Hypothermia blunts acetylcholine increase in CSF of traumatically brain injured rats

Bruce G Lyeth, Ji Y. Jiang, Susan E. Robinson, Hongzhi Guo, Larry W. Jenkins

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


Activation of muscarinic acetylcholine (ACh) receptors contributes to the pathophysiological consequences of moderate experimental traumatic brain injury (TBI). Hypothermia (30°C) provides protection in experimental TBI. We measured ACh levels in CSF and plasma 5 min after moderate fluid percussion TBI under normothermic or hypothermic conditions, because ACh in the CSF has been correlated with the severity of behavioral deficits after TBI. Three groups were examined: TBI with hypothermic brain (30°C), TBI with normothermic brain (37°C), or sham TBI with normothermic brain (37°C). ACh concentrations in CSF were significantly higher in 37°C TBI rats, but not in 30°C TBI rats compared to shams. ACh concentratons in plasma did not differ between groups. These results suggest that a contributing factor to the neuroprotective effects of moderate hypothermia in TBI may be related to the reduction of excessive ACh levels in the central nervous system following injury.

Original languageEnglish (US)
Pages (from-to)247-256
Number of pages10
JournalMolecular and Chemical Neuropathology
Issue number3
StatePublished - Apr 1993
Externally publishedYes


  • acetylcholine
  • choline
  • CSF
  • hypothermia
  • plasma
  • Traumatic brain injury

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Molecular Biology


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