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Results for “5-Methoxytryptamine”

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At least 19 recordsLinked to original sources
PubMed1979

MAO inhibition and the effects of centrally administered LSD, serotonin, and 5-methoxytryptamine on the conditioned avoidance response in rats.

Pretreatment with the MAO-inhibitors iproniazid, clorgyline, or deprenyl abolishes the effects of LSD on the conditioned avoidance response (CAR) in rats. The effects of serotonin (5-HT) and 5-methoxytryptamine (5-MT) are greatly potentiated by these substances. Brain levels of LSD are not affected by MAO inhibition whereas levels of 5-HT and 5-MT are significantly elevated. It is postulated that the decreased behavioral response to LSD is the result of 'MAO inhibitor-induced' changes whereas the increased response of 5-HT and 5-MT results from increased brain levels of these compounds.

5-Methoxytryptamine↗
PubMed1979

N-Chloroacetyl 5-methoxytryptamine (isamide): a selective antagonist of 5-hydroxytryptamine in the rat uterus.

Isamide, the N-chloroacetyl derivative of 5-methoxytryptamine, produced a dose-dependent competitive blockade of uterine contractions in vitro induced by 5-HT. The pA2 value for the 5-HT-isamide interaction was 4.42. The blockade was short-lasting and reversible; after recovery, a dose-dependent increase in the uterine sensitivity to 5-HT was found. The blockade proved to be selective to the 5-HT receptor. The simultaneous application of 5-HT plus isamide partially prevented the 5-HT-induced auto blockade phenomenon. In addition, isamide did not affect the contractile responses of the uterus to oxytocin or bradykinin or the contractile effects of the rat vas deferens to adrenaline.

5-Methoxytryptamine↗
PubMed1975

Radioprotective and toxic effects of a mixture of AET and 5-methoxytryptamine in mice.

The authors studied the radioprotective efficacy and toxicity of an AET + 5-methoxytryptamine mixture and its effect on the course of respiratory exchange, using different weight ratios of the two components. The optomum was found to be 150 mg AET/kg b.w + 25 mg 5-MOT/kg b.w. This mixture gave very good protection in the supralethal exposure range and markedly prolonged its duration. The high toxicity of this mixture was abolished by the pre-administration of glutathione. Raised and longer protection was also manifested in the course of respiratory exchange, showing that an association exists between changes in energy metabolism and raised radioresistance of the organism.

5-Methoxytryptamine↗
PubMed1979

Fast axonal transport in rat sciatic nerve. Inhibition by pineal indoles.

The effect of pineal indoles on fast axoplasmic transport of proteins in the sciatic nerve was examined in rats injected with [3H]leucine in the sixth lumbar dorsal root ganglion. Melatonin (350-1100 nmol) applied locally in the sciatic nerve impaired significantly axonal transport. At a 350-nmol dose all other indoles tested (i.e., 5-hydroxyindoleacetic acid, 5-methoxyindoleacetic acid, serotonin, N-acetylserotonin, tryptamine, 5-methoxytryptamine) were less potent than melatonin to impair fast axonal flow. Vinblastine injected either into the ganglion or in the sciatic nerve markedly inhibited axonal transport.

5-Methoxytryptamine↗
PubMedDate not supplied

Participation of 5-hydroxytryptamine in anticonvulsive action of benzodiazepines.

The influence of several compounds activating or producing hypofunction of the serotonergic system was studied on the convulsive threshold and anticonvulsive action of benzodiazepines (chlordiazepoxide, diazepam, oxazepam, nitrazepam) in the pentylenetetrazol test. No changes in the convulsive threshold either for clonic, nor for tonic phase were found. However, the anticonvulsive action of benzodiazepines was enhanced by 5-hydroxytryptophan, 5-methoxytryptamine (given together with pargyline), or fenfluramine. p-Chlorophenylalanine and methergoline did not affect, but cyproheptadine enhanced the anticonvulsive action of most of benzodiazepines tested.

5-Hydroxytryptophan↗
PubMed1978

High-affinity 3H-serotonin binding to caudate: inhibition by hallucinogens and serotoninergic drugs.

The specific binding of 3H-serotonin to calf caudate homogenate was studied. The dissociation constant was 2nM and the number of specific sites was 14fmoles/mg protein. Of many drugs tested, inhibition of specific 3H-serotonin binding occurred almost exclusively with serotonin agonists and antagonists. The concentrations for 50% inhibition of 3H-serotonin binding by serotonergic agonists follow: bufotenin, 6nM; 5-methoxytryptamine, 12 nM; psilocin, 35nM; dimethyltryptamine, 220 nM; and tryptamine, 270 nM. The concentrations for the antagonists were: LSD 9.5 nM; methysergide 16nM and metergoline 25nM.

Animals↗
PubMed1979

The central action of pizotifen.

The central action of the potential antidepressant drug pizotifen (Sandomigran) was studied in mice, rats and rabbits. Pizotifen in doses up to 10 mg/kg i.p. was ineffective in classic tests for antidepressant activity. It neither antagonized the effects of reserpine in rats (hypothermia, ptosis) nor potentiated the effects of amphetamine (in mice and rats), nialamide or L-dopa (in mice) on locomotor activity. However, its antidepressant activitiy was found in the 'despair test' in rats. On the other hand, pizotifen inhibited the head twitch reaction induced by L-5-hydroxytryptophan in mice (ED50 = 0.009 mg/kg, i.p.) and by 5-methoxytryptamine (+ tranylcypromine) in rats (ED50 = 0.45 mg/kg, i.p.). It also antagonized tryptamine-induced clonic convulsions of fore-paws in rats (ED50 = 0.35 mg/kg, i.p.), and in doses of 5--10 mg/kg s.c. inhibited hyperthermia produced by LSD in rabbits. Finally, pizotifen (0.1--0.3 mg/kg, i.v.) inhibited or abolished LSD- or quipazine-induced stimulation of the hind limb flexor reflex of spinal rats; the above effect was not due to noradrenolytic action of the drug. These results suggest that pizotifen strongly blocks the central postsynaptic serotonin receptors.

Amphetamine↗
PubMed1975

Studies on serotonin binding proteins of nerve ending membranes.

Synaptic membranes were isolated from rat brain homogenates by differential and density gradient centrifugation. Membrane proteins were solubilized by detergent buffer and assayed for serotonin-binding activity by adsorption of free 5-HT on charcoal. When the membrane extract was incubated with serotonin at +4 degrees C for various times, equilibrium was reached within 10 min. With increasing serotonin concentrations the specific part of binding was saturable whereas the non-specific part increased linear with the total 5-HT added. Kinetic analysis of the data revealed two different classes of binding sites with the apparent dissociation constants Kd1 = 5.3X10(-7) M and Kd2 = 1.1X10-5 M. The disociation reaction followed first order kinetics in two steps. The first step was very rapid, the second step proceeded with a half life time t1/2 of 16 min and a dissociation rate constant of k-1 = 7.2X10(-4) s-1. the binding was sensitive to heat and SH-blocking reagents and displaceable by serotonin in excess, d-LSD, and to a lower extent by 5-methoxytryptamine and tryptamine. The significance and localization of the binding sites at the membrane are discussed.

Animals↗
PubMedDate not supplied

Alpha-MSH and MIF-2 effects on serotonin levels and accumulation in various rat brain areas.

Levels as well as accumulation of serotonin (5-HT) were measured in various brain regions of the rat after administration of alpha-melanocyte-stimulating hormone (MSH) and Pro-Leu-Gly-NH2 (MIF-I). The method used in determining the serotonin measured both 5-OH-tryptamine (5-HT) and 5-methoxytryptamine (5-MT). No statistically significant changes in levels or accumulation of serotonin after pargyline injection were found when unoperated control rats were treated with either MSH or MIF-I. Similar treatment of hypophysectomized rats indicated that both peptides significantly (p less than 0.05) lowered serotonin accumulation only in the area of the frontal cortex; a similar but smaller, not statistically significant, decrease was seen in the hypothalamus and hippocampus of the hypophysectomized rat. Since only hypophysectomized rats were affected, no correlation between the behavioral effects of these peptides (which has been found to occur in both unoperated and hypophysectomized rats) and the biochemical changes could be made.

Animals↗
PubMed2026

Resurrection biology: Melatonin as a modulator of anastasis (Review).

Although apoptosis is regarded as an irreversible and terminal process, recent research has identified anastasis as a cellular mechanism that enables cell recovery even after the activation of executioner caspases. While important in supporting tissue homeostasis following mild or transient injury, anastasis presents significant challenges in oncology, as cancer cells may exploit this phenomenon to evade chemotherapy, subsequently acquiring aggressive traits such as genomic instability, stem‑like properties, and increased metastatic capacity. N‑acetyl‑5‑methoxytryptamine (melatonin), recognized for its antioxidant activity and role as a mitochondrial regulator, has been associated with several biological processes that overlap with pathways involved in anastasis, including mitochondrial bioenergetics, redox homeostasis, and DNA repair mechanisms. However, direct evidence supporting a role for melatonin in regulating anastasis remains limited. The present review consolidated current insights into the molecular regulation of anastasis, examining its biphasic transcriptional profile and oncogenic consequences, while exploring the mechanistic links between melatonin biology and pathways relevant to apoptotic recovery and evaluating the therapeutic prospects of melatonin in targeting anastasis as a strategy to mitigate tumor recurrence and improve clinical outcomes.

Melatonin↗
PubMed1975

Physiological and pharmacological evidence for a serotonergic projection to the hippocampus.

Rat hippocampal pyramidal cells were studied for their response to serotonin applied iontophoretically and to stimulation of the midbrain raphe nuclei. Ninety-two percent of the cells studied were inhibited by serotonin. Fourty-eight percent of the cells responded by inhibition to dorsal and median raphe stimulation. The inhibitory response to raphe stimulation was absent when the rats were pretreated with p-chlorophenylalanine (PCPA), a serotonin synthesis inhibitor; PCPA effects were alleviated by 5-HTP or 5-HT administration. The response to raphe stimulation was blocked by emthysergide and cyproheptadine. The responses to raphe stimulation were potentiated by chlorimipramine, a serotonin reuptake blocker. These data satisfy several of the criteria required to identify serotonin as the inhibitory neurotransmitter for the raphe-hippocampal pathway

5-Hydroxytryptophan↗
PubMed1977

Effects of 5-hydroxytryptamine on the lower esophageal sphincter in vivo: evidence for multiple sites of action.

Intravenous administration of 5-hydroxytryptamine (5-HT) caused a dose-dependent contraction in the lower esophageal sphincter in the opossum. The smallest dose of 5-HT which caused a detectable contraction of the sphincter was 0.5 mug/kg, and a maximal sphincter contraction was produced by a dose of 40 mug/kg. Methysergide converted the contractile effect of 5-HT to a dose-dependent fall in the sphincter pressure; maximal inhibition of 77.2 +/- 7.2% of the resting pressure occurred with a dose of 40 mug/kg. The inhibitory effect of 5-HT was antagonized by tetrodotoxin, 5 MeO-DMT, and 5-HT tachyphylaxis. 5 MeO-DMT enhanced 5-HT-induced contraction of the sphincter. In the presence of 5 MeO-DMT and methysergide, 5-HT still caused a brief contraction of the sphincter; this contraction appeared to be due to stimulation of postganglionic cholinergic neurons as it was antagonized by tetrodotoxin or atropine. Reserpinization caused enhancement of the sphincter contraction by 5-HT. In the reserpinized animals in the presence of methysergide, 5-HT caused a small initial contraction followed by prolonged inhibition; atropine antagonized the initial contraction, while inhibition was antagonized by 5 MeO-DMT. These studies are consistent with the view that 5-HT exerts several different effects on the sphincter. 5-HT causes contraction of the sphincter by its direct action on the muscle and also by stimulation of cholinergic excitatory neurons. In addition, 5-HT inhibits the sphincter by stimulation of nonadrenergic inhibitory neurons.

5-Methoxytryptamine↗
PubMed1976

Relation of pH to fluorescence of serotonin, melatonin, and other indole compounds reacted with o-phthaldialdehyde.

We distinguished serotonin, malatonin, and other indole compounds by their markedly different fluorescence behavior when heated with o-phthaldialdehyde in different concentration of HCl, or after the subsequent addition of alkali. Fluorescence may increase, disappear, or change from blue to orange-red. Only melatonin developed significant fluorescence (at less than 0.5 mug/liter) when heated with the reagent in 50 mmol/liter HCl. Serotonin and 5-hydroxyindole compounds with a C-3 aliphatic chain lost their blue fluorescence when brought from strong to weakly acid and alkaline pH. Intense reddish fluorescence developed in strongly alkaline solution. C-5 methoxy derivatives, such as melatonin, maintained their blue fluorescence in alkaline solution. Differences in fluorescence color (and RF) also characterized these compounds on silica gel plates. The use of toluene decreased blank fluorescence, while sample preparation in dim light, as often recommended, resulted in diminished and less-stable fluorescence.

5-Methoxytryptamine↗