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At least 19 recordsLinked to original sources
PubMed1978

Decreased platelet monoamine oxidase activity in chronic schizophrenia, shown with novel substrates.

Platelet monoamine oxidase (MAO) was kinetically evaluated in chronic schizophrenics and matched controls, using substrates of major physiologic importance and substrates of particular interest in the study of schizophrenia, such as serotonin (5-ht), N,N-dimethyltryptamine (DMT), 5-methoxytryptamine (5-MT), and dopamine (DA). Substrates were measured at six concentrations; values for maximal velocity (Vmax) and Michaelis constant (Km) were obtained by using Lineweaver-Burk plots. The Vmax was decreased for all substrates in chronic schizophrenia and the Km was decreased for DA, 5-HT, and DMT, but remained unchanged for 5-MT. The value of Km/Vmax was similar for schizophrencis and normal persons when DA, 5-HT, and DMT were used as substrates, which may indicate that "uncompetitive" inhibition is responsible for the observed decrease in activity among chronic schizophrenics. The finding of a decreased Vmax but unchanged Km with 5-MT would be consistent with noncompetitive inhibition.

5-Methoxytryptamine↗
PubMed1979

Increased excretion of dimethyltryptamine and certain features of psychosis: a possible association.

The excretion of the hallucinogen dimethyltryptamine (DMT) and its precursor N-methyltryptamine (NMT) was studied among 74 recently admitted psychiatric patients and 19 normal persons. Both compounds were detected in 24-hour urine samples from all subjects. Dimethyltryptamine excretion was greatest in schizophrenia, mania, and "other psychosis" and tended to decline as clinical state improved. Psychotic depressives excreted smaller amounts of DMT more akin to those excreted by neurotic and normal subjects. Urinary NMT excretion was unrelated to psychiatric diagnosis. Ratings on the Present State Examination (PSE) also indicated that increased excretion of DMT was associated with psychotic rather than neurotic psychopathology. Forty-three percent of the variance in urinary DMT levels could be explained in terms of six of the 38 PSE syndromes. Syndromes suggesting elation, perceptual abnormalities, and difficulty in thinking and communicating were most correlated with raised urinary DMT excretion.

Adolescent↗
PubMed1978

Quantitative assay of the N-methylated metabolites of tryptamine and serotonin by gas chromatography mass spectrometry as applied to the determination of lung indoleethylamine N-methyltransferase activity.

A specific and sensitive method is described for the identifcation and quantification of the N-mono- and dimethylated derivatives of tryptamine and serotonin by gas chromatography mass spectrometry. Deuterated analogues of the amines have been prepared for use as internal standards. The technique has been applied to the determination of indoleethylamine N-methyltransferase activity in rabbit and human lung. No interference from the beta-carboline formation or other side reactions between the substrates and the methyl donor was observed.

Animals↗
PubMed1976

[Comparison of altered states of consciousness induced by the hallucinogens (--)-delta9-trans-tetrahydrocannabinol (delta9-THC) and N,N-dimethyltryptamine (DMT) (author's transl)].

The study compares altered states of consciousness induced by the hallucinogens (--)delta9-trans-Tetrahydrocannabinol (delta9-THC) and N,N-Dimethyltryptamine (DMT) using two placebo control groups. A total of 24 subjects received 250 mug delta9-THC p.o./kg body weight and 26 subjects were treated with 250 mug DMT i.m./kg. Placebo was given to 24 subjects. The effects were assessed by a questionnaire administered following the experimental conditions. Questionnaire items were combined into the following eight scales according to their content and several cirteria of the theory of mental testing: visual hallucinations (illusions), auditory hallucinations (illusions), impairment of memory and attention, depersonalization syndrome, deprealization syndrome, changes of body image, euphoric state and anxious-depressive state. The two hallucinogen groups differed significantly from placebo on all eight scales. No difference, however, between delta9-THC and DMT was significant. On the scale "optical hallucinations (illusions)" a tendency that DMT might have stronger effects than delta9-THC was found. Methodological problems of comparing different hallucinogens are discussed.

Cognition Disorders↗
PubMed1977

Factors affecting the urinary excretion of endogenously formed dimethyltryptamine in normal human subjects.

The hallucinogenic substance N',N'-dimethyltryptamine and its precursor N-methyltryptamine were found in 24-h specimens of urine from 19 normal human subjects; the mean excretion rates were 386 ng 24 h(-1) and 856 ng 24 h(-1) respectively. The urinary excretion of both compounds was unrelated to age, sex, urinary volume, or creatinine, nor was any consistent diurnal pattern observed. Rates for the mono and dimethylated compounds were not correlated. Diet and the intestinal flora were excluded as a source of urinary dimethyltryptamine. Administration to 4 subjects of sufficient ammonium chloride to increase the H ion concentration of the urine caused a transient increase in dimethyltryptamine excretion but no consistent increase in the rate for N-methyltryptamine. Acidification of the urine did not appear to be the determining factor in this result since in one subject the same drop in urinary pH was achieved by feeding methionine without any increase in dimethyltryptamine excretion.

Adult↗
PubMed1979

Severe aggression in rats induced by mescaline but not other hallucinogens.

Pairs of male Sprague-Dawley rats were administered mescaline, lysergic acid diethylamide (LSD), psilocin, N,N-dimethyltryptamine (DMT), 3,4-dimethoxyphenylethylamine (DMPEA), or 5-hydroxydopamine (5-OHDA) IP prior to being placed in a shock-elicited aggression situation. When foot shock was delivered, controls struck each other with their forepaws, but never engaged in either biting or injurious fighting. Mescaline-treated rats (50 or 250 mg) rarely struck each other, but engaged in nearly lethal biting. While LSD (25--400 micrograms/kg), psilocin (2.0 mg/kg), and DMT (5 mg/kg) produced some biting, this did not significantly differ from controls and never resulted in injuries. At higher doses, psilocin, DMT, and DMPEA decreased the amount and intensity of fighting. Rats treated with 5-OHDA (8--200 mg/kg) or LSD (25--400 micrograms/kg) did not differ from controls. These results suggest that mescaline's ability to induce pathological aggression in rats exposed to foot shock is not shared by other hallucinogens or nonhallucinogenic mescaline analogues.

Aggression↗
PubMed1976

Dimethyltryptamine levels in blood of schizophrenic patients and control subjects.

A gas chromatographic-mass spectrometric determination of blood N,N-dimethyltryptamine in normal controls and schizophrenic patients was carried out with a sensitivity limit of 0.05 ng/ml whole blood. Although the results appear to suggest that the mean DMT level was higher in the total patient group, those patients with acute psychosis, female patients and patients with suspiciousness scores on the BPRS of 4 or over, the differences were not statistically significant.

Female↗
PubMed1979

Naloxone enhancement of DMT and LSD-25 induced suppression of food-rewarded bar pressing behavior in the rat.

The narcotic antagonist naloxone was tested to determine its possible interaction with N,N-dimethyltryptamine (DMT) and lysergic acid diethylamide-25 (LSD) in adult male Holtzman rats trained to press a bar on a fixed-ratio four schedule (FR4), i.e., every fourth press earned a reward of 0.01 ml sugar sweetened milk. LSD (0.1 mg/kg) or increasing doses of DMT (1.0, 3.2, and 10.0 mg/kg) were administered i.p. to disrupt food-rewarded fixed ratio bar pressing in a dose related fashion. Pretreatment (5--10 min) with behaviorally ineffective doses of naloxone (1.0--5.6 mg/kg) dramatically enhanced the effects of DMT and LSD. The content of DMT in the brain and liver of rats injected with DMT alone (10 mg/kg) and with a 5 min pretreatment of naloxone (3.2 mg/kg) was determined by radiochemical analysis at 30 and 90 min after 14C-DMT injection. There was no significant difference for either brain or liver 14C-DMT levels when control DMT rats were compared with the naloxone pretreated rats. These results seem to rule out interference by naloxone with the metabolism of DMT as a mechanism of the observed behavioral potentiation.

Animals↗
PubMed1979

Serotonergic function in mouse head twitches induced by lithium and reserpine.

We examined the relationship between lithium-induced head twitches and serotonergic neurons. Head twitches were elicited by combined treatment with lithium chloride (2 or 5 mEq/kg x 5, s.c. administered hourly) and rauwolfia alkaloids, i.e., reserpine (5 mg/kg, s.c.), tetrabenazine (20 mg/kg, s.c.), and syrosingopine (10 mg/kg, s.c.). Neither lithium nor the alkaloid alone induced the twitches; nor did combined administration of lithium with methamphetamine or p-chloroamphetamine. The head twitches induced by lithium in combination with reserpine were strongly inhibited by antiserotonin drugs, methysergide and cyproheptadine, and also by a serotonin synthesis inhibitor, p-chlorophenylalanine (PCPA), when administered between lithium and reserpine. When PCPA was administered before lithium for 3 days, the head twitches were potentiated. In addition, the head twitches were potentiated by a serotonin receptor stimulant, 5-methoxy-N,N-dimethyltryptamine. The results imply that lithium can induce head twitches in the presence of rauwolfia alkaloids and may exert its effect in part by acting on the serotonergic neuron system.

Acetylcholine↗
PubMed1978

Stimulation of rat prolactin secretion by indolealkylamine hallucinogens.

The hallucinogenic indoleamine drugs N,N-dimethyltryptamine (N,N-DMT), psilocybin, bufotenin, 5-methoxy-N,N-dimethyltryptamine, and N-methyltryptamine, increased rat plasma prolactin (PRL) levels. The increase in plasma PRL produced by N,N-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 N,N-DMT, and psilocybin. Parachloroamphetamine, a relatively selective toxin for serotonin neurons, also stimulated the increase in PRL produced by N,N-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 which promote PRL secretion may be outside the blood-brain barrier or that the central 5-HT receptors which mediate PRL secretion may be especially responsive to bufotenin.

Animals↗
PubMed1979

A characteristic effect of hallucinogens on investigatory responding in rats.

The disruption of the temporal distribution of investigatory responses by rats in a novel hole-board following lysergic acid diethylamide-25 (LSD), as described in a companion paper (Geyer and Light, 1979), was found to be a characteristic effect of a variety of hallucinogens. Similar effects were produced by indoleamine hallucinogens, such as LSD, N,N-dimethyltryptamine, and psilocin, and by phenylethylamine hallucinogens, such as mescaline or 2,5-dimethoxy-4-methylamphetamine (DOM). Congeners of DOM that are inactive in humans had no significant effects. Furthermore, of a variety of other psychoactive drugs tested, only apomorphine produced an effect similar to that of the hallucinogens. These results suggest that a simple behavioral measure of exploration in a hole-board may provide a useful animal model with which to examine the common effects of hallucinogens.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1975

New characteristics of harmaline inhibition of intestinal transport systems.

Harmaline strongly inhibits the uptake of phenylalanine by slices of guinea-pig intestine in vitro. The lowest concentration having a significant effect is 0.1 mM. The drug also inhibits the unidirectional flux of phenylalanine from the mucosal to serosal face of the tissue provided it is added to the solution bathing the mucosal surface. The unidirectional flux of sodium from the mucosa to the serosa was similarly reduced. Ion and water absorption in the perfused dog intestine in vivo is also diminished in the presence of harmaline. These results support the hypothesis, previously proposed in view of the rapid onset of harmaline inhibition of sodium-dependent uptake mechanisms in a variety of tissues, that harmaline interacts with the sodium-site of non-electrolyte carrier complexes. The effect of harmaline on phenylalanine uptake by the intesting is duplicated by other psychotropic indole analogues. The actions of harmine and harnalol are similar to that of harmaline, despite great differences in the liposolubility of the different compounds. N:N-dimethyl-tryptamine is equally inhibitory, but serotonin is inactive. Mescaline and lysergic acid diethylamide also inhibit phenylalanine transport, but to a much lesser extent than harmaline.

Alkaloids↗
PubMed1976

The effects of quipazine on 5-HT metabolism in the rat brain.

Since quipazine is a potent 5-HT agonist in peripheral organs, its possible stimulatory effects on serotoninergic receptors in the rat brain were investigated. Quipazine administration (10 mg/kg, i.p.) induced a significant decrease in the synthesis and turnover rates of serotonin in the brain stem as well as in the forebrain. It is not likely that these changes were mediated by a negative feed-back mechanism triggered by a direct action of quipazine on central 5-HT postsynaptic receptors. Indeed, in contrast to LSD and 5-methoxy-N,N-dimethyltryptamine, this compound failed to activate the 5-HT sensitive adenylate cyclase in colliculi homogenates of newborn rats. However, quipazine exerted direct effects on serotoninergic terminals. It inhibited competitively the reuptake process in synaptosomes (Ki=1.38 X 10(-7) M) and stimulated the K+ evoked release of newly synthesized 3H-5-HT in slices of the brain stem. Injected in vivo in a dose which affected 5-HT uptake and release, quipazine did not modify MAO activity. However, this activity was non-competitively inhibited by high concentratin of the drug in vitro (Ki=3.0 X 10(-5) M). These actions are very likely indirectly responsible for the stimulation of central 5-HT receptors.

Adenylyl Cyclases↗
PubMed1976

Elevation of brain GABA concentrations with amino-oxyacetic acid; effect on the hyperactivity syndrome produced by increased 5-hydroxytryptamine synthesis in rats.

Pretreatment of rats with aminooxyacetic acid (AOAA; 40 mg/kg) raised the concentration of rat brain GABA and inhibited the hyperactivity produced by increasing brain 5-hydroxytryptamine (5-HT) concentration by administration of tranylcypromine and L-tryptophan. The maximum effect was seen 90 min after AOAA injection with smaller effects 30 and 180 min after injection. AOAA did not affect the rate of 5-HT accumulation in the brain, but did inhibit the hyperactivity response which follows injection of the 5-HT agonist 5-methoxy-N,N-dimethyltryptamine, suggesting that post-synaptic 5-HT responses were being inhibited. AOAA also inhibited the locomotor activity which follows administration of tranylcypromine and L-dopa. Blockade of GABA receptors by injection of picrotoxin (2.5 mg/kg) enhanced the dopamine hyperactivity. Since a dopaminergic system has been shown to be involved in the 5-HT hyperactivity syndrome and appears to act post-synaptically to the 5-HT neurones initiating the syndrome it is suggested that inhibition of the 5-HT hyperactivity syndrome may be due to accumulation of GABA distal to the dopaminergic receptors.

Acetates↗