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PubMed1992

Stimulatory and inhibitory effects of serotonergic hallucinogens on spinal mono- and polysynaptic reflex pathways in the rat.

The effects of two 5-HT-related hallucinogens on rat spinal mono- and polysynaptic reflex pathways in the rat were investigated. 5-Methoxy-N,N-dimethyltryptamine (5-MeODMT, 1 and 100 micrograms/kg, i.v.), an indolealkylamine agent, produced a dose-dependent decrease in the monosynaptic reflex, whereas 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI, 1-100 micrograms/kg), a phenylalkylamine agent, produced a dose-dependent increase in the monosynaptic reflex. Both agents increased the polysynaptic reflex. The 5-HT2 receptor antagonists ketanserin (100 micrograms/kg) and ritanserin (100 micrograms/kg) blocked the effects of DOI on the monosynaptic reflex but only partially blocked the 5-MeODMT-induced effect on the monosynaptic reflex. These antagonists inhibited the change in polysynaptic reflex, induced by DOI but not by 5-MeODMT. Neither propranolol (1 mg/kg) nor 3-tropanyl-3,5-dichlorobenzoate (MDL 72222, 1 mg/kg) antagonized the effect of either agent. 5-Methoxy-N,N-dimethyltryptamine and DOI increased the excitability of motoneurons and this effect was inhibited by ketanserin. These results indicate that the two types of hallucinogens possess both common and distinct characteristics, with regard to their action on the spinal reflex: (1) both increase the activity of motoneurons through 5-HT2 receptors but (2) only 5-MeODMT has an inhibitory action on the pathway of the monosynaptic reflex.

Amphetamines↗
PubMed1987

(+)-8-OH-DPAT and 5-MeODMT induced analgesia is antagonised by noradrenaline depletion.

In experiments with both rats and mice the 5-HT agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and 5-methoxy-N,N-dimethyl-tryptamine (5-MeODMT) were shown to produce reliable analgesic effects after acute administration (1 mg/kg SC) in the tail-flick, hot-plate and shock-titration tests of nociception. Prior treatment with the noradrenaline neurotoxin, N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4), systemically administered to both rats and mice abolished the analgesic effects of both the 5-HT agonist compounds in all the tests of nociception used. Intrathecal 6-hydroxydopamine (6-OHDA) treatment also abolished the analgesic effects of 8-OH-DPAT and 5-MeODMT; in the tail-flick test the analgesia induced by 8-OH-DPAT was reversed to an hyperalgesia. Biochemical analyses confirmed notable noradrenaline depletions in the spinal cord. It is concluded that an important interaction between presynaptic noradrenergic terminals and serotonergic receptor sites, possibly 5-HT1A, mediates spinal nociception processes.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Cyclic-ratio schedule analysis of a serotonin agonist and depletor on consummatory behaviour.

Four male Wistar rats, 180 days old at the start of the experiment, at 85% of their free-feeding body weight were trained to respond on a geometric cyclic-ratio schedule comprised of the following ratio values: 2, 4, 8, 16, 32 and 64, for 0.1 ml of 5% sucrose reinforcement. The response functions (response rates plotted against reinforcement rates) were linear and of negative slope over the range of ratio values from 2 to 16. IP administration of 1.0 mg/kg 5-MeODMT reduced the x- and y-intercepts of the linear portion of the response function without altering the slope relative to 2.0 ml/kg 0.85% saline IP. This was interpreted as a perceived palatability effect. IP administration of 100 mg/kg pCPA elevated the reinforcement rate intercept but also decreased the slope of the response function. This finding was interpreted as an increase in the perceived palatability of the reinforcer, coupled with a decrease in motivation at higher schedule conditions, possibly due to peripheral effects of pCPA.

Animals↗
PubMed1994

Physical exercise as a novel antidepressant agent: possible role of serotonin receptor subtypes.

Long-term exercise is associated with an antidepressant effect in patients with mild to moderate forms of nonbipolar depression and appears to be a promising new approach to its treatment. Adaptive changes in serotonin (5-HT) receptor functioning appears to play an important role in mediating the action of various antidepressant treatments. We investigated the adaptive changes in behavioral sensitivity of the 5-HT receptor subtype following 4 weeks of swimming exercise in normal rats, as well as in an animal model of depression (3 week, variety of chronic stressors). 5-HT1A autoreceptor sensitivity was assessed by hyperphagic response induced by 8-OH-DPAT (0.25 mg/kg, IP); 5-HT1A postsynaptic receptor by 5-HT syndrome induced by 8-OH-DPAT (0.75 mg/kg, IP), and 5 Me-ODMT (5 mg/kg, IP); and 5-HT2 receptor by wet dog shakes response induced by quipazine (1 mg/kg, IP) and 5MeODMT (5 mg/kg, IP). It was observed that exercise training in normal rats resulted in enhanced sensitivity of the 5-HT2 receptors along with subsensitivity of 5-HT1A autoreceptors. Exercise, given prophylactically along with chronic stressors, was able to prevent the development of behavioral deficit in the open-field test, and the animals developed remarkably enhanced sensitivity of 5-HT2 receptors. This adaptive supersensitivity of 5-HT2 receptor is also seen after various antidepressant treatments and may play an important role in mediating the antidepressant action of exercise.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1984

Ontogeny of N,N-dimethyltryptamine and related indolealkylamine levels in neonatal rats.

The present study deals with the measurement of the brain levels of the two potent hallucinogens N,N-dimethyltryptamine (DMT) and 5-methoxy-N,N-dimethyltryptamine (OMB), the biogenic amine tryptamine (TA), and its condensation product 1,2,3,4-tetrahydro-beta-carboline (THBC) in rats of various ages. Using gas chromatography-mass spectrometry with isotope dilution, we detected DMT, OMB, and THBC in neonatal rats from birth. DMT levels remained low until days 12 and 17 at which time they increased significantly and then returned to the initial low levels for all subsequent ages. The levels of OMB were higher than those measured for DMT with the highest levels being observed at days 12 and 17, and also on day 31. However, the levels for OMB showed much more variation. Although elevated levels of DMT and OMB have been correlated with stress, there are no known functions for these compounds. TA levels remained below detection limits until day 19. THBC levels were observed to be highest on days 22 and 31. The role that THBC plays in mammalian tissues is not known.

Aging↗
PubMed1980

Evidence that respiratory depression by serotonin agonists may be exerted in the central nervous system.

Resting with CO2 stimulated respiration were measured by means of a whole body plethysmograph in rats lightly anesthetized with halothane. The respiratory effects of different doses of the serotonin precursor 5-HTP, and the serotonin agonist 5-methoxy-N,N-dimethyltryptamine were studied as well as the effects of a serotonin antagonist methysergide and p-chlorophenylalanine, an inhibitor of serotonin synthesis. The serotonergic agonists decreased tidal volume and minute volume in a dose dependent manner and produced a respiratory acidosis. The respiratory depressant effect was antagonized by methysergide, and the serotonergic antagonist and synthesis inhibitor alone stimulated respiration. Rats given intraventricular 5-methoxy-N,N-dimethyltryptamine also evidenced a decrease in tidal volume, and this response was greater in animals given 5,7-dihydroxytryptamine. It seems likely that CNS serotonin receptors are involved in the control of both basal and CO2 stimulated respiration.

5-Hydroxytryptophan↗
PubMed1980

Circling produced by serotonin and dopamine agonists in raphe lesioned rats: a serotonin model.

The serotonin (5-HT) receptor agonists quipazine and 5-methoxy-N,N-dimethyltryptamine caused slow, contralateral circling, which was not dose-related, when given to rats with an asymmetric electrolytic lesion of the midbrain medial raphe nucleus. No circling was recorded after administration of fenfluramine, a compound that releases 5-HT. The dopamine drugs apomorphine and d-amphetamine caused vigorous circling in raphe lesioned rats which was increased further by quipazine but antagonized by fenfluramine. The effects of the 5-HT drugs on d-amphetamine circling were closely dose-related. The results suggest that modulation of d-amphetamine circling by 5-HT agonists in rats with a specific, asymmetric 5-HT lesion could provide the basis for a 5-HT rotation model.

Animals↗
PubMed1980

Effects of 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (6-MeO-THbetaC) on audiogenic seizures in DBA/2J mice.

It was found previously that 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (6-MeO-THbetaC) increased brain concentration of the neurotransmitter serotonin (5-HT) and decreased the concentration of its metabolite 5-hydroxyindole acetic acid (5-HIAA) at the same time the compound attenuated audiogenic seizures (AGS) in DBA/2J mice. In the present study we determined the time-course and dose-response effects of 6-MeO-THbetaC for blockade of AGS. Drugs sharing common effects with 6-MeO-THbetaC were also tested. At a dose of 100 mg/kg, 6-MeO-THbetaC blocked AGS between 10 min and 12 hr after injection, with maximal inhibition at 1 hr at which time a dose-related decrease in AGS was also demonstrated. All of the drugs tested which blocked AGS, including 6-MeO-THbetaC, THbetaC, 5-Hydroxytryptophan, chlorimipramine and pargyline, have biochemical similarities suggesting that facilitating serotonin function may be responsible for seizure-attenuating effects.

5-Hydroxytryptophan↗
PubMed1981

Antagonism of ethanol-induced decrease in LH by para-chlorophenylalanine: lack of correlation with altered serotonergic mechanisms.

Acute administration of ethanol lowers plasma levels of luteinizing hormone (LH) in several species. Since ethanol may interact with central serotonergic (5HT) neurons, and since 5HT systems have been found to play a role in modulating LH release, we examined the possible role of central serotonergic neurons in the ethanol-induced depression of LH. Acute PCPA (400 mg/kg, 20 hr before 2.0 g/kg ethanol) was effective in preventing the ethanol-induced depression of LH, suggesting that ethanol activates 5HT systems to lower LH. In support of this, the central 5HT agonist 5-methoxy-N, N-dimethyltryptamine (5MDMT) depressed LH in a dose-dependent manner. However, while the effects of a sub-maximal dose of 5MDMT were blocked by prior administration of methysergide, this 5HT receptor antagonist was unable to prevent the post-ethanol fall in LH. Additionally, because other doses of PCPA (250 mg/kg 20 hr prior to ethanol, and 100 mg/kg P.O. x 3 days before ethanol) produced similar reductions in hypothalamic 5HT but did not block the ethanol effect, and because electrolytic lesions of the median raphe nucleus were also ineffective in preventing the post-ethanol depression of LH, we conclude that activation of serotonergic systems does not play a major role in the ethanol induced depression of LH.

5,7-Dihydroxytryptamine↗
PubMed1982

Possible mechanism of 5-methoxy-N,N-dimethyltryptamine-induced turning behaviour in DRN lesioned rats.

5-Methoxy-N,N-dimethyltryptamine (5-MeODMT) (7.5 mg/kg SC) caused a contralateral turning in rats with a unilateral lesion of the dorsal raphe nucleus (DRN). This turning behaviour was blocked by pretreatment with putative 5-HT antagonists, methysergide, cyproheptadine and cinanserin. The peripheral 5-HT antagonist, xylamidine, also prevented the response to 5-MeODMT. Of the other neurotransmitter antagonists, only haloperidol was active, hyoscine, picrotoxin, naloxone and strychnine were ineffective. Pretreatment with alpha-methyl-p-tyrosine (alpha-MT) also significantly reduced the turning response to 5-MeODMT. These results indicate that a central dopaminergic system is involved in 5-MeODMT-induced turning behaviour. This suggestion is supported by the finding that an ipsilateral turning in response to 5-MeODMT was observed in the rats with additional 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle (MFB). The possible mechanisms by which 5-MeODMT induced turning in DRN lesioned rats are discussed.

Animals↗
PubMed1982

Beta-adrenoceptor antagonists may attenuate hyponeophagia in the rat through a serotonergic mechanism.

The unconditioned inhibition of feeding in a novel setting (hyponeophagia) was reduced by propranolol and another potentially centrally acting beta-adrenoceptor antagonist, pindolol but not by a peripherally acting one, atenolol. A similar attenuation of hyponeophagia was seen following the 5-HT antagonist methysergide but no consistent effects were observed following some dopamine antagonist drugs. 5-Methoxy N,N-dimethyltryptamine (5-MeODMT), a compound with central 5-HT agonist properties, consistently potentiated hyponeophagia, an effect which was reversed by the centrally acting beta-adrenoceptor antagonists and by methysergide. The results are interpreted as evidence for a 5-HT mediation of hyponeophagia and for a probable central 5-HT antagonist role for propranolol and pindolol.

Adrenergic beta-Antagonists↗
PubMed1982

Discriminative stimulus properties of DOM and several molecular modifications.

Rats trained to discriminate racemic 2,5-dimethoxy-4-methylphenylisopropylamine, (+/-)-DOM (1.0 mg/kg), from saline in a two-lever drug discrimination task were challenged with the optimal isomers of DOM as well as with several related agents which represent minor molecular modifications of the DOM structure. Generalization of the (+/-)-DOM stimulus was found to occur to R(-)-DOM, S(+)-DOM, (+/-)-2,5-dimethoxyphenylisopropylamine (2,5-DMA), R(-)-2,-5-DMA, and the 2-demethyl derivative of (+/-)-DOM. The 3-methyl positional isomer of (+/-)-DOM was found to produce only 34% DOM-appropriate responding at the highest dose tested while administration of S(+)-2,5-DMA and the 5-demethyl derivative of (+/-)-DOM resulted in disruption of behavior.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1983

Effects of apomorphine, clonidine or 5-methoxy-NN-dimethyltryptamine on approach and escape components of lateral hypothalamic and mesencephalic central gray stimulation in two inbred strains of mice.

The effects of intraperitoneal injections of increasing doses of apomorphine, clonidine or 5-methoxy-NN-dimethyltryptamine (5-m-DMT) on approach and escape reactions induced by lateral hypothalamic (LH) or mesencephalic central gray (CG) stimulation were compared in BALB/c and DBA/2 mice. Apomorphine increased both the approach latency for LH stimulation and the escape latency for CG stimulation; the BALB/c strain was more reactive than DBA/2 animals. Clonidine reduced the approach latency for LH stimulation only in the BALB/c strain. 5-m-DMT increased escape latency both for LH and CG stimulation only in the DBA/2 strain. These results suggest that the neurochemical regulation of escape reactions respectively generated by LH or CG activation is partially different: dopamine seems to be involved only in CG aversion, whereas serotonin (5-HT) modulates both LH and CG escape reactions. Moreover, our results demonstrate a noradrenergic influence on the appetitive component of LH stimulation. Finally, they confirm that approach and escape reactions, particularly when induced from lateral hypothalamus, depend on distinct neuronal populations.

Animals↗
PubMed1983

Serotonin receptor activation in rats previously deprived of REM sleep.

The effects of serotonin precursors (L-5-hydroxytryptophan and L-tryptophan, with or without MAO inhibitors) and of agonists (quipazine and 5-methoxy-N,N-dimethyltryptamine-MeO-DMT) were studied in 3 day REM-deprived or control rats, by recording the presence of the serotonin syndrome and the number of head shakes. The REM sleep-deprived rats showed a larger incidence of the serotonin syndrome and a greater number of head shakes in comparison to the control animals, when challenged with the serotonin precursors. Conversely, REM sleep deprivation did not modify the responsiveness of rats to 0.75-6.0 mg/kg of MeO-DMT and to 2.4-6.0 mg/kg of quipazine. However, REM-deprived rats reacted less than controls to 0.3-1.25 mg/kg of quipazine. Increased turnover due to REM sleep deprivation could explain the augmented responsiveness of the rats to the serotonin precursors. Conversely, the decreased responsiveness to quipazine could result from receptor hyposensitivity due to intense receptor activation, caused by the increased turnover, during the 3 day period of REM sleep deprivation.

5-Hydroxytryptophan↗
PubMed1985

Altered responses to serotonergic agents in Fawn-Hooded rats.

The incidence of "wet dog" shakes elicited by quipazine, the hyperthermic response induced by 5-methoxy-N,N-dimethyltryptamine (5MeODMT) and the hypothermic response to 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were compared in rats of the Fawn-Hooded (FH) and Sprague-Dawley (SD) strains. The behavioral responses of FH rats to quipazine and 5MeODMT were significantly greater than those of SD rats. On the other hand, the hypothermic effect of 8-OH-DPAT in FH rats was significantly less than that elicited in SD animals. The present results are supportive of the view that the responsiveness of serotonergic mechanisms in the CNS of FH rats differs markedly from those in SD animals.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

Further studies on the dose-dependent stimulus properties of 5-methoxy-N,N-dimethyltryptamine.

Twenty-two rats were trained to discriminate either 1.5 mg/kg of 5-methoxy-N,N-dimethyltryptamine (5-OMe DMT) from saline in a standard two-lever operant procedure. Once responding was stable, various doses of several serotonin (5-HT) antagonists, i.e., cyproheptadine (CYP), methysergide (UML), cinanserin (CIN), and methergoline (MCE), were administered in combination with 5-OMe DMT, to assess the ability of each antagonist to attenuate each 5-OMe DMT-stimulus. The 5-OMe DMT-stimulus at 1.5 mg/kg was completely antagonized by CYP, and was partially attenuated by CIN and MCE. UML had negligible effects on 5-OMe DMT-appropriate responding. In the 3.0 mg/kg 5-OMe DMT-trained rats, UML and MCE partially blocked the 5-OMe DMT-stimulus; CYP and CIN had no significant effect on 5-OMe DMT-appropriate responding. The results suggest that until the in vivo effects and mechanism of action of 5-OMe DMT and certain 5-HT antagonists are better understood, caution is advised when conclusions are drawn from studies employing these agents.

Animals↗
PubMed1986

Prenatal stress increases the behavioral response to serotonin agonists and alters open field behavior in the rat.

Female rats were exposed to mild stress throughout pregnancy and the offspring tested at 60 days of age. In an open field test the prenatal stress group showed increased locomotion and increased rearing compared to control rats confirming that the prenatal stress treatment was sufficient to produce persistent behavioural changes in the offspring. The prenatal stress offspring also showed an increased behavioural response to injections of 5-hydroxy-L-tryptophan (wet-dog shakes) and an enhanced 5-HT syndrome following treatment with the 5-HT agonist 5-methoxy-N,N- dimethyltryptamine. These results provide further evidence that maternal stress produces long-lasting changes in the functioning of central 5-HT neurons in the offspring.

5-Hydroxytryptophan↗