In vivo [125I]-iodobenzovesamicol binding reflects cortical cholinergic deficiency induced by specific immunolesion of rat basal forebrain cholinergic system
Autor: | Jochen Heinicke, Peter Georgi, Ingrid Kämpfer, Dietlind Sorger, Reinhard Schliebs, Steffen Rossner, C. Dannenberg |
---|---|
Rok vydání: | 2000 |
Předmět: |
Cancer Research
medicine.medical_specialty Cerebellum Tetrahydronaphthalenes Striatum Biology Iodine Radioisotopes chemistry.chemical_compound Prosencephalon Piperidines Internal medicine Vesicular acetylcholine transporter medicine Animals Receptors sigma Radiology Nuclear Medicine and imaging Receptors Cholinergic Tissue Distribution Cholinergic neuron Rats Wistar Basal forebrain Analysis of Variance Acetylcholinesterase Rats Radiography Endocrinology medicine.anatomical_structure nervous system chemistry Cholinergic Fibers Molecular Medicine Cholinergic Autoradiography Female Neuroscience Acetylcholine medicine.drug |
Zdroj: | Nuclear medicine and biology. 27(1) |
ISSN: | 0969-8051 |
Popis: | In this study, radiolabeled iodobenzovesamicol (IBVM), which is known to bind with high affinity to the vesicular acetylcholine transporter, was tested for its usefulness in imaging cortical cholinergic deficits in vivo. To induce reductions in cortical cholinergic input, the cholinergic immunotoxin 192IgG-saporin was employed. This has been shown to selectively and efficiently destroy basal forebrain cholinergic neurons in rats. The efficiency of the immunolesion was verified by histochemical acetylcholinesterase staining. [125I]-IBVM binding before and after lesioning was measured using autoradiography. Basal forebrain cholinergic cell loss resulted in a considerable reduction in [125I]-IBVM binding in the cholinoceptive target regions, but not in the striatum and cerebellum, brain regions that do not receive a cholinergic input by the basal forebrain cholinergic nuclei, suggesting that [123I]-IBVM has potential in imaging cortical cholinergic deficits in vivo, at least in animals. |
Databáze: | OpenAIRE |
Externí odkaz: |