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[H]ketanserin binding increases in monkey cortex following basal forebrain lesions with ibotenic acid |
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| Authors: | Gary L. Wenk Kathrin L. Engisch Lisa D. McCall Susan J. Mitchell Thomas G. Aigner Robert L. Struble Donald L. Price David S. Olton |
| Affiliation: | * Department of Psychology, The Johns Hopkins University, Baltimore, MD 21218, U.S.A. † Laboratory of Neuropsychology, National Institute of Mental Health, Bethesda, MD 20205, U.S.A. ‡ Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. § Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. |
| Abstract: | The present study investigated the effects of damage to the basal forebrain cholinergic system upon [3H]ketanserin binding in the neocortex and hippocampus of monkeys. [3H]Ketanserin specifically binds to serotonin type-2 receptor sites. Lesions were placed in the medial septal area, nucleus basalis, or both regions. Ten months later, [3H]ketanserin binding was increased in the neocortex, but not in the hippocampus, while levels of choline acetyltransferase (acetyl-CoA: choline O-acetyltransferase, EC 2.3.1.6) activity decreased in the neocortex and hippocampus. Changes in the levels of choline acetyltransferase and [3H]ketanserin binding were correlated significantly in the neocortex (r = −0.64, P < 0.025), but not in the hippocampus. The data suggest that degeneration of the basal forebrain cholinergic system may alter serotonergic function in the neocortex. |
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