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α‐1 Adrenoceptors are decreased in human epileptic foci
Author(s) -
Brière Richard,
Sherwin Allan L.,
Robitaille Yvon,
Olivier André,
Quesney Luis F.,
Reader Tomas A.
Publication year - 1986
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410190106
Subject(s) - beta (programming language) , alpha (finance) , receptor , endocrinology , prazosin , adrenergic receptor , medicine , epilepsy , chemistry , biology , neuroscience , antagonist , surgery , construct validity , computer science , patient satisfaction , programming language
Abstract Cortical α‐1 adrenoceptors were measured in tissues obtained from 10 patients immediately following temporal lobectomy for intractable partial epilepsy. At operation each patient exhibited spontaneous spiking restricted to either the anterior (n = 5) or posterior (n = 5) portion of the first two temporal gyri. Control samples were obtained from the nonspiking half of the same gyrus. Receptor‐binding assays were performed on isolated cortical membranes using [ 3 H]prazosin. There was a reduction ( p < 0.01) in the receptor density (β max ) of the sites in the epileptic foci without any change in affinity (mean ± SEM): spiking—β max , 160.5 ± 11.3 fmol/mg protein; affinity, 0.17 ± 0.04 n M ; nonspiking—β max , 218.8 ± 15.6 fmol/mg protein; affinity 0.17 ± 0.04 n M . This relative decrease in α‐1 adrenoceptor density may be the substratum of a noradrenergic hyposensitivity that could contribute to a localized diminution in inhibitory mechanisms in epileptic foci.