Neurotransmitter-mediated mechanisms of traumatic brain injury: acetylcholine and excitatory amino acids.
Research into traumatic brain injury (TBI), focusing on changes in energy metabolism, cerebrovascular dysfunction, and brain parenchymal morphology, has not produced complete descriptions of mechanisms mediating the pathophysiology of TBI. New studies indicate that neurochemical alterations mediate important components of brain physiology associated with TBI, and these alterations may be responsive to pharmacologic therapy. We discuss rodent models of TBI, review current experimental evidence of muscarinic cholinergic and excitatory amino acid (EAA) receptor involvement in its pathophysiology, and address issues relevant to the interpretation of these data.
Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond.
R L
RL
Hayes
L W
LW
Jenkins
B G
BG
Lyeth
D000109:Acetylcholine / Q000502:physiology*; D000596:Amino Acids / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000503:physiopathology*; D001930:Brain Injuries / Q000503:physiopathology*; D004195:Disease Models, Animal; D006801:Humans; D008959:Models, Neurological; D018377:Neurotransmitter Agents / Q000502:physiology*; D017981:Receptors, Neurotransmitter / Q000502:physiology
D000596:Amino Acids; D018377:Neurotransmitter Agents; D017981:Receptors, Neurotransmitter; D000109:Acetylcholine