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 alpha-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.