Concussion in rats causes an immediate change in occupancy but not affinity of hypothalamic cholinergic receptors.
Experimental concussion in rats is associated with subsequent enhanced binding in vitro of certain ligands to hypothalamic tissue but not to other brain regions. Scatchard analysis shows that the number of specific binding sites for [3H]quinuclidinylbenzilate increases within 3 s after concussion with no significant change in binding affinity. The apparent increase in receptors is likely the result of a deficit in binding of endogenous ligand. We propose that concussion produces a pressure wave that deforms cholinergic and possibly other receptors selectively in the hypothalamus, resulting in a transient deficit in transmitter binding and interruption of neuronal circuits concerned with the state of consciousness.
D000818:Animals; D001924:Brain Concussion / Q000378:metabolism*; D007031:Hypothalamus / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000378:metabolism; D011813:Quinuclidinyl Benzilate / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011950:Receptors, Cholinergic / Q000378:metabolism*; D011976:Receptors, Muscarinic / Q000378:metabolism*
D011950:Receptors, Cholinergic; D011976:Receptors, Muscarinic; D011813:Quinuclidinyl Benzilate