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Morrow AL, Norman AB, Battaglia G, Loy R, Creese I. 
“Up-Regulatlon of Serotonergic Binding Sites Labeled By [3H]WB4101 Following Fimbrial Transection And 5,7-Dihydroxytryptamine-Induced Lesions”. 
Life Sciences. 1985 Sep;37(20):1913-1922.
Lesions of the serotonergic afferents to the hippocampus, by fimbrial transection or by 5,7-dibydroxytryptamine treatment, produce an increase in the Bmax of 3H]WB4101 to its nanomola; affinity binding site, with no effect on its picomolar affinity binding site or on [3H]prazasin binding. The nanomolar site is serotonergic as the serotonergic agonists, serotonin and 8-hydroxydipropylaminotetraline (8-OH-DPAT have nanomolar affinity for [3HljWB4101 binding when studied in the presence of a prazasin mask (30nM) of the alpha1 component of 3HJWB4101 binding. The serotonin receptor antagonists metergoline, lysergic acid diethylamide and lisuride also have high nanomolar affinities while ketanserin, yohimbine, prazosin and noradrenergic agonists have affinities in the micromolar range. Fimbrial transection or 5,7-diLydroxytryptamine injections produced 32% and 44 0ncreases in the Bmax of [3H]NVB4101 binding in the presence of a prazosin mask. Serotonin competition for [3H]WB4101 binding was identical in control and experimental tissue from each lesion experiment. Although specific binding of [3H]WB4101 was increased, there was no change in the affinities or the percentages of the two binding components for serotonin competition with [3H]WB4101. These data suggest that removal of the serotonergic input to the hippocampus produces an increase in the Bmax of serotonin receptor binding sites labeled by [3H]WB4101.
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