Psychedelic Abstracts

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Serotonin release contributes to the locomotor stimulant effects of 3,4-methylenedioxymethamphetamine in rats.
J Pharmacol Exp Ther. 1990 Aug; 254(2): 456-64
Methylenedioxymethamphetamine (MDMA) is a phenylethylamine with novel mood-altering properties in humans. MDMA shares the dopamine-releasing properties of amphetamine but has been found to be a more potent releaser of serotonin (5-HT). The present study undertook to determine the relative roles of dopamine and 5-HT release in MDMA-induced locomotor hyperactivity. S-(+)MDMA produced dose-dependent increases of rat locomotion. Investigatory behaviors such as holepokes and rearings were suppressed by (+)MDMA. Pretreatment with the selective 5-HT uptake inhibitors fluoxetine, sertraline and zimelidine inhibited (+)MDMA-induced locomotor hyperactivity but failed to antagonize the reduction of holepokes and rearings. Because 5-HT uptake inhibitors have been found previously to block the MDMA-induced release of 5-HT in vitro, and because fluoxetine was found to have no effect on (+)amphetamine-induced hyperactivity, the present results suggest that (+) MDMA-induced locomotor hyperactivity is dependent on release of endogenous 5-HT. Additionally, prior depletion of central 5-HT with p-chlorophenylalanine partially antagonized the (+)MDMA-induced hyperactivity, although catecholamine synthesis inhibition with alpha-methyl-p-tyrosine did not block the effects of (+)MDMA. Taken together, these studies suggest that (+)MDMA increases locomotor activity via mechanisms that are dependent on the release of central 5-HT and that are qualitatively different from the mechanism of action of (+)amphetamine.

Serotonin release contributes to the locomotor stimulant effects of 3,4-methylenedioxymethamphetamine in rats.
Journal of Pharmacology and Experimental Therapeutics; 1990 Aug Vol 254(2) 456-464
Examined dopamine and 5-hydroxytryptamine (5-HT) release in methylenedioxymethamphetamine (MDMA) induced hyperactivity in male rats. S-(+)MDMA produced dose-dependent increases in locomotion. Investigatory behaviors such as holepokes and rearings were suppressed by (+)MDMA. Pretreatment with fluoxetine, sertraline, and zimelidine inhibited (+)MDMA-induced locomotor hyperactivity but failed to antagonize the reduction of holepokes and rearings. Results suggest that (+)MDMA-induced locomotor hyperactivity was dependent on release of endogenous 5-HT. Prior depletion of central 5-HT with p -chlorophenylalanine partially antagonized the (+)MDMA-induced hyperactivity, although catecholamine synthesis inhibition with alpha-methyl- p -tyrosine did not block the effects of (+)MDMA. (+)MDMA increased locomotor activity via mechanisms that are dependent on the release of central 5-HT and that are qualitatively different from the mechanism of action of (+)amphetamine.

Central alpha 1-adrenergic stimulation in relation to the behaviour stimulating effect of modafinil; studies with experimental animals.
Eur J Pharmacol. 1990 May 3; 180(1): 49-58
Single administration of the new drug modafinil was followed by an increase in locomotor activity in mice and in nocturnal activity in monkeys. Stereotyped behaviour in mice and rats, and potentiation of amphetamine-induced stereotyped behaviour were not observed; however, at the highest dose used, a slight potentiation of apomorphine-induced stereotyped behaviour was observed in rats. The modafinil-induced increase in locomotor activity in mice was prevented by the centrally acting alpha 1-adrenoceptor antagonists, prazosin and phenoxybenzamine, and by reserpine but not by the mixed dopamine D-1/D-2 antagonist, haloperidol, the dopamine D-2 antagonist, sulpiride, the peripherally acting alpha 1-adrenoceptor antagonist, phentolamine, the alpha 2-adrenoceptor antagonist, yohimbine, the beta-adrenoceptor antagonist, propranolol, or by the catecholamine synthesis inhibitor, alpha-methyl-p-tyrosine. Likewise, the modafinil-induced increase in nocturnal activity in monkeys was prevented by prazosin. Interestingly, modafinil did not produce obvious peripheral sympathetic effects in mice and rats (no salivation, no contraction of the pilomotor muscles, slight mydriasis only at high doses). Therefore, modafinil appears to produce a strong stimulating effect in rodents and in primates. These effects could be linked to modulation (stimulation) of central alpha 1-adrenoceptors unaccompanied by peripheral sympathetic effects, which is unexpected.

Purity of street LSD
'Psychedelic Drugs Reconsidered'; 1979
According to data compiled by the PharmChem Research Foundation, a California organization, the only psychedelic drugs now generally available on the street are LSD, PCP, and to a lesser extent MDA. Almost no one takes the trouble to manufacture mescaline or psilocybin, because their effects resemble those of LSD and the much larger amounts required make the expense too great. Mescaline is available only in the form of peyote buttons and psilocybin only in the form of psychedelic mushrooms, which have been discovered growing all over the United States; they are increasingly sought after in the wild (see Pollock 1975 a; Weil 1977 a) and, with difficulty, can also be cultivated (see Oss and Oeric 1976). (Many 'psilocybin mushrooms,' incidentally, are just commercial mushrooms laced with LSD.) Anything labeled as pure or synthetic mescaline, psilocybin, or THC is almost certainly either LSD or PCP, or else contains no drug. Some chemicals closely related to LSD have been synthesized to sidestep the law; the one most often available is the acetylated variant, ALD-52, which is almost as potent as LSD itself. As for the quality of illicit LSD, adulterants and substitutes must be distinguished from products of improper synthesis. Since the variable physical and psychological effects of LSD sometimes resemble those of strychnine, belladonna, or amphetamine, there are rumors that illicit LSD often contains these substances. But laboratory analysis, especially the work of PharmChem Research Foundation, shows that illicit LSD rarely contains adulterants, although the advertised dose is usually two to five times the actual one. The major problem is imputities that are by-products of careless or inadequate synthesis. In the manufacturing process, ergotamine or other ergot alkaloids are reduced to lysergic acid (d-lysergic acid monohydrate), which is then converted to LSD. The whole procedure, and especially the last stage, in which LSD is separated from iso-LSD by chromatography, is rather delicate; it requires skill and good equipment. The government has tried to cut off the supply of chemical precursors; but illicit chemists are usually able to obtain enough, because several ergot derivatives are used as medicines and the quantities needed are small: by on estimate, 70 kg of ergotamine tartrate is enough to supply the American LSD market for a year (McGlothlin 1974 b). The only impurity regularly found by the PharmChem Laboratory, aside from occasional traces of ergotamine, is iso-LSD: it is very similar to LSD in chemical structure (the same atoms in a slightly different arrangement) but pharmacologically inactive. It is rarely present in a proportion of more than 15 percent and appears to have no effect on the drug action. So street LSD seems to be reasonably pure.

Stimulation of rat prolactin secretion by indolealkylamine hallucinogens.
Psychopharmacology; 1978 Vol 56(3) 255-259
The hallucinogenic indoleamine drugs N,N-dimethyltryptamine (DMT), psilocybin, bufotenin, 5-methoxy-N,N-dimethyltryptamine, and N-methyltryptamine increased plasma prolactin (PRL) levels in male Sprague-Dawley rats. The increase in plasma PRL produced by DMT, psilocybin, and bufotenin was inhibited by methysergide, a serotonin receptor blocker. Parachlorophenylalanine (PCPA), an inhibitor of serotonin synthesis, significantly potentiated the increase in PRL produced by DMT and psilocybin. Parachloroamphetamine, a relatively selective toxin for serotonin neurons, also stimulated the increase in PRL produced by DMT. These results suggest that the indole hallucinogens stimulate PRL secretion by a serotonergic agonist mechanism. Bufotenin has been reported to pass the blood/brain barrier poorly, but of the indoles studied it had the most potent effect on PRL secretion. This raises the possibility that the serotonin receptors that promote PRL secretion may be outside the blood/brain barrier or that the central 5-hydroxytryptamine receptors that mediate PRL secretion may be especially responsive to bufotenin.

New iodinated amphetamines by rapid synthesis for use as brain blood flow indicators.
J. Lab. Cmpds. and Radiopharm. 19: 1307. (1982) [#132]
[No Abstract]

Sargent, T., A. T. Shulgin, and C. A. Mathis.
New iodinated amphetamines by rapid synthesis for use as brain blood flow indicators.
J. Lab. Cmpds. and Radiopharm. 19: 1307. 132 (1982.)

Antagonism of the neurotoxicity due to a single administration of methylenedioxymethamphetamine.
Eur J Pharmacol. 1990 May 31; 181(1-2): 59-70
The role of transmitter release in the serotonergic neurotoxicity of methylenedioxymethamphetamine (MDMA) was examined using treatments altering MDMA-induced release or its consequences. The long-term decrease in 5-HT concentrations and tryptophan hydroxylase activity produced by MDMA was antagonized by depletion of vesicular monoamines with reserpine or interruption of monoamine synthesis with the decarboxylase inhibitor, monofluoromethyl DOPA (dihydroxyphenylalanine). Similar results were achieved by selectively inhibiting dopamine synthesis with alpha-methyl-p-tyrosine or through bilateral lesions of the substantia nigra with 6-hydroxydopamine. The dopamine receptor antagonist haloperidol was also effective in this regard. Although these results strongly implicate dopamine release in the long-term neurochemical effects of MDMA, protection was also provided by selective 5-HT2 antagonists indicating that the neurotoxicity is dependent upon the release of both dopamine and 5-HT.

Schmidt, Christopher J; Kehne, John H
Neurotoxicity of MDMA: Neurochemical effects.
Annals of the New York Academy of Sciences; 1990 Oct Vol 600 665-681
The acute neurochemical effects of 3,4-methylenedioxymethamphetamine (MDMA) begin immediately after administration with a rapid decline in the activity of the rate-limiting enzyme for 5-hydroxytryptamine (5-HT) synthesis, tryptophan hydroxylase. There is also an increase in carrier-mediated efflux of 5-HT that may be responsible for the behavioral effects of MDMA. An acute imbalance in the redox state of the serotonergic nerve terminal may be involved in the development of MDMA's long-term effects. The immediate effects of p -chloroamphetamine (PCA) and MDMA at resistant terminals are similar regardless of their sensitivity to neurotoxic effects. A difference between sensitive and resistant terminals may explain differences in sensitivity to PCA and MDMA.

Stanford, Mark W
Designer drugs: Medical aspects and clinical management.
Alcoholism Treatment Quarterly; 1988 Win Vol 4(4) 97-125
Discusses designer drugs (i.e., illegally manufactured psychoactive compounds that are chemically manipulated for the consumer) that are currently circulating within the chemically dependent population, including analogs of fentanyl, meperidine, phencyclidine, and MDA/MDMA (93-4-methylenedioxyamphetamine and its N-methyl analog, respectively). Drug classifications, kinetics, central nervous system (CNS) effects, patterns of abuse, and treatment suggestions are outlined for each drug. As no one can attest to the kitchen chemist's knowledge of chemical synthesis, the products' potency, purity, or toxic potentiation for cellular damage is unknown.

Stimulus properties of phenethylamine hallucinogens and lysergic acid diethylamide: The role of 5-hydroxytryptamine.
Journal of Pharmacology and Experimental Therapeutics; 1978 Feb Vol 204(2) 416-423
Investigated the effects on mescaline-mediated stimulus control of BC-105 and cinanserin, 2 chemically distinct antagonists of 5-hydroxytryptamine (5-HT) and of parachlorophenylalanine (PCPA), an inhibitor of 5-HT synthesis. Stimulus control was established by assigning 2 conditions to each female CFN rat. One treatment was the stimulus in whose presence responses were reinforced, and the other was the stimulus in whose presence responses were punished. In Groups 1 and 2, the conditions were mescaline (10 mg/kg) and saline; in Groups 3 and 4, they were amphetamine and saline. In Ss trained to discriminate the effects of mescaline and saline, BC-105 and cinanserin blocked mescaline-mediated stimulus control and the degree of antagonism was positively correlated with the dose of antagonist. Pretreatment with PCPA failed to produce significant effects. An indication of the specificity of action of BC-105 was provided by its failure, over a range of doses, to antagonize the stimulus of amphetamine. Doses of LSD, 2,5-dimethoxy-4-methylamphetamine, and 2,5-dimethoxy-4-ethylamphetamine which mimicked mescaline in mescaline-trained Ss were blocked by the same doses of either BC-105 or cinanserin found to be effective against mescaline. Data suggest that a serotonergic mechanism plays a significant role in stimulus control induced by mescaline. Drugs that mimic mescaline, whether of indoleamine or phenethylamine class, appear to do so via the same mechanism.

Serotonergic function in mouse head twitches induced by lithium and reserpine.
Psychopharmacology; 1979 Vol 61(3) 255-260
Examined the relationship between lithium-induced head twitches (HTs) and serotonergic neurons in male ddY albino mice. HTs were elicited by combined treatment with lithium chloride (2 or 5 mEq/kg in 5 hourly sc injections) and rauwolfia alkaloids (i.e., reserpine, 5 mg/kg; tetrabenazine, 20 mg/kg; and syrosingopine, 10 mg/kg; all given sc). Neither lithium nor the alkaloid alone induced the HTs, nor did administration of lithium combined with methamphetamine or parachloroamphetamine. HTs induced by lithium in combination with reserpine were strongly inhibited by the antiserotonin drugs methysergide and cyproheptadine and also by a serotonin synthesis inhibitor, parachlorophenylalanine (PCPA), when administered between lithium and reserpine. When PCPA was administered before lithium for 3 days, HTs were potentiated. In addition, the HTs were potentiated by a serotonin receptor stimulant, 5-methoxy-N,N-dimethyltryptamine. Results imply that lithium can induce HTs in the presence of rauwolfia alkaloids and may exert its effect in part by acting on the serotonergic neuron system.

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