Lisuride

Fig 2 Reflectance scan of a chromatogram track with 90 ng of each substance per chromatogram zone 1 = lisuride dihydrogen maleate, 2 = methyseigide maleate, 3 = dihydroeigotamine mesylate, 4 = ergotamine tartrate. 

Lisuride dihydrogen maleate (h/Jj 30-35), methysergide maleate (h/ij 40-45), dihydroergotamine mesylate (hRf 45-50) and ergotamine tartrate (hRj 70-75) appeared as blue violet chromatogram zones on a yellow background. The detection limits — calculated for free base — were 3-4 ng substance per chromatogram zone. 

Hetey, L., Schwitzlowsky, R., and Oelssner, W., Influence of psychotomimetics and lisuride on synaptosomal dopamine release in the nucleus accumbens of rats, Eur. J. Pharmacol., 93, 213, 1983. 

Herrman, W. M., Horowski, R., Dannehl, K., Kramer, U., and Lurati, K. (1977) Clinical effectiveness of lisuride hydrogen maleate A double-blind trial versus methysergide. Headache, 17 54-60. 

Horowski, R., and Wachtel, H. (1979) Pharmacological effects of lisuride in rodents Mechanism of action and influence of chronic treatments with lisuride. In Dopaminergic Ergot Derivates and Motor Function, edited by K. Fuxe and D. B. Caine, pp. 237-251. Pergamon Press, New York. 

Kehr, W., and Speckenbach, W. (1978) Effect of lisuride and LSD on monoamine synthesis after axotomy or reserpine treatment in rat brain. Naunyn Schmiedebergs Arch. Pharmacol., 301 163-169. 

White, F. J., and Appel, J. B. (1982) Lysergic acid diethylamide (LSD) and lisuride Differentiation of their neuropharmacological actions. Science, 216 535-537. 

Limb flicks in cats, production by hallucinogens of, 61-63 receptor systems that mediate, 62-63 Limb jerks, in primates, production by hallucinogens of, 63-64 Lisuride, behavioral affects of, 54-55 Locomotor behavior, effects of hallucinogens on, 49-51... 

Itil, T. M., Herrmann, W. M and Akpinar, S. (1975) Prediction of psychtropic properties of lisuride hydrogen maleate by quantitative pharmaco-electroencephalogram. Int. J. Clin. Pharmacol., 12 221-223. 

Six patients with Parkinson s disease were withdrawn from their antiparkinsonian medications (L-DOPA/carbidopa, bromocriptine, or lisuride) (Rabey et al. 1992, 1993). After 12 hours off medication, the subjects ate 250 g of cooked fava beans. Significant improvements in motor symptoms were noted, comparable to those seen with 125 mg of L-DOPA and 12.5 mg of carbidopa. In fact, three subjects developed severe dyskinesias after fava ingestion, akin to those seen after larger doses of pharmaceutical L-DOPA. Plasma levels of L-DOPA increased after fava ingestion in a manner comparable to that seen with administration of oral L-DOPA. These results suggest that the L-DOPA contained in fava beans was transported into the CNS and converted to dopamine. In five nonparkinsonian, healthy volunteers, a similar increase in plasma L-DOPA was observed after fava ingestion, although much lower. The difference in plasma L-DOPA between normal volunteers and parkinsonian patients is apparently due to a residual effect of carbidopa in the subjects with Parkinson s disease. Without carbidopa, the L-DOPA from fava is rapidly converted to dopamine in the blood stream and never crosses the blood-brain barrier. 

Egan CT, Herrick-Davis K, Miller K, Glennon RA, Teitler M. (1998). Agonist activity of LSD and lisuride at cloned 5HT2A and 5HT2C receptors. Psychopharmacology (Berlin). 136(4) 40 14. 

Welsh SE, Kachelries WJ, Romano AG, Simansky KJ, Harvey JA. (1998). Effects of LSD, ritanserin, 8-OH-DPAT, and lisuride on classical conditioning in the rabbit. Pharmacol Biochem Behav. 59(2) 469-75. 

Bromocriptine (11), pergolide (12), cabergoline (13) and lisuride (14) are examples of compounds which have been developed in this way and are now used clinically. The pharmacological differences between the compounds is not very great. All are D2-dopamine receptor agonists, although... 

The involvement of dopaminergic neurotransmission in AD has led to the use of agonists such as bromocriptine, lisuride, and pergolide, with poor results. A selective monoamine oxidase B inhibitor (MAO-B) such as deprenyl has also been employed. Little solid information exists on the effects of deprenyl on AD. Unfortunately, all information available comes from small studies. In a double-blind study, Tariot et al. (1987) observed that, with a daily dose of 10 mg in 17 patients with AD, a significant reduction in the scores for anxiety, depression, tension, and excitement was achieved. Burke et al. (1993), in a study of more than 20 patients with AD during a period of 15 months, found no behavioral changes in the progression of the illness nor in its scores. 

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