• 1 January 1982
    • journal article
    • research article
    • Vol. 222  (3) , 670-673
Abstract
Amygdala-kindled seizures reduced significantly the total number of [3H]quinuclidinyl benzilate [a muscarinic cholinergic antagonist] binding sites in both dentate and hippocampal gyri compared to electrode-implanted, unstimulated controls. Both high and low affinity carbachol displaceable binding site populations were significantly reduced in hippocampal gyrus. Using a computerized nonlinear least-squares curve-fitting model, a selective decline of low affinity sites was found in dentate gyrus membranes. The selectivity of the decline in dentate but not hippocampal gyrus underscores the specificity of this molecular response to amygdala-kindled seizures. These receptor alterations evidently underlie adaptive mechanisms which antagonize kindled epileptogenesis.