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PubMed1991

[Study by the intracerebral microdialysis method of the effects of atypical neuroleptics and anxiolytics on striatal release and metabolism of dopamine in awake rats].

Using brain microdialysis in awake rats effects of risperidone, ritanserin, buspirone, sulpiride and 5-methoxy-N,N-dimethyltryptamine (MeODMT) on striatal dopamine (DA) release and metabolism were studied. Risperidone, sulpiride and buspirone increased levels of DA, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). Ritanserin failed to affect DA release, while increased DOPAC and HVA levels. MeODMT had no effect on striatal DA release and metabolism. Possible interaction between DA and serotonin systems is discussed.

Animals↗
PubMed1990

[Hemodynamic profile of 8-OH-DPAT and 5-HT1 agonists in the anesthetized dog].

In anaesthetized dogs, intravenous administration of 8-OH-DPAT (1-300 micrograms/kg i.v.) induced dose-dependent decrease in blood pressure (BP) and total peripheral resistance (TPR). Heart rate (HR) and cardiac output (CO) changed little. 5-Carboxamidotryptamine (5-CT) (0.3-3 micrograms/kg i.v.) dose-dependently decreased BP and TPR but increased HR, CO, myocardial contractility and pulmonary arterial pressure (PAP). 5-MeODMT and RU 24969 decreased BP only after the highest dose used (300 micrograms/kg i.v. and 1 mg/kg i.v. respectively) but significantly increased PAP at all doses used. These results indicated that in dogs as in other animal species, 8-OH-DPAT decreases BP by systemic vasodilatation without a reflex activation of the myocardium. This lack of a reflex tachycardia suggests a centrally-mediated effects of 8-OH-DPAT. In contrast to 8-OH-DPAT, the vasodilatation induced by 5-CT triggers a reflex tachycardia. The increase in PAP induced by 5-MeODMT, RU 24969 and--to a lesser extent--5-CT, may be due to a direct stimulation of 5-HT2 receptors. However, a 5-HT1 component could not be ruled out.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1987

Effects of an atypical barbiturate (valofan) on spontaneous and stimulated locomotor activity and on brain serotonin metabolism in mice.

The effects of an atypical barbiturate, 2-allophanyl-2-allyl-4-valerolactone (valofan), have been studied on spontaneous locomotor activity and amphetamine-induced hypermotility in mice. Some serotonergic agents were employed in order to evaluate the possible involvement of serotonin on its mechanism of action. Valofan (250 and 500 mg/kg) always reduced spontaneous locomotion and amphetamine-induced hypermotility; after the administration of L-tryptophan (10 mg/kg) and tranylcypromine (1 mg/kg) both locomotions decreased; when administered in combination with valofan they resulted in an additive effect. Similar results have been obtained by administration of 5-methoxy-N,N-dimethyltryptamine (1 mg/kg) and pindolol (5 mg/kg) alone or combined with valofan. Valofan affected the serotonin metabolism increasing 5-HT and 5-HIAA concentrations in a dose dependent way in the cortex, in the brainstem or in total brain. No correlation seems to exist between the effects of valofan, on its own or combined with serotonergic agents, on motor activity and its effects on the accumulation of 5-HT and 5-HIAA. We can therefore suggest that valofan manifests its central effects by an unclear mechanism which cannot completely be accounted for its metabolic effects on cerebral serotonin and dopamine.

Animals↗
PubMedDate not supplied

Serotonin-mediated behavior in rats chronically treated with (-) deprenyl.

(-) Deprenyl given in small (0.25 mg/kg) daily doses for 30 days to rats left the serotonin (5-HT) and the 5-hydroxyindoleacetic acid (5-HIAA) levels in the striatum unchanged. The postsynaptic 5-HT receptor responsiveness, as measured with 5-methoxy-N,N-dimethyl-tryptamine (5-MeODMT), remained also unaltered. In (-) deprenyl-treated rats the p-chloroamphetamine (PCA)-induced 5-HT syndrome was significantly increased and this enhancement of the PCA effect was not abolished by the reserpine-induced depletion of the 5-HT stores.

Animals↗
PubMedDate not supplied

Pharmacological effects of oxaprotiline enantiomers on the central serotonin system.

The study examined the effect of both oxaprotiline (OXA) enantiomers on the serotonin system in rats and mice. (+)-OXA and (-)-OXA partly inhibit the behavioral syndrome induced by 8-OH-DPAT and 5-methoxy-dimethyltryptamine (5-MeODMT) in normal and reserpinized rats. Imipramine and desipramine produced a similar but less potent effect. (+)-OXA and, to a lesser extent, (-)-OXA antagonized the m-chlorophenylpiperazine (m-CPP)-induced hypothermia in mice. Imipramine and desipramine produced no such effect. (+)-OXA attenuated the head-twitch response to L-5-HTP in mice, but (-)-OXA has no such action. Neither enantiomer inhibited the fenfluramine-induced hyperthermia in rats nor antagonized m-CPP-induced stimulation of hind limb flexor reflex of spinal rat. The obtained results indicate that both enantiomers may have a 5-HT1B-antagonistic action and a less potent 5-HT1A-antagonistic one; on the other hand, they shown no 5-HT2-antagonistic activity.

5-Hydroxytryptophan↗
PubMed1989

Effect of gepirone and ipsapirone on the stimulated and unstimulated secretion of prolactin in the rat.

Previous studies have demonstrated that the 5-hydroxytryptamine1A (5-HT1A) agonist buspirone stimulated rat prolactin (PRL) secretion. Administration of the 5-HT1A agonists gepirone (GEP) or ipsapirone (IPS) s.c. in doses from 1 to 10 mg/kg had no effect on PRL secretion in male rats. However, pretreatment with GEP (10 mg/kg) or IPS (10 mg/kg) significantly attenuated the increase in serum PRL concentration elicited by the 5-HT agonists 5-methoxy-N,N-dimethyltryptamine or 6-chloro-2-(1-piperazinyl)-pyrazine (MK-212). To determine whether the inhibitory effect of GEP or IPS was related to a serotonergic mechanism or a more general inhibitory effect on PRL secretion, the ability of GEP and IPS to inhibit the haloperidol- or alpha-methyl-p-tyrosine-induced increase in PRL secretion was studied. GEP (1, 3 and 10 mg/kg) and IPS (10 mg/kg) inhibited the increase in PRL secretion produced by either haloperidol (0.25 mg/kg) or alpha-methyl-p-tyrosine (75 mg/kg). Furthermore, GEP produced a concentration-dependent inhibition of PRL secretion from anterior pituitary tissue incubated in vitro. The inhibitory effect of GEP was comparable to that of dopamine in this system. Moreover, haloperidol blocked completely the GEP-mediated suppression of PRL secretion in this preparation. These data suggest agonist properties of both GEP and IPS at D2 dopamine receptors. In light of other evidence that GEP has D2 antagonist effects in vivo, we hypothesize that GEP and perhaps IPS are partial dopamine agonists which may contribute to their antianxiety and/or antidepressant properties.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

[Changes in 5-HT2 receptor density induced by repeated treatment with 5-HT uptake inhibitor or 5-HT agonist].

It has been known that many antidepressant drugs which have serotonin (5-HT) antagonistic activities and 5-HT antagonists can induce the reduction of 5-HT2 receptor binding by their acute or successive administration. We investigated the effects of repeated treatment with 5-HT agonists on 5-HT2 receptors in rat cerebral cortex. We used citalopram as selective 5-HT uptake inhibitor, 5-hydroxytryptophan as 5-HT precursor, and 5-methoxy-N,N'-dimethyltryptamine as 5-HT2 agonist. The 5-HT2 receptor density was decreased by repeated treatment with these respective drugs. So it may be supposed that the reduction of 5-HT2 receptor binding is induced not only by 5-HT antagonists but also by 5-HT agonists.

5-Hydroxytryptophan↗
PubMed1989

Different behavioral reactivity of 5-HT1 sites between killer and non-killer rats after midbrain raphe lesion.

A behavioral reactivity study on 5-HT1 and 5-HT2 sites of isolated killer and non-killer rats and on raphe lesioned killer and non-killer animals was undertaken, 5-HT1 reactivity was measured by a rank intensity scale on the forepaw treading and hind-limb abduction induced by 5-MeODMT. 5-HT2 reactivity was determined by the "shaking" behavior following 5-HTP. No behavioral differences on 5-HT1 and 5-HT2 sites were observed between isolated killer or non-killer animals. Similarly, comparable values of "shakes" were obtained on killer and non-killer lesioned rats. On the contrary, 5-MeODMT, induced a lower behavioral response on lesioned killer as compared to lesioned non-killer. This different behavioral response can not be explained by a probable difference of 5-HT terminals denervation since a similar reduction of 5-HT brain uptake was observed between both groups of rats. Finally, the decreased reactivity of 5-HT1 sites may be an index of a lower 5-HT neurotransmission and could therefore provide an explanation of the appearance of muricidal activity in some but not in all the lesioned rats.

5-Hydroxytryptophan↗
PubMed1987

Potentiation in phencyclidine-induced serotonin-mediated behaviors after intracerebroventricular administration of 5,7-dihydroxytryptamine in rats.

Phencyclidine (PCP)-induced behaviors were compared with 5-methoxy-N,N-dimethyltryptamine (5-MeODMT)- and p-chloroamphetamine-induced behaviors in rats pretreated with ritanserin or 5,7-dihydroxytryptamine (5,7-DHT) in order to investigate whether PCP interacts with 5-hydroxytryptamine2 (5-HT2) receptors. Head-twitch and wet-dog shake induced by p-chloroamphetamine, a 5-HT releaser, and head-twitch induced by PCP were blocked completely by pretreatment with ritanserin, a specific 5-HT2 receptor blocker, but other behaviors induced by p-chloroamphetamine, PCP and 5-MeODMT, a 5-HT agonist, were not. The intensity of head-weaving, turning, backpedalling and hind-limb abduction induced by 5-MeODMT and the intensity of head-weaving, turning and head-twitch induced by PCP were markedly greater in the rats 2 weeks after the 5,7-DHT, a 5-HT neurotoxin-injection. Contrarily, 5-HT-mediated behaviors induced by p-chloroamphetamine were attenuated in the 5,7-DHT-treated rats. 5,7-DHT-treatment increased the number of 5-HT1 ([3H]-5-HT), 5-HT2 ([3H]ketanserin) and PCP ([3H]PCP) binding sites in the synaptic membrane of rat brain, but decreased the brain level of 5-HT (41% of control). These results may indicate that PCP as a 5-HT2 agonist induces head-twitch via 5-HT2 receptors, and that PCP induces head-weaving and turning via 5-HT1 receptors and/or some other mechanisms in rats.

5,7-Dihydroxytryptamine↗
PubMedDate not supplied

Participation of sympathetic and vagal tones in the hypotensive and bradycardic effects of some 5-HT1-like receptor agonists in the rat.

In normotensive anaesthetized rats, 8-OH-DPAT, RU 24969 and 5-MeODMT, three 5-HT1-like receptor agonists, decreased blood pressure and heart rate. The decrease in blood pressure was suppressed by pithing or pretreatment with hexamethonium. Bilateral section of the vagus nerves, pretreatment with a beta-adrenoceptor blocking agent or with atropine, combination of bivagotomy plus beta-adrenoceptor blockade strongly reduced the bradycardia. These results are compatible with a centrally-mediated decrease in sympathetic tone and increase in vagal tone, as the cause of the hypotension and bradycardia induced by these 5-HT1-like receptor agonists in normotensive anaesthetized rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMedDate not supplied

Comparative study of the effects of stimulation or blockade of beta-adrenoceptors on the head-twitches induced in mice by 5-hydroxytryptophan versus 5-methoxy-N, N-dimethyltryptamine.

This study aimed at comparing the effects of blockade or stimulation of beta-adrenoceptors on the head-twitch response induced in mice by direct (5-MeODMT) or indirect (5-HTP) activation of serotonergic receptors shows that: beta-agonists (clenbuterol and salbutamol) increased the 5-HTP-induced head-twitches and decreased the response to 5-MeODMT. beta-agonists (propranolol and penbutolol) reduced the head-twitches elicited by 5-HTP but enhanced those induced by 5-MeODMT. Under our experimental conditions, desipramine behaved like the beta-agonists studied. Prior intracerebroventricular injection of 5,7-DHT enhanced the response to 5-MeODMT but did not prevent the antagonism of clenbuterol against 5-MeODMT-induced head-twitches. These findings suggest that beta-receptors are in a position to regulate differentially serotonin transmission.

5,7-Dihydroxytryptamine↗
PubMed1988

Three serotonin responses in cultured mouse hippocampal and striatal neurons.

Serotonin (5-HT) produced 3 different types of responses in neurons of mouse hippocampal and striatal cell cultures. These 3 responses have been characterized in terms of their pharmacological specificity, physiological mechanism, and dependence on cytoplasmic components. The most frequently observed response was inhibitory and was the result of a receptor-mediated activation of an inwardly rectifying potassium conductance. Typically, the response peaked within 1-3 sec of agonist application and did not exhibit desensitization. 5-Methoxy-N,N-dimethyltryptamine also produced this response in both striatal and hippocampal cultures and had no effect on the other 5-HT currents observed in this study. The selective 5-HT agonists--8-hydroxy-2-(di-n-propylamino)-tetralin, 1-(m-chlorophenyl) piperazine, and 1-(2-methoxyphenyl) piperazine--did not activate this outward current response. Methysergide did not block the 5-HT-activated outward current and often acted as an agonist. The response was lost in low-series-resistance recordings which facilitate solution exchange between the patch electrode and the cell. The loss of this response was prevented by using high-resistance patch electrodes, which retard this exchange. The 2 other responses described in this study were excitatory. They were seen less often than the inhibitory response. One of the excitatory responses was fast, with a time to peak of approximately 200 msec and a duration of 2-4 sec. The other was slow, with a time to peak of 7-10 sec and a duration of approximately 30-40 sec. Both of these responses were accompanied by a conductance increase. The fast excitatory response reversed at depolarized potentials and desensitized with a rate that varied with voltage. Metoclopramide and d-tubocurarine completely and reversibly blocked this fast excitatory response, while methysergide had no effect. The fast excitatory response was not lost during intracellular dialysis of cells in cultures from either striatum or hippocampus. In cultures from both brain regions, the slow excitatory response was blocked by methysergide. The slow excitatory response was lost even in patch-clamp recordings with high-resistance electrodes. This response was similar to responses to dopamine, norepinephrine, and forskolin, all of which are known to activate adenylate cyclase in the CNS.

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

[Effect of long-term lithium treatment on serotonin syndrome in rats].

Brain 5-HT receptors are reported to play an important role in the therapeutic effect of Li in manic-depressive illness. In the present study we examined the effect of Li on 5-HT syndrome which is postulated to be the physiological response of 5-HT1 receptors. Intraperitoneal injection of the 5-HT receptor agonist 5-MeODMT elicited 5-HT syndrome in a dose-dependent manner. Then the incidence of 5-HT syndrome elicited by 2 mg/kg of 5-MeODMT was measured in animals under long-term Li treatment. Four out of six abnormal behaviors of the 5-HT syndrome, i.e. forepaw treading, resting tremor, rigidity, and head weaving, were significantly increased by the 9-day treatment with Li. On the 17th day of Li treatment, the incidence of all six behaviors, including hindlimb abduction and straub tail, were significantly enhanced. This Li-induced supersensitivity of 5-HT1 receptor-mediated behaviors inconsistent with the previous reports of the down-regulation of 5-HT1 receptors measured by receptor binding assay. The reason for this discrepancy is obscure. Further examination of the effect of Li on the signal-transduction system from the receptor to the behavior will be necessary.

Animals↗
PubMed1984

Justicia pectoralis: a study of the basis for its use as a hallucinogenic snuff ingredient.

The use of Justicia pectoralis var. stenophylla as a Virola snuff admixture and also as the sole ingredient of a snuff was investigated. Extracts of the plant did not contain alkaloids, although the ubiquitous compound, betaine, was isolated because of its reaction with alkaloid reagents. Nor did extracts have any significant effect upon the gross behavioral effects, or increased spontaneous motor activity, elicited in mice by 5-methoxy-N,N-dimethyl-tryptamine (5-MeODMT), the primary psychotropic constituent of the Virola resin snuff. Coumarin and umbelliferone were identified because they are major constituents of the plant and because of their ability to relax smooth muscle.

Alkaloids↗