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Schwarcz R, Bennett JP, Coyle JT. 
“Loss of striatal serotonin synaptic receptor binding induced by kainic acid lesions: correlations with Huntington's Disease”. 
J.Neurochem.. 1977;28(4):867-69.
The effects of kainic acid (KA) on striatal serotonin (5-HT) synaptic receptor binding were studied. 2 mcg KA (Sigma-Chem.) was injected into the rat caudate nucleus. After decapitation, performed 10 days later, the brains were removed and dissected. The lesioned striate and contralateral non-lesioned striate were analyzed for 5-HT uptake, using KrebsRinger-Tris medium. (3H)5-HT (Arnersham Searle) was added. Non-specific (3H)-5-HT uptake was estimated using 10 mcM Lilly 1 1 0140. 5-HT synaptic receptor binding was determined by homogenizing the frozen striate in Tris-hydrochloride buffer. Aliquots of homogenate were incubated with (3H)-LSD (New England Nuclear) or (3H)-5-HT and binding determined. Results Specific binding of (3H)-LSD and (3H)-5-HT to membrane preparations from KA-lesioned caudate nuclei was reduced 60-70% below values for contralateral un-lesioned caudate nuclei. Binding of both ligands was inhibited approxirna tely the same percentate in lesioned and non-lesioned tissue by unlabeled LSD, 5-HT and 2bromo-LSD. The integrity of presynaptic 5-HT terminals determined by synaptosomal high-affinity (3H)-5-HT uptake was not changed by the lesions. Conclusion Since the decreases in (3H)-LSD and (3H)-5-HT binding to KAlesioned caudate nuclei were similar in magnitude to those decreases found in neuronally depleted Huntington's disease caudate nuclei, this strengthened the usefulness of striatial KA lesions as an animal model for Huntington's disease.
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