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PubMed1984

Behavioral effects of intracerebroventricular administration of LSD, DOM, mescaline or lisuride.

The effects on a fixed ratio-40 (FR-40) operant behavior of intracerebroventricular (ICV) administration of the hallucinogens lysergic acid diethylamide (LSD), 2,5-dimethoxy-4-methylamphetamine (DOM), mescaline or the non-hallucinogenic LSD-analogue lisuride were compared with intraperitoneal (IP) administration. Infusion of LSD (8.5 to 34 micrograms) into the left lateral ventricle produced a dose-dependent decrease in reinforcers and an increase in 10-sec periods of non-responding (pause intervals). The time-course of LSD showed a shorter latency to onset after ICV than IP administration. The ED50 for doses increasing pause intervals by ICV administration was 15 micrograms. This disruption was greater than that produced by IP administration of equivalent doses of LSD (IP ED50: 19 micrograms). DOM (40 to 120 micrograms) infused into the lateral ventricle also produced a dose-dependent disruption of FR-40 behavior. ICV DOM also showed a rapid onset to peak effects, but a slower offset than LSD, and was 3 times more potent than systemic administration (ED50s: 58 micrograms ICV vs. 153 micrograms IP). Mescaline was much more potent in disrupting FR-40 behavior by the ICV route than by IP administration. The ICV ED50 for doses of mescaline increasing pause intervals was 74 micrograms, in contrast to an ED50 following systemic administration of 2251 micrograms, demonstrating a 30-fold difference in potency. Lisuride administered via the ICV route was no more potent than by IP administration with ED50s of 4 micrograms ICV and 4 micrograms IP. Lower doses of lisuride administered by both routes had a similar effect over time on pause intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed2005

DPP IV inhibitor blocks mescaline-induced scratching and amphetamine-induced hyperactivity in mice.

Dipeptidyl peptidase IV (DPP IV) is a ubiquitous membrane-bound enzyme that cleaves the two N-terminal amino acids from peptides with a proline or alanine residue in the second position from the amino end. Potential substrates for DPP IV include several neuropeptides, suggesting a role for DPP IV in neurological processes. We have developed a potent DPP IV inhibitor (IC50 = 30 nM), 1-(2-amino-3-methyl-butyryl)-azetidine-2-carbonitrile (AMAC), which has shown efficacy in two established models of psychosis: mescaline-induced scratching and amphetamine-induced hyperactivity. In the mescaline-induced scratching model, AMAC treatment before mescaline administration reduced the number of scratching paroxysms by 68% (P < 0.01). The compound showed a dose-dependent effect, inhibiting significantly at 6, 20 and 60 mg/kg (37%, 39% and 68%, respectively). In the amphetamine-induced hyperactivity model, 50 and 60 mg/kg AMAC, given before injection of amphetamine, significantly reduced hyper-locomotion by 65% and 76%, respectively. Additionally, AMAC showed no significant activity in binding assays for 20 receptors thought to be involved in the pathology of schizophrenia, including dopamine, serotonin and glutamate. A structurally similar analog, 1-(2-dimethylamino-3-methyl-butyryl)-azetidine-2-carbonitrile (DAMAC), that does not inhibit DPP IV, was inactive in both models. Taken together, these data suggest that the antipsychotic effects of AMAC are the result of DPP IV inhibition.

Amphetamine↗
PubMed1981

Sulfur analogues of psychotomimetic agents. Monothio analogues of mescaline and isomescaline.

Two monothio analogues of mescaline and three monothio analogues of 2,3,4-trimethoxyphenethylamine (isomescaline) have been synthesized and characterized. Only the two mescaline analogues (3-and 4-thiomescaline) were found to be psychotomimetics in man, being 6 and 12 times more potent than mescaline, respectively. All five compounds can serve as substrates for bovine plasma monoamine oxidase in vitro, but no positive correlation is apparent between the extent of enzymatic degradation and human psychotomimetic potency.

Adult↗
PubMed2003

The analysis and distribution of mescaline in postmortem tissues.

Mescaline (3,4,5-trimethoxyphenethylamine) is a hallucinogenic alkaloid found in the peyote cactus. This report documents mescaline distribution in a death caused by multiple gunshot wounds. Mescaline was extracted with a butyl chloride liquid-liquid method and identified by mass spectrometry. Quantitative analysis was performed by gas chromatography using a nitrogen-phosphorus detector. Concentrations of the drug were 2.95 mg/L, 2.36 mg/L, 8.2 mg/kg, and 2.2 mg/kg in blood, vitreous, liver, and brain, respectively.

Forensic Medicine↗
PubMed1976

Potentiation by desipramine of neuronal responses to mescaline.

The effect of desipramine on responses of single cortical neurones to mescaline was studied by the microelectrophoretic technique. Both potentiation and antagonism of responses to mescaline by desipramine were observed. The antagonism may be related to the alpha-adrenolytic action of desipramine. The potentiation is unlikely to reflect the uptake blocking action of desipramine, since desipramine does not block the uptake of mescaline in the cerebral cortex. It is suggested that the potentiation may be due to a post-synaptic action of desipramine.

Animals↗
PubMed1981

Phencyclidine, lysergic acid diethylamide, and mescaline: cerebral artery spasms and hallucinogenic activity.

Phencyclidine (PCP), lysergic acid diethylamide (LSD), and mescaline produced potent contractile responses on isolated basilar and middle cerebral arteries, where, in terms of potency, LSD greater than mescaline greater than PCP. All three drugs produced cerebrovasospasm in a concentration range which parallels that needed for their psychotomimetic and intoxicating actions. Specific receptors for PCP, which subserve contraction and differ from those for LSD and mescaline, are found in cerebral arteries. Concentrations of PCP that produced near-maximum contractile responses on cerebral arteries were similar to those in the blood and brain of human subjects who had died from PCP overdoses. A specific calcium antagonist, verapamil, readily prevented (and reversed) PCP-induced vasospasm. This study provides direct evidence for PCP receptors in cerebral blood vessels, the biologic action of which can be reversed by a calcium antagonist; the clinical use of the latter could prove invaluable in treating PCP-intoxicated victims.

Animals↗
PubMed1990

[Some analytical aspects of mescaline].

Mescaline was extracted from a vegetal powder, seazed on the "Côte d'Azur", then analyzed by several techniques (thin layer chromatography, infra-red spectrometry, gas chromatography/mass spectrometry) and determined by high performance liquid chromatography with methyl-amphetamine as internal standard. The powder contained 0.76% of mescaline. The presence of a possible isomer was noted in the powder as well as in a "old" sample of mescaline.

Chromatography, Thin Layer↗
PubMed1989

Effects of mescaline and its derivative N-[3,4,5-trimethoxyphenylethyl]-aziridine on the spatial orientation of rats in a T-maze.

The central effect of mescaline and of its derivative N-[3,4,5- trimethoxyphenylethyl]-aziridine (FAZ) after their stereotaxic administration into the lateral ventricle of the brain was studied in behavioural experiments on rats. The effect of the two substances was tested by a method studying memory elicitation in response to appetitive motivation in a multiple T-maze. The results show that both substances worsened the behaviour in question. The negative effect of mescaline (lengthening of the time of passage through the maze) was manifested both immediately and several weeks after a single dose. FAZ likewise worsened the test reaction, but its effect was less pronounced than that of mescaline.

Animals↗
PubMed1979

[Effect of mescaline on cerebral cholinesterases and on exploratory behavior in rats].

In this study the Authors had the purpose to evaluate the action of a psychotomimetic substance (mescaline) on behavior (exploring behaviour and spontaneous motility) and on cerebral biochemistry (cholinesterase activity) of rat. The mescaline has shown to be active both on behaviour (increasing the spontaneous motility) and on biochemistry (decreasing the total cholinesterase activity). From the examination of the results of this work it could be cautiously assumed the hypothesis that the behavioural effects of mescaline are related (at least partially) to modifications of the cholinergic system at the cerebral level.

Acetylcholinesterase↗
PubMed1976

Synthesis of potential mescaline antagonists.

1-[2-(3,4,5-Trimethoxyphenyl)ethyl]-3-pyrroline, 2-(3,4,5-trimethoxybenzyl)-1,2,3,6-tetrahydropyridine, N-n-propylmescaline, N-cyclopropylmethylmescaline, and N-allylmescaline were synthesized as potential mescaline antagonists. The ability of these compounds to antagonize mescaline-induced disruption of swim behavior is also given.

Animals↗
PubMed1983

Synthesis and action on the central nervous system of mescaline analogues containing piperazine or homopiperazine rings.

Structural juxtaposition of the 3,4,5-trimethoxyphenyl group in the same molecule with a piperazine or homopiperazine ring has been realized in a series of mescaline analogues (I-IV) as part of an investigation into the pharmacological properties of the seven-membered perhydro-1,4-diazepines (homopiperazines). The analogous six-membered piperazines were synthesized and tested as reference substances to determine whether the seven-membered ring conveyed special properties. A variety of pharmacological tests of action on the CNS showed that replacement of the amino group in mescaline by the heterocycles significantly alters the biological activity. In particular, both the piperazine and the homopiperazine derivatives displayed sedative activity to about the same extent.

Animals↗
PubMed1976

Parachlorophenylalanine potentiates facilitatory effects of mescaline on shuttlebox escape/avoidance in rats.

Acute parachlorophenylalanine (pCPA) pretreatment (150 mg/kg, i.p., 24 h beforehand) potentiated facilitatory effects of mescaline (39.6 mg/kg i.p.) on shuttlebox escape/avoidance in hooded rats, tested in two different situations: 1. during aquisition of avoidance behavior (Experiment 1); and 2. in stable pretrained poor avoiders (Experiment 2). pCPA alone did not influence avoidance behavior in either situation. Mescaline, with pCPA pretreatment, may be associated with long-term behavioral effects; all rats treated with this combination were later found to be poor avoiders, unable to achieve a stable baseline of good avoidance. pCPA significantly depleted brain norepinephrine and dopamine, as well as serotonin, measured after testing in the second situation.

Animals↗
PubMed1975

Does increasing stress change the behavioral action of mescaline from disruption to facilitation?

This experiment is related to the hypothesis of Bridger and of Wray that hallucinogens have facilitatory effects on animal behavior when stress is part of the experiment and have disruptive effects otherwise. Male Long-Evans rats were trained to high (above 89%), stable base line rates of shuttlebox avoidance, then given each of four treatments at 6-day intervals after returning to base line avoidance rates: 1. saline (1 ml i.p.), 2. saline+stressor, 3. mescaline hydrochloride (36.6 mg/kg i.p.), 4. mescaline (39.6 mg/kg i.p.)+stressor. Stress treatment was 1.0 mA footshock (1 sec duration) every 20-30 sec for 15 min between injection and session. Sessions (100 trials) began 20 min after injection. Treatments 1 and 2 had no effect on avoidance rate. Treatments 3 and 4 significantly decreased avoidance rate, with the latter causing significantly more decrease than the former. None of the treatments affected presession (5 min adaptation period) or intertrial crossings of the shuttlebox or latency on escape trials. These results suggest that exposure to a stressor, per se, is not the crucial factor causing hallucinogens to have facilitatory effects on animal behavior.

Adaptation, Psychological↗
PubMed1983

Mescaline elicits behavioral effects in cats by an action at both serotonin and dopamine receptors.

The characteristic behavioral effects of mescaline in cats were nearly completely blocked by pretreatment with low doses of either a specific serotonin antagonist (methysergide) or a dopamine specific antagonist (haloperidol). These blocking effects were not due to non-specific actions, since methysergide did not block the behavioral effects of apomorphine, and haloperidol did not block the behavioral effects of 5-methoxy-N,N-dimethyltryptamine. Thus, it appears that the behavioral effects of mescaline are dependent upon the simultaneous action of the drug at both serotonin and dopamine receptors.

5-Methoxytryptamine↗
PubMedDate not supplied

A new view of the structural relationship between LSD and mescaline.

An examination of the effects of S-(-) and R-(+) 2-amino-1,2,3,4-tetrahydronaphthalene (2-AT) on mouse spontaneous activity and rabbit EEG has shown that the S-(-) enantiomer shows selective central effects similar to those of hallucinogens like mescaline. A stereochemical analysis of these results indicates that the structural relationship between mescaline, or other phenethylamine type hallucinogens, may involve correspondence between the aromatic ring of the phenethylamines and the pyrrole portion of the indole nucleus in LSD.

Animals↗
PubMed1997

Dihydrobenzofuran analogues of hallucinogens. 4. Mescaline derivatives.

Dihydrobenzofuran and tetrahydrobenzodifuran functionalities were employed as conformationally restricted bioisosteres of the aromatic methoxy groups in the prototypical hallucinogen, mescaline (1). Thus, 4-(2-aminoethyl)-6,7-dimethoxy-2,3-dihydrobenzofuran hydrochloride (8) and 1-(8-methoxy-2,3,5,6-tetrahydrobenzo[1,2-b:5,4-b']difuran-4-yl)-2- aminoethane hydrochloride (9) were prepared and evaluated along with 1 for activity in the two-lever drug discrimination (DD) paradigm in rats trained to discriminate saline from LSD tartrate (0.08 mg/kg). Also, 1, 8, and 9 were assayed for their ability to displace [3H]ketanserin from rat cortical homogenate 5-HT2A receptors and [3H]8-OH-DPAT from rat hippocampal homogenate 5-HT1A receptors. In addition, these compounds were evaluated for their ability to compete for agonist and antagonist binding to cells expressing cloned human 5-HT2A, 5-HT2B, and 5-HT2C receptors. Finally, agonist efficacy was assessed by measurement of phosphoinositide hydrolysis in NIH 3T3 cells expressing the rat 5-HT2A or 5-HT2C receptors. Although 1 fully substituted for LSD in the DD assays (ED50 = 33.5 mumol/kg), neither 8 nor 9 substituted for LSD, with just 50% of the rats administered 8 selecting the drug lever, and only 29% of the rats administered 9 selecting the drug lever. All of the test compounds had micromolar affinity for the 5-HT1A and 5-HT2A receptors in rat brain homogenate. Curiously, the rank order of affinities of the compounds at 5-HT2A sites was opposite their order of potency in the behavioral assay. An evaluation for ability to stimulate phosphoinositide turnover as a measure of functional efficacy revealed that all the compounds were of approximately equal efficacy to serotonin in 5-HT2C receptors. At 5-HT2A receptors, however, 8 and 9 were significantly less efficacious, eliciting only 61 and 45%, respectively, of the maximal response. These results are consistent with the proposed mechanism of action for phenethylamine hallucinogens, that such compounds must be full agonists at the 5-HT2A receptor subtype. In contrast to the 2,5-dimethoxy-substituted phenethylamines, where rigidification of the methoxy groups had no deleterious effect on activity, the loss of activity in the 3,4,5-trioxygenated mescaline analogues may suggest that the 3 and 5 methoxy groups must remain conformationally mobile to enable receptor activation.

3T3 Cells↗
PubMed1995

3,4,5-Trimethoxyphenylacetaldehyde, an intermediate metabolite of mescaline, is a substrate for microsomal aldehyde oxygenase in the mouse liver.

3,4,5-Trimethoxyphenylacetaldehyde, an intermediate metabolite of mescaline, was oxidized to 3,4,5-trimethoxyphenylacetic acid by mouse hepatic microsomes. The reaction was NADPH-dependent, and inhibited by SKF 525-A, metyrapone and disulfiram. A P450 isozyme in mouse hepatic microsomes, P450 MUT-2 (CYP2C29), catalyzed the reaction (0.96 nmol/min/nmol P450) in which NADPH and NADPH-cytochrome c reductase were essential for the catalytic activity. The reaction was confirmed to be an oxygenation since molecular oxygen was incorporated into the carboxylic acid metabolite formed under oxygen-18 gas by GC-MS analysis. By addition of antibody against CYP2C29 to the microsomes (3.2 mg/mg microsomal protein) the MALDO activity was inhibited by 35% of the control value with preimmune serum, suggesting that CYP2C29 or an immunologically-related isozyme(s) plays a major role in the NADPH-dependent oxidation of 3,4,5-trimethoxyphenylacetaldehyde to 3,4,5-trimethoxyphenylacetic acid by mouse hepatic microsomes. Pharmacological experiments on mescaline and its deaminated metabolites using mice indicated that the metabolites were much less active or were inactive in cataleptogenic effect and pentobarbital-induced sleep prolongation as compared with the parent compound.

Acetaldehyde↗
PubMed1978

[Effects of mescaline and lysergide on the mechanical responses of isolated organs of the rat to catecholamines and the role of calcium transfers in these phenomena].

On isolated Rat vas deferens the contracting responses of noradrenaline and dopamine are increased by mescaline (23 micromoles) and decreased by lysergide (15 micromoles). Similarly, on isolated Rat duodenum previously decalcified the hypertonic responses of recalcification are modified in the opposite direction by the two agonists. On the other hand, mescaline such as lysergide increase the fall of tonus which ensues the decalcification of isolated duodenum.

Animals↗