Traumatic brain injury reduces hippocampal α7 nicotinic cholinergic receptor binding

Changes in the expression of central nervous system (CNS) neurotransmitter receptors may contribute to behavioral and physiological deficits that occur following traumatic brain injury (TBI). Studies investigating the neurochemical 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 calcium channel expression. Quantitative autoradiography was used to determine the effects of CCI on receptor expression, 48 h following injury. The most robust and consistent change in receptor binding was in the density of α7 nicotinic receptors as determined by α-[¹²⁵I]-bungarotoxin (BTX) binding. Bilateral deficits in BTX binding were present following both mild and moderate levels of injury. In contrast, changes in the density of α3/α4 nAChr's, muscarinic AChr's, NMDA-type glutamate receptors, and L-type calcium channel expression were more regionally restricted and lower in magnitude, as compared to changes in BTX binding. The high calcium permeability of the α7 nAChr may be related to the extensive decrease in BTX binding that occurs following TBI.