Cerebrospinal fluid of brain trauma patients inhibits in vitro neuronal network function via NMDA receptors.
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.
Otto
Frauke
F
Department of Neurology, Heinrich-Heine University, Düsseldorf, Germany.
Illes
Sebastian
S
Opatz
Jessica
J
Laryea
Maurice
M
Theiss
Stephan
S
Hartung
Hans-Peter
HP
Schnitzler
Alfons
A
Siebler
Mario
M
Dihné
Marcel
M
D000293:Adolescent; D000328:Adult; D000368:Aged; D001930:Brain Injuries / Q000134:cerebrospinal fluid* / Q000503:physiopathology*; D002478:Cells, Cultured; D002555:Cerebrospinal Fluid / Q000378:metabolism / Q000502:physiology*; D053595:Embryonic Stem Cells / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009415:Nerve Net / Q000378:metabolism / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000096:biosynthesis / Q000502:physiology*
D016194:Receptors, N-Methyl-D-Aspartate