Differential modulation of carbachol and trans-ACPD-stimulated phosphoinositide turnover following traumatic brain injury

M. Delahunty, Ji Y. Jiang, Raiford T. Black, Bruce G Lyeth

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

In the fluid percussion model of traumatic brain injury (TBI), we examined muscarinic and metabotropic glutamate receptor-stimulated polyphosphoinositide (PPI) turnover in rat hippocampus. Moderate injury was obtained by displacement and deformation of the brain within the closed cranial cavity using a fluid percussion device. Carbachol and (±)-1-Aminocyclopentane-trans-1,3.-dicarboxylic acid (trans-ACPD)-stimulated PPI hydrolysis was assayed in hippocampus from injured and sham-injured controls at both 1 hour and 15 days following injury. At 1 hour after TBI, the response to carbachol was enhanced in injured rats by up to 200% but the response to trans-ACPD was diminished by as much as 28%. By contrast, at 15 days after TBI, the response to carbachol was enhanced by 25% and the response to trans-ACPD was enhanced by 73%. The ionotropic glutamate agonists N-methyl-D-aspartate (NMDA), and α-amino-3 hydroxy-5-methyl-4-isoxazolepropionate (AMPA), did not increase PPI hydrolysis in either sham or injured rats and injury did not alter basal hydrolysis. Thus, hippocampal muscarinic and metabotropic receptors linked to phospholipase C are differentially altered by TBI.

Original languageEnglish (US)
Pages (from-to)405-411
Number of pages7
JournalNeurochemical Research
Volume20
Issue number4
DOIs
StatePublished - Apr 1995
Externally publishedYes

Keywords

  • hippocampus
  • inositol phosphates
  • metabotropic glutamate receptor
  • Muscarinic receptor
  • traumatic brain injury

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry

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