Traumatic brain injury reduces hippocampal alpha 7 nicotinic cholinergic receptor binding

Changes in the expression of central nervous system (CNS) neurotransmitter receptors may contribute to behavioral and physiological deficits that occu r following traumatic brain injury (TBI), Studies investigating the neuroch emical basis for the protracted cognitive dysfunction that follows TBI have focused in part on cholinergic mechanisms. The present study compared the effects of mild and moderate cortical contusion injury (CCI) on the density of cholinergic receptor subtypes, NMDA-type glutamate receptors, and calci um channel expression. Quantitative autoradiography was used to determine t he effects of CCI on receptor expression, 48 h following injury. The most r obust and consistent change in receptor binding was in the density of alpha 7 nicotinic receptors as determined by alpha-[I-125]-bungarotoxin (BTX) bin ding. Bilateral deficits in BTX binding were present following both mild an d moderate levels of injury. In contrast, changes in the density of alpha3/ alpha4 nAChr's, muscarinic AChr's, NMDA-type glutamate receptors, and L-typ e calcium channel expression were more regionally restricted and lower in m agnitude, as compared to changes in BTX binding. The high calcium permeabil ity of the alpha7 nAChr may be related to the extensive decrease in BTX bin ding that occurs following TBI.