Summary ,1. Human blood platelets have been shown to take up dopamine by an energydependent, saturable process that is inhibited by 5-hydroxytryptamine (5-HT), desipramine and other drugs. 2. Platelets from parkinsonian subjects receiving oral L-DOPA also took up dopamine.3. When the responses of normal and parkinsonian platelets were compared, the parkinsonian cells showed the following differences: increased affinity for the dopamine transport process; decreased equilibrium concentrations of dopamine after incubation for 90 min, and greater efflux of dopamine from loaded platelets during a 10 min incubation. 4. There were no differences in the uptake of 5-HT by parkinsonian platelets, but endogenous 5-HT was significantly reduced; ATP was normal. 5. In two out of three samples of platelets from parkinsonian subjects, traces of a dopamine-like substance were detected, but this finding requires confirmation. 6. If the platelet is a valid model for dopaminergic brain neurones, then the results described would suggest that dopamine uptake and storage may be abnormal in brain neurones in Parkinson's disease.

Attempts to isolate the putative endogenous ligand for the benzodiazepine receptor from bovine urine resulted in the identification of three isoflavans: equol (1), 3',7-dihydroxyisoflavan (2), and 4'-hydroxy-7-methoxyisoflavan (9), as "diazepam-like" compounds. 3-Chloro-9H-carbazole (17) was found to enhance the binding of diazepam in the benzodiazepine receptor binding assay. Pinosylvine monomethyl ether (18), indigo (20), and indirubin (21) were isolated as inactive compounds.

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SUMMMARY1. Blood platelets from normal children and children with the trisomy 21 form of Down's syndrome (mongolism) were studied to determine the cause of the well established reduction in platelet 5-HT in the disease.2. Concentrations of endogenous 5-HT in the platelets from mongols were 25-3 % of the concentrations found in normal children.3. The net accumulation of 5-HT in the mongol cells was decreased to 52*7 % of normal. This reduction was probably due, in part, to a defect in 5-HT transport, because the initial rates of 5-HT uptake at plasma concentrations of 10-and 10-5 M were significantly slower. 4. Experiments on the efflux of 5-HT from mongol platelets loaded with amine showed that the rate of loss was initially 2-6 and later 7-8 times faster than normal.5. Platelet ATP in mongol cells was 26 % of normal, and the reduction of ATP and 5-HT was in the molar ratio of 3:1.6. It is considered that the low platelet 5-HT in Down's syndrome is due to a defective 5-HT transport mechanism and impaired 5-HT binding, resulting from a reduction in the essential binding substance, ATP.