Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MESCALINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

Action of a chronic administration of mescaline in dynamic behavioural situations.

The modifications of the rat behaviour caused by a chronic administration of mescaline were studied in two schedules of operant conditioning. In the "periodic conditioning" test, the schedule of reinforcement was changed from a fixed ratio to a fixed interval schedule. Mescaline (4 mg/kg/day and 10 mg/kg/day) caused no modification of the ability of the rat to adapt its behaviour to the new experimental situation. In the "reversal test" the contingency for food delivery was switched from one lever, where responses were previously reinforced to the other lever where responses had no programmed consequences. A chronic administration of mescaline (4 mg/kg/day) caused a total incapacity of the rat to switch to the lever which became reinforced in the reversal trial. A chronic administration of 9 mg/kg/day of mescaline had an excitatory effect and the number of reinforced responses in the II and III reversals exceeded the unreinforced responses in a measure greater than in the controls.

Animals↗

C-(4,5,6-trimethoxyindan-1-yl)methanamine: a mescaline analogue designed using a homology model of the 5-HT2A receptor.

A conformationally restricted analogue of mescaline, C-(4,5,6-trimethoxyindan-1-yl)-methanamine, was designed using a 5-HT(2A) receptor homology model. The compound possessed 3-fold higher affinity and potency than and efficacy equal to that of mescaline at the 5-HT(2A) receptor. The new analogue substituted fully for LSD in drug discrimination studies and was 5-fold more potent than mescaline. Resolution of this analogue into its enantiomers corroborated the docking experiments, showing the R-(+) isomer to have higher affinity and potency and to have efficacy similar to that of mescaline at the 5-HT(2A) receptor.

Animals↗

Nootropic candidates inhibit head-twitches induced by mescaline in mice.

The effects of various nootropic candidates on mescaline-induced head-twitches were studied in mice. The number of head-twitches induced by mescaline (100 mg/kg, s.c.) was significantly reduced by idebenone (32 and 100 mg/kg, i.p.), minaprine (0.32-10 mg/kg, p.o.) and nebracetam (100 mg/kg, p.o.). Cholinesterase inhibitors such as tetrahydroaminoacridine (1 and 10 mg/kg, p.o.), NIK-247 (10 and 18 mg/kg, p.o.) and physostigmine (0.32 mg/kg, i.p.) also suppressed the head-twitch response to mescaline. These results suggest that the direct or indirect cholinergic-activating effects of these drugs may be involved in inhibiting mescaline-induced head-twitches.

Animals↗

Mescaline: a survey.

The hallucinogen mescaline is found in the peyote and San Pedro cacti, which are prevalent in Mexico and the southwestern United States. In a survey of middle-class, predominantly white adolescents in a drug treatment facility, 18 percent of the respondents indicated that they had taken mescaline. Much of the purported mescaline was probably another hallucinogen, usually LSD. The effects of equipotent doses of mescaline and LSD are almost indistinguishable.

Adolescent↗

[Estimation of mescaline and pellotine in Lophophora coulter plants (Cactaceae) by means of the oscillographic polarography].

Oscillographic polarography has been applied for the mescaline and pellotine estimation. These alkaloids produce in 0.5 N NaOH electrolyte a sharp peak within the cathode region of the oscillogram, each of them showing different potential. It makes possible to estimate them at a concentration of 5.10(-6) g/ml. All the forms of Lophophora williamsii were found to contain mescaline and lower content of pellothine, L. jourdaniana--to have equal content of both alkaloide, L. diffusa and L. fricii--to contain pellotine and only traces of mescaline. Plants grown in the greenhouse accumulated the same amount of alkaloids as native plants. Grafting on roodstock which does not produce essential amount of the alkaloids, does not affect the ability of Lophophora to synthesize mescaline and pellotine.

Alkaloids↗

Teratogenic effects of mescaline, epinephrine, and norepinephrine in the hamster.

Mescaline was administered orally at doses of 16 and 32 mg/kg on the seventh through tenth days of gestation to pregnant cream-strain hamsters. This treatment resulted in a dose-dependent effect on reproductive success and skeletal ossification. The effect of mescaline on reproductive success included an increased number of resorptions resulting in a decreased litter size. The 32 mg/kg dose of mescaline caused 48.8% resorptions, while 16 mg/kg and control animals had 12.0% and 6.4% resorptions, respectively. Litter size was decreased from 12.0 pups in controls to 10.3 (16 mg/kg) and 6.5 (32 mg/kg) pups per litter in treated groups. No gross abnormalities were observed at necropsy; there was, however, a dose-dependent increased delay in the ossification of the skull, sternum, and metatarsals. Both epinephrine and norepinephrine caused a decrease in reproductive success when administered at 500 micrograms/kg. Epinephrine appeared to cause a trend toward preimplantation wastage as indicated by an increased corpora lutea to implantation site ratio (from 1.3-1.9). Norepinephrine, however, caused an increased number of resorptions (29.1% in controls). Both norepinephrine and epinephrine produced similar delays in ossification.

Animals↗

Mescaline: excitatory effects on acoustic startle are blocked by serotonin2 antagonists.

The ability of serotonin2 (5-HT2) antagonists to block the excitatory effects of mescaline on the acoustic startle reflex were analyzed. Mescaline (20 mg/kg) caused a consistent increase in the amplitude of the acoustic startle reflex. This effect was blocked in a dose-related fashion by the 5-HT2 antagonist ritanserin (ED50 dose = 0.25 mg/kg IP). In contrast, even a high dose of ritanserin (2.0 mg/kg) did not block the excitatory effects of amphetamine on startle. Other 5-HT2 antagonists (ketanserin, cinanserin, LY 53857) also blocked mescaline's effect, whereas the 5-HT1 antagonist pindolol (5 mg/kg) did not. These results support the hypothesis that the behavioral effects of hallucinogens are mediated by agonist actions at 5-HT2 receptors.

Animals↗

Stimulation of human prolactin secretion by mescaline.

Prolactin (PRL) and Growth Hormone (GH) secretions were studied in human serum after the oral administration of 5 mg/kg mescaline (3,4,5-trimethoxy-beta-phenylethylamine) or 2,3,4-trimethoxy-beta-phenylethylamine (2,3,4-TMPEA) respectively. Mescaline stimulated the secretion of PRL more than four-fold above base-line levels. Peak concentrations were found 90--120 min after drug intake. Five hours later serum PRL was still markedly increased. Mescaline also triggered GH secretion. There was no alteration of serum PRL and GH concentrations after intake of the non-hallucinogenic 2,3,4-TMPEA.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗

Cross tolerance to antinociception elicited by intracerebroventricular administration of mescaline and morphine to rabbits, and EEG correlates.

Tolerance and cross tolerance to the antinociceptive effect of equipotent doses of morphine (10 mug/kg) and mescaline (100 mug/kg) are shown in the rabbit after their repeated intracerebroventricular administration. The recording of the electrical activity of different brain areas indicates that a partial tolerance also develops to the EEG effects in animals undergoing chronic treatment with mescaline. The comparison of certain of the mescaline-induced effects with those of morphine suggests that some biochemical and neural patterns are common to the 2 drugs.

Analgesia↗

Hapten-immunological studies on mescaline.

Antibodies with mescaline binding specificity were raised in rabbits by immunization with conjugates of bovine serum albumin with mescaline or its analogue 3,4,5-trimethoxyphenylacetic acid. Immunized rats were given mescaline and their behavior was compared to that of non-immunized controls.

Absorption↗

Inescapable shock alters mescaline's disruption of active avoidance acquisition.

Rats were tested on a two-way avoidance acquisition with or without inescapable shock given 24 h prior to training. Mescaline given to nonshock rats disrupted acquisition in a dose-dependent fashion and tolerance developed to this disruption. Mescaline given to shock rats had no effect on acquisition even though levels of acquisition were the same for both shock and nonshock rats without drug. Moreover, subchronic treatment (5 days facilitated acquisition. These experiments demonstrate an interaction between shock, which presumably is a stressor, and mescaline. The data are consistent with the observation that when animals are exposed to presumptive stressors (e.g., shock, handling) hallucinogens can facilitate behavior, while in other situations, hallucinogens disrupt behavior.

Animals↗

6-Hydroxydopamine inhibits some effects of mescaline centrally administered to rabbits.

The narcotic antagonist naloxone does not antagonize antinociception elicited in the rabbit by 100 microgram/kg of mescaline centrally administered, whereas pretreatment with 6-hydroxydopamine (6-OHDA) inhibits this mescaline effect. Stereotyped behavior of rabbits following central mescaline administration is also prevented by 6-hda pretreatment. Since 6-OHDA in known to produce a degeneration of catecholamine containing nerve terminals, a crucial role of catecholamines is suggested in the complex of effects seen in the rabbit after central administration of the hallucinogen.

Animals↗

LSD mescaline and serotonin injected into medial raphe nucleus potentiate apomorphine hypermotility.

Microinjections of LSD (0.05 microgram), mescaline (0.5 microgram) and serotonin (10 microgram) into the medial raphe nucleus of rats resulted in a strong potentiation of apomorphine (1 mg/kg i.p.)-induced hypermotility. The potentiating effect of LSD or serotonin was suppressed by simultaneous injections of methysergide (0.05 microgram) or cyproheptadine (0.05 microgram) into the medial raphe nucleus. The same doses of LSD injected into the dorsal raphe nucleus and of LSD and mescaline injected into the nucleus accumbens failed to influence locomotor activity, whereas injections of higher doses of LSD and mescaline into the nucleus accumbens inhibited spontaneous and apomorphine-stimulated locomotor activity. It is concluded that the potentiating effect of systemically administered low doses of hallucinogens was triggered by preferential actions on the serotonergic system in the medial raphe nucleus.

Animals↗

Mescaline-induced motor impairment in rats, assessed by two different methods.

Motor impairment, especially ataxia, is often mentioned as a 'side effect' of doses of psychoactive drugs which depress animal behaviour; it is difficult to determine it accurately from visual observation, but relatively few attempts have been made to measure it objectively and quantitatively. Mescaline, in moderate to large doses, can induce biphasic--depressant followed by stimulant--effects on learnt and other performance of laboratory rodents. Motor impairment, using three doses, was accordingly measured during the depressant phase by two methods. An 'ataxia' test, involving analyses of footprints, showed few irregularities of gait splay due to mescaline, but the drug markedly reduced the length of steps ('stride') in a dose-related manner. In a 'tilt plane' test for general motor control, the animals' ability to cling to a tilted plane decreased with 25 mg/kg mescaline, at 30 and 40 minutes after administration. Deficits of this kind can be relevant to interpreting drug actions on forms of behaviour which involve movements for responding, and they also have interesting potential in their own right.

Animals↗

Effects of mescaline and some of its analogs on cholinergic neuromuscular transmission.

Mescaline (3,4,5-trimethoxyphenylethylamine; MES) and its analogs, anhalinine (ANH) and methylenemescaline trimer (MMT) were investigated, using sciatic-sartorius preparations of the frog and cortical tissue from the rat. The effects of MES and its analogs were examined with respect to muscle twitch, resting membrane potential and nicotinic receptor binding. Mescaline and its analogs (10-100 microM) blocked both directly and neurally evoked twitches but their effects on neurally evoked twitches were greater than those on directly evoked twitches. Mescaline, ANH and MMT decreased amplitude of the miniature endplate and endplate potentials, decreased acetylcholine (ACh) quantal content, hyperpolarized the resting membrane potential and prolonged duration of the action potential. They did not significantly displace the binding of [125I]-alpha-bungarotoxin (alpha-BTX) to nicotinic receptors, at concentrations which blocked neuromuscular transmission. These results suggest that MES and its analogs inhibit cholinergic neuromuscular transmission by blocking release of ACh; they also affect K+ conductance.

Acetylcholine↗

Pharmacological and behavioral components of tolerance to LSD and mescaline in rats.

A fixed-ratio schedule of water reinforcement (FR-10) was used to examine the relative contributions of pharmacological and behavioral mechanisms in the development of tolerance to the disruptive effects of LSD and mescaline in the rat. Rats treated daily with LSD or mescaline before operant testing developed tolerance to the impairement of responding, while rats treated daily after each session did not display tolerance when the drugs were administered before testing. These results indicate that behavioral compensatory mechanisms may be involved in the development of tolerance to the disruptive effects of LSD and mescaline on fixed-ratio (FR-10) performance.

Animals↗

Mescaline produces pathological aggression in rats regardless of age or strain.

Several measures of aggressive behavior were investigated in three ages (40-50, 90-110, and 180-200 days old) and in three strains (Sprague-Dawley, Wistar, and Long-Evans) of rats before and following the administration of mescaline hydrochloride in a shock-elicited aggression situation. The measures included the number of fights, duration of fighting, latency of fighting, number of bites inflicted, and a composite index of pathological aggression. During predrug baseline testing it was found that older rats, regardess of strain, engaged in more frequent fights that were longer in duration and more intense than younger animals. When the animals were tested with mescaline, they engaged in significantly more fights, biting, and pathological aggression than during baseline testing regardless of their age of strain. These results suggest that mescaline-induced pathological aggression in rats is a robust phenomenon.

Age Factors↗

Naloxone potentiates the disruptive effects of mescaline on operant responding in the rat.

Food-deprived male rats were trained to press a lever on a fixed ratio-40 (FR-40) operant schedule for food reinforcement. Administration of mescaline (4.0--10.0 mg/kg) immediately before the start of the operant session resulted in a cessation of responding for some portion of the 40-min period ("hallucinatory pause"). The duration of this pause was found to be dose-dependent. Although administration of naloxone alone (1.0-8.0 mg/kg, five minutes prior to the start of the session) had no effect on FR-40 responding per se, pretreatment with this agent significantly potentiated the disruptive effects of mescaline. This potentiation by naloxone was further shown to be dose-dependent. These data suggest that the effects of the phenethylamine hallucinogen mescaline are potentiated by pretreatment with the narcotic antagonist naloxone.

Animals↗