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Serotonin: all studies

Page 97 of 400: studies 961 to 970 of 3,999, newest first. Back to the serotonin overview

Research

Methylenedioxymethamphetamine induces opposite changes in central pre- and postsynaptic 5-HT1A receptors in rats.

European Journal of Pharmacology July 1, 1995 Norberto Aguirre, J L Galbete, Berta Lasheras et al.

The present study examined the short- and long-term effects of single and repeated administration of 3,4-methylenedioxy-methamphetamine (MDMA, 'ecstasy') on somatodendritic and postsynaptic 5-HT1A receptors of the rat brain. [3H]8-Hydroxy-2-(di-n-propylamino)tetralin ([3H]8-OH-DPAT) was used to label 5-HT1A receptors in the brain stem region containing the dorsal raphe nucleus and in the...

DOI: 10.1016/0014-2999(95)00303-3 (opens in new tab) Raphe nuclei Frontal lobe Dendrites Synapses +8

Modulation of methylenedioxymethamphetamine-induced striatal dopamine release by the interaction between serotonin and gamma-aminobutyric acid in the substantia nigra.

Journal of Pharmacology and Experimental Therapeutics June 1, 1995 Bryan K. Yamamoto, J F Nash, Gary A. Gudelsky

The effects of the amphetamine analog, 3,4-methylenedioxymethamphetamine (MDMA) were compared to the effects of d-amphetamine on the in vivo release of dopamine and gamma-aminobutyric acid (GABA) in the striatum and substantia nigra. The brain region-dependent role of the 5-HT2 receptors in the striatum and substantia nigra in regulating MDMA-induced dopamine and GABA release also was studied....

DOI: 10.1016/s0022-3565(25)09555-2 (opens in new tab) Serotonin Substantia nigra Corpus striatum Animals +6

The monoamine oxidase-B inhibitor L-deprenyl protects against 3,4-methylenedioxymethamphetamine-induced lipid peroxidation and long-term serotonergic deficits.

Journal of Pharmacology and Experimental Therapeutics May 1, 1995 J E Sprague, D E Nichols

3,4-Methylenedioxymethamphetamine (MDMA)-induced serotonergic neurotoxicity was assessed in the striatum, hippocampus and frontal cortex of rats by using [3H]paroxetine binding to label serotonin (5-HT) uptake sites and 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels as markers of serotonergic function. NMDA (40 mg/kg) induced a significant decrease in both [3H]paroxetine binding Bmax and...

Activation of glycogen phosphorylase by serotonin and 3,4-methylenedioxymethamphetamine in astroglial-rich primary cultures: involvement of the 5-HT2A receptor

Brain Research May 1, 1995 Jose C Poblete, Efrain C. Azmitia 52 citations

Neurotransmitters, neuropeptides, and ions regulate glycogen levels in the brain by modulating the activity of glycogen synthase (GSase) and glycogen phosphorylase (GPase). GPase is co-localized with glial fibrillary acidic protein (GFAP), an astroglia-specific marker, suggesting that glycogen is localized in astroglial cells. Additionally, functional serotonin (5-HT) receptors are found in...

3,4-methylenedioxymethamphetamine (‘Ecstasy’) promotes the translocation of protein kinase C (PKC): requirement of viable serotonin nerve terminals

Brain Research May 1, 1995 H Kenneth Kramer, Jose C Poblete, Efrain C. Azmitia 22 citations

The metabolic effects of the neurotoxic, ring-substituted amphetamine 3,4-methylenedioxy-methamphetamine (MDMA or 'Ecstasy') were examined in vivo. In this study, we focused on the ability of MDMA to induce a translocation of the calcium and phospholipid-dependent protein kinase C (PKC) from the cytosol to the cortical plasma membrane. Two injections of MDMA (20 mg/kg; 10 h apart; s.c.)...

Role of hypothermia in the mechanism of protection against serotonergic toxicity. I. Experiments using 3,4-methylenedioxymethamphetamine, dizocilpine, CGS 19755 and NBQX.

Journal of Pharmacology and Experimental Therapeutics February 1, 1995 G. Farfel, Lewis S. Seiden

High doses of 3,4-methylenedioxymethamphetamine (MDMA) have been shown to cause long-lasting depletions of central serotonin (5-HT) which are indicative of neuronal toxicity. The noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (DZ) attenuates depletions of 5-HT induced by MDMA. Because DZ has been shown to induce hypothermia in rat models of ischemia, the purpose of...

The selective 5-HT2A receptor antagonist MDL 100,907 counteracts the psychomotor stimulation ensuing manipulations with monoaminergic, glutamatergic or muscarinic neurotransmission in the mouse--implications for psychosis.

Journal of neural transmission. General section 1995 M L Carlsson

The present study has shown that a subthreshold dose of the uncompetitive N-methyl-D-aspartate (NMDA) antagonist MK-801, combined with a subthreshold dose of LSD, produces marked locomotor stimulation in monoamine-depleted mice. Likewise, MK-801, as well as the muscarine receptor antagonist atropine and the alpha-adrenoceptor agonist clonidine, were found to interact synergistically with the...

Identification of a primary metabolite of ibogaine that targets serotonin transporters and elevates serotonin.

Life Sciences 1995 Deborah C. Mash, J K Staley, Michael H. Baumann et al. 108 citations

Ibogaine is a hallucinogenic indole with putative efficacy for the treatment of cocaine, stimulant and opiate abuse. The purported efficacy of ibogaine following single dose administrations has led to the suggestion that a long-acting metabolite of ibogaine may explain in part how the drug reduces craving for psychostimulants and opiates. We report here that 12-hydroxyibogamine, a primary...

The effect of ibogaine on kappa-opioid- and 5-HT3-induced changes in stimulation-evoked dopamine release in vitro from striatum of C57BL/6By mice.

Brain Research Bulletin 1995 Henry Sershen, Audrey Hashim, Ábel Lajtha 25 citations

Ibogaine is an indole alkaloid that has been suggested to have potential efficacy for interrupting dependency on stimulant drugs. The kappa-opioid and serotonin 5-HT3 systems may be involved in the action of ibogaine, related to their modulation of dopaminergic transmission. The kappa-opioid agonist U 62066 attenuated the in vitro stimulation-evoked efflux of tritium label from striatal tissue...

p-Chloroamphetamine (PCA), 3,4-methylenedioxy-methamphetamine (MDMA) and d-fenfluramine pretreatment attenuates d-fenfluramine-evoked release of 5-HT in vivo.

Psychopharmacology December 1994 Hugh Series, P J Cowen, Trevor Sharp

Previous work has suggested that repeated treatment with substituted amphetamines including PCA, MDMA and d-fenfluramine produces a persistent neurodegeneration which is relatively selective for the fine serotoninergic terminals arising from the dorsal raphe nucleus. The aim of the present study was to investigate whether the acute releasing effect of d-fenfluramine might also be sensitive to...