frauke Otto MD1,
  2. Sebastian Illes MSc1,
  3. Jessica Opatz PhD1,
  4. Maurice Laryea PhD2,
  5. Stephan Theiss MSc1,
  6. Hans-Peter Hartung MD1,
  7. Alfons Schnitzler MD1,3,
  8. Mario Siebler MD1,
  9. Marcel Dihné MD1,*

Article first published online: 20 JUL 2009

DOI: 10.1002/ana.21808

Issue

Annals of Neurology

Annals of Neurology

Volume 66, Issue 4, pages 546–555, October 2009

Additional Information

How to Cite

Otto, F., Illes, S., Opatz, J., Laryea, M., Theiss, S., Hartung, H.-P., Schnitzler, A., Siebler, M. and Dihné, M. (2009), Cerebrospinal fluid of brain trauma patients inhibits in vitro neuronal network function via NMDA receptors. Annals of Neurology, 66: 546–555. doi: 10.1002/ana.21808

Author Information

  1. 1

    Department of Neurology, Heinrich-Heine University, Düsseldorf, Germany

  2. 2

    Department of General Pediatrics, Heinrich-Heine University, Düsseldorf, Germany

  3. 3

    Institute of Clinical Neuroscience and Medical Psychology, Heinrich-Heine University, Düsseldorf, Germany

*Department of Neurology, Heinrich-Heine University, Moorenstr. 5, 40225 Düsseldorf, Germany

  1. †

    Potential conflict of interest: Nothing to report.

Publication History

  1. Issue published online: 8 OCT 2009
  2. Article first published online: 20 JUL 2009
  3. Accepted manuscript online: 20 JUL 2009 12:00AM EST
  4. Manuscript Received: 17 SEP 2009
  5. Manuscript Accepted: 10 JUL 2009
  6. Manuscript Revised: 1 JUL 2009

Funded by

  • Bundesministerium für Bildung und Forschung. Grant Number: BMBF, 01GN0503
  • Christiane & Claudia Hempel-Stiftung für Klinische Stammzellforschung
  • Hannelore-Kohl-Stiftung ZNS
  • Forschungskommission der medizinischen Fakultät der Heinrich-Heine-Universität Düsseldorf

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Abstract

Neurological diseases frequently induce pathological changes of cerebrospinal fluid (CSF) that might secondarily influence brain activity, as the CSF–brain barrier is partially permeable. However, functional effects of CSF on neuronal network activity have not been specified to date. Here, we report that CSF specimens from patients with reduced Glasgow Coma Scale values caused by severe traumatic brain injury suppress synchronous activity of in vitro-generated neuronal networks in comparison with controls. We present evidence that underlying mechanisms include increased N-methyl-D-aspartate receptor activity mediated by a CSF fraction containing elevated amino acid concentrations. These proof-of-principle data suggest that determining effects of CSF specimens on neuronal network activity might be of diagnostic value. Ann Neurol 2009;66:546–555

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