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D E Nichols

9 papers in the library · 507 citations · publishing 1981-1996

Papers

Stereochemical effects of 3,4-methylenedioxymethamphetamine (MDMA) and related amphetamine derivatives on inhibition of uptake of [3H]monoamines into synaptosomes from different regions of rat brain.

Biochemical pharmacology July 15, 1987 T D Steele, D E Nichols, G K Yim 179 citations

MDMA and related compounds block the reuptake of serotonin and norepinephrine more potently than dopamine, setting them apart from both amphetamine and the hallucinogen DOM. The S-(+) enantiomer of MDMA and MDA inhibits dopamine uptake, while the alpha-ethyl homolog MBDB does not. Both stereoisomers of MDMA, MDA, and MBDB strongly inhibit serotonin and norepinephrine uptake, whereas DOM has no effect on any monoamine uptake. These findings suggest MDMA's mechanism is closer to amphetamine than to DOM, and that serotonin and norepinephrine systems underlie its pharmacological effects.

Amphetamine derivatives induce locomotor hyperactivity by acting as indirect serotonin agonists.

Psychopharmacology January 1, 1991 C W Callaway, M P Johnson, L H Gold et al. 70 citations

MBDB, a derivative of amphetamine that releases little or no dopamine, caused rats to become hyperactive and suppressed their exploratory behaviors, similar to the effects of MDMA. This hyperactivity lasted over 60 minutes at higher doses. Pretreatment with fluoxetine, a serotonin reuptake inhibitor, blocked MBDB-induced hyperactivity, indicating that the behavioral effects depend on serotonin release rather than dopamine release. Fluoxetine also blocked hyperactivity from related drugs S-(+)3,4-methylenedioxyamphetamine and p-chloroamphetamine. Tissue measurements showed decreased serotonin and its metabolite 5-HIAA after MBDB or S-(+)MDMA, which was prevented by fluoxetine. S-(+)MDMA increased dopamine levels in a fluoxetine-sensitive manner, suggesting serotonin release may indirectly influence dopamine.

p-methylthioamphetamine is a potent new non-neurotoxic serotonin-releasing agent.

European journal of pharmacology December 8, 1992 X Huang, D Marona-Lewicka, D E Nichols 62 citations

p-Methylthioamphetamine (MTA) is a potent and selective serotonin releaser that appears to lack the serotonin neurotoxic effects seen with p-chloroamphetamine (PCA). MTA was about twice as potent as PCA at inhibiting serotonin uptake, but 7 to 10 times less potent at inhibiting dopamine and norepinephrine uptake. In drug discrimination tests, MTA was nearly as effective as PCA in animals trained to recognize MDMA or related compounds. MTA also caused dose-dependent serotonin release from rat brain slices similar to PCA. However, a high dose of PCA reduced serotonin and its metabolite by 70-90% in brain regions, while twice the molar dose of MTA had no such effect, suggesting MTA is not neurotoxic to serotonin neurons.

[125I]-2-(2,5-dimethoxy-4-iodophenyl)aminoethane ([125I]-2C-I) as a label for the 5-HT2 receptor in rat frontal cortex.

Pharmacology, biochemistry, and behavior January 1, 1990 M P Johnson, C A Mathis, A T Shulgin et al. 56 citations

A radiolabeled compound, [125I]-2C-I, was used to label low-density 5-HT2 agonist binding sites in brain tissue. The nonhydrolyzable GTP analog GppNHp inhibited high-affinity binding, and serotonin along with several 5-HT2 agonists and antagonists showed high affinity for the site. At 37°C, the number of binding sites (Bmax) decreased compared to 24°C, while binding affinity (KD) remained unchanged. Structure-activity relationships for displacing [125I]-2C-I supported the receptor's role in hallucinogen action. The findings demonstrate [125I]-2C-I as a useful radioligand and provide further evidence linking the 5-HT2 receptor to hallucinogenic activity.

Hallucinogenic and stimulatory amphetamine derivatives: fingerprinting DOM, DOI, DOB, MDMA, and MBDB by spectral analysis of brain field potentials in the freely moving rat (Tele-Stereo-EEG).

Psychopharmacology January 1, 1989 W Dimpfel, M Spüler, D E Nichols 42 citations

Hallucinogenic amphetamine derivatives (R-DOB, R-DOM, R-DOI) and nonhallucinogenic amphetamine derivatives (S-MBDB, S-MDMA, S-amphetamine) produce distinct brain activity patterns in freely moving rats. Nonhallucinogens generally decreased power in field potentials across frontal cortex, hippocampus, striatum, and reticular formation, with the most prominent changes in alpha2 and delta frequency bands. In contrast, hallucinogens increased power specifically in the alpha1 frequency band, especially in the striatum. Because increases in alpha1 power have been linked to serotonergic control mechanisms, these results support the hypothesis that 5-HT2 receptors, which are abundant in the striatum, may be involved in the hallucinogenic action of drugs.

Comparison of solution conformational preferences for the hallucinogens bufotenin and psilocin using 360-MHz proton NMR spectroscopy.

Journal of medicinal chemistry February 1, 1981 G P Migliaccio, T L Shieh, S R Byrn et al. 34 citations

NMR spectroscopy reveals that the side-chain conformations of bufotenin and psilocin differ in solution. In water, both compounds have similar populations of trans and gauche rotamers. In chloroform, bufotenin shows a slight preference for the trans rotamer, while psilocin strongly favors the gauche form, stabilized by about 1 kcal/mol, possibly due to a weak hydrogen bond. The difference in biological activity between the two compounds is largely explained by their different basicities: the amino group pKa of psilocin is 8.47, compared to 9.67 for bufotenin, which affects their partitioning behavior.

Behavioral effects of the highly selective serotonin releasing agent 5-methoxy-6-methyl-2-aminoindan.

European journal of pharmacology June 2, 1994 D Marona-Lewicka, D E Nichols 32 citations

MMAI (5-methoxy-6-methyl-2-aminoindan) appears to be a selective serotonin releaser without psychostimulant or hallucinogenic effects. In rats trained to discriminate MMAI from saline, only other serotonin-releasing drugs fully mimicked MMAI's effects. MMAI did not produce amphetamine-like or LSD-like stimulus effects. Depleting serotonin with p-chlorophenylalanine blocked MMAI's discriminative cue for about a week, and selective serotonin reuptake inhibitors reduced its discriminability. Behavioral observations showed MMAI induced a syndrome similar to that caused by serotonin precursors or receptor agonists, including hypolocomotion, catalepsy-like posture, and flat body posture. The findings suggest MMAI acts primarily by releasing serotonin rather than directly activating or blocking neurotransmitter receptors.

Neurotoxic effects of the alpha-ethyl homologue of MDMA following subacute administration.

Pharmacology, biochemistry, and behavior May 1, 1989 M P Johnson, D E Nichols 26 citations

A behaviorally equipotent dose of the MDMA analogue MBDB (25 mg/kg) produced significant decreases in serotonin, its metabolite 5-HIAA, and serotonin uptake sites in rat cortex, similar to the nearly 60% reductions caused by MDMA (20 mg/kg) two weeks after treatment. However, MBDB appeared slightly less neurotoxic than MDMA. Unlike MDMA, MBDB did not cause a significant increase in dopamine levels three hours after a single injection. The findings suggest that dopamine release may play a role in MDMA's neurotoxicity.

(+/-)-1-(2,5-Dimethoxy-4-ethylthiophenyl)-2-aminopropane (ALEPH-2), a novel putative anxiolytic agent lacking affinity for benzodiazepine sites and serotonin-1A receptors.

Naunyn-Schmiedeberg's archives of pharmacology November 1, 1996 M Reyes-Parada, C Scorza, V Romero et al. 6 citations

The novel amphetamine derivative ALEPH-2, a putative anxiolytic, produced serotonergic syndrome symptoms like forepaw treading and flat body posture in rats, along with decreased motor activity. No significant effect on head shakes was observed, though variability was high. In mice, higher doses (4 mg/kg) caused significant hypothermia. The drug showed nanomolar affinity for 5-HT2A/2C receptors (Ki = 173 nM) but only micromolar or lower affinity for 5-HT1A, benzodiazepine, and GABAA receptors. These findings suggest ALEPH-2's anxiolytic-like effects involve serotonergic mechanisms, particularly 5-HT2A/2C receptor interactions.