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Persson SA. 
“The Effect of LSD and 2-Bromo LSD on the Striatal Dopa Accumulation after Decarboxylase Inhibition in Rats”. 
Europ.J.Pharmacol.. 1977;43(1):73-83.
Effects of LSD and 2-bromo LSD (BL; 50th Sandoz) on striatal DOPA accumulation after decarboxylase inhibition in rats were investigated. Methods Cerebral hemisection at the caudate hypothalamus was performed in male Sprague-Dawley rats (188-298 g) under ether anesthesia. In vivo tyrosine hydroxylation was determined via measurement of striatal DOPA levels. 3Hydroxybenzylhydrazine (NSD-1015), a carboxylase inhibitor, was given and striate were removed after death. DOPA was isolated and determined fluorometrically. All drugs were administered via i.p. injection. Results NSD-1015 induced striatal DOPA accumulation. LSD and BL (both 2 mg/kg) increased DOPA levels. BL (2-4 mg/kg) had a significantly greater effect, which was similar to that of haloperidol (Leo) (0.5 mg/kg). Apomorphine (Sandoz) decreased DOPA levels. LSD with BL had a similar effect to that of BL alone. LSD and BL (0.5-2 mg/kg) overcame the effect of apomorphine (5 mg/kg) dose-dependently. LSD and BL did not alter striatal DOPA levels due to haloperidol (5 mg/kg). Increase in DOPA at 4 and 24 hr after reserpine (Serpasil, CIBA) (5 mg/kg) was inhibited by LSD (0.5 mg/kg) and apomorphine(O.05mg/kg). BL had no effect. LSD (0.5 mg/kg) inhibited increased DOPA levels in the sectioned side of the brain, while BL increased levels in the other side. y-butyrolactone (Sigma-Chem.) (750 mg/kg) increased DOPA accumulation, which was inhibited dosedependently by apomorphine and LSD. Haloperidol, BL and promethazine (Lergigan, Recip) did not have any effect. Haloperidol, but not BL orpromethazine, inhibited the effect of apomorphine. Promethazine and BL antagonized the LSD -induced fall in DOPA levels following y-butyrolactone administration.
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