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At least 523 records · Page 29Linked to original sources
PubMed2002

Discriminative stimulus properties of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(+/-)DOI] in C57BL/6J mice.

RATIONALE: The drug discrimination procedure has proven to be a valuable tool for studying the mechanism of action of psychoactive drugs. Recently, mice with targeted gene mutations have been developed that may also prove useful in evaluating the role of specific receptors in mediating the actions of drugs. We were interested in studying the effects of hallucinogens in genetically modified mice using the drug discrimination procedure. OBJECTIVE: To establish the training procedures and characterize the stimulus properties of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(+/-)DOI] versus saline in wild-type mice. METHODS: Using a two-lever drug discrimination procedure, C57BL/6J mice were trained to discriminate (+/-)DOI (2.5 mg/kg) from saline on a VI 30-s schedule of reinforcement. RESULTS: The acquisition function was orderly and similar to that found previously with rats, although the training dose required for the mice was four times higher (2.5 versus 0.75 mg/kg). The dose-response relationship indicated that percent drug lever responding was dose-dependent. Two other hallucinogens, LSD and (-)DOB, substituted fully for (+/-)DOI. Mice were tested for their ability to discriminate (+/-)DOI following pretreatment with the 5-HT(2A) receptor antagonist MDL 100,907, or with 5-HT(2C) selective antagonists, SB 206,553 or SB 242,084. A dose of 0.25 mg/kg MDL 100,907 essentially completely blocked the discriminative stimulus effects of 2.5 mg/kg (+/-)DOI. Surprisingly, both SB 206,553 and SB 242,084 also attenuated the effect of 2.5 mg/kg (+/-)DOI. The effect of SB 206,553 was surmountable at 5.0 mg/kg (+/-)DOI. CONCLUSIONS: These data agree with the results from studies with rats indicating a prominent role for the 5-HT(2A) receptors in mediating the discriminative stimulus effects of (+/-)DOI but in addition, suggest a small but significant role for the 5-HT(2C) receptor in mice.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed2003

Swim stress inhibits 5-HT2A receptor-mediated head twitch behaviour in mice.

RATIONALE: Several studies have shown that swim stress lowers the convulsant potency of different convulsants. The involvement of alpha(2)-()adrenoceptors has been proposed. Drugs active at alpha(2)-adrenoceptors are known to modulate the head twitch response, the behaviour supposedly mediated by 5-HT(2A) receptors. OBJECTIVES: We tested whether swim stress modulates head twitch behaviour in mice and whether alpha(2)-adrenoceptors interfere with this effect. METHODS: The mice were stressed (10 min swimming at 18-19 degrees C), and the head twitch response was produced by 5-hydroxytryptophan (5-HTP, the precursor of serotonin) or by 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI, a selective 5-HT(2) receptor agonist) administered IP before or after swimming. Yohimbine (a non-selective alpha(2)-adrenoceptor antagonist), idazoxan (a selective alpha(2)-adrenoceptor antagonist) and diazepam were also used. RESULTS: Swim stress inhibited profoundly the 5-HTP-induced head twitch behaviour in mice. alpha(2)-Adrenoceptor antagonists and diazepam failed to counteract this effect. The head twitch behaviour produced by DOI given before or after stress was also inhibited. Repeatedly stressed mice had only a mild inhibition of the head twitch response. CONCLUSIONS: The results demonstrate that swim stress inhibits, by an alpha(2)-adrenoceptor unrelated mechanism, 5-HT(2A) receptor-mediated head twitch behaviour in mice, suggesting that this effect and the swim stress-induced anticonvulsant effect are produced by two separate and independent mechanisms.

5-Hydroxytryptophan↗
PubMed2004

Attenuation of nicotine's discriminative stimulus effects in rats and its locomotor activity effects in mice by serotonergic 5-HT2A/2C receptor agonists.

RATIONALE: Reports have indicated that administration of nicotine inhibits, while withdrawal of chronically administered nicotine augments effects of serotonergic 5HT2A/2C agonists. OBJECTIVE: It was our objective to determine whether 5HT2A/2C agonists can modulate the discriminative stimulus effects of nicotine in rats or its locomotor activity effects in mice. METHODS: Adult male Sprague-Dawley rats were trained to discriminate 0.3 mg/kg nicotine base from saline in a two-lever, fixed-ratio (FR10), food-reinforced, operant-conditioning task during daily (Monday-Friday) 15-min experimental sessions. After characterizing a dose-response curve for nicotine, we tested the ability of the 5HT(2A/2C) agonists (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCL (DOI; 0.18-1.0 mg/kg) and 1-(4-bromo-2, 5-dimethoxyphenyl)-2-aminopropane (DOB; 0.1-1.0 mg/kg), the 5HT2C agonist 6-chloro-2-(1-piperazinyl)pyrazine hydrochloride (MK 212; 0.1 mg/kg-1.0 mg/kg), and the 5HT1A agonist (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT; 0.01 mg/kg-1.0 mg/kg) to modulate nicotine's discriminative stimulus effects. After finding that DOI was able to attenuate the percentage nicotine lever responding (%NLR), we tested for it to also reverse nicotine's effects on locomotor activity in mice. RESULTS: The 5HT2A/2C agonists-in particular DOI-dose dependently attenuated %NLR. The effects of DOI were reversed by the 5HT2A/2C antagonist ketanserin. MK 212 and 8-OH-DPAT had irregular effects among rats and only reduced %NLR to below 50% levels at doses markedly suppressing responding. DOI also dose dependently blocked nicotine's acute rate-lowering locomotor activity effects. CONCLUSIONS: These results indicate that activation of serotonin 5HT2A/2C receptors can blunt the discriminative stimulus and locomotor activity effects of nicotine and presents the possibility that activation of these receptors might also be able to attenuate other effects of nicotine.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2006

Role of atypical opiates in OCD. Experimental approach through the study of 5-HT(2A/C) receptor-mediated behavior.

RATIONALE: The selective serotonin (5-HT) reuptake inhibitors (SSRIs) represent the first-line pharmacotherapy for obsessive-compulsive disorder (OCD), and atypical antipsychotic drugs, which block 5-HT2A receptors, are used in augmentation strategies. Opiate drugs are also effective in treatment-refractory OCD and Tourette syndrome. The 5-HT2A-related behavior (i.e., head twitch) has been related with tics, stereotypes, and compulsive symptoms observed in Tourette syndrome and OCD. OBJECTIVES: The aim of this study was to explore whether 5-HT2A-related behavior is affected by atypical opiate drugs. MATERIALS AND METHODS: Head-twitch response was induced in mice by administration of either 5-hydroxytryptophan (5-HTP) or the 5-HT2A/C agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). Dose-effect curves of atypical opiate drugs [(+/-)-tramadol, (-)-methadone and levorphanol], morphine, and other psychoactive drugs (fluvoxamine, desipramine, nefazodone, and clozapine) were performed. Opioid mechanisms were investigated by administration of naloxone. RESULTS: All the opiates tested reduced both 5-HTP and DOI-induced behavior in a naloxone-reversible fashion, atypical opiates being more effective. The effects of the other drugs depended on the protocol, clozapine being the most effective. CONCLUSIONS: Combined 5-HT and opioid properties result in a greater efficacy in antagonizing 5-HT2A-related behavior. These results provide behavioral evidence to support convergent effects of the 5-HT and opioid systems in discrete brain areas, offering the potential for therapeutic advances in the management of refractory stereotypes and compulsive behaviors.

5-Hydroxytryptophan↗
PubMed2001

Effects of nicotine on head-shakes and tryptophan metabolites.

RATIONALE: Nicotine appears to ameliorate the tics of Tourette syndrome. There is evidence that plasma concentrations of the tryptophan metabolite kynurenine may be elevated in this condition. Rodent head-shakes have been proposed as a putative model of Tourette syndrome and are potentiated by kynurenine. OBJECTIVES: To determine the effects of acute and chronic nicotine on mouse head-shakes, and to study whether nicotine influences brain and plasma levels of kynurenine and certain of its further metabolites in this species. METHODS: Behavioural and biochemical studies. RESULTS: Acute (-10 min) administration of (-)-nicotine, or the nicotinic agonist (+)-epibatidine, dose dependently attenuated head-shakes induced by the 5-HT2A/2C receptor agonist +/-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). This attenuation was inhibited by the nicotinic receptor antagonist mecamylamine. Acute nicotine did not affect either spontaneous head-shakes or plasma and brain kynurenine. Fifteen hours after the last of twice daily injections of nicotine (1.6 mg/kg for 7 days), the frequency of spontaneous and DOI-induced head-shakes was significantly potentiated and there was a significant elevation of both plasma and brain kynurenine, although no differences were detected in plasma concentrations of tryptophan, kynurenic acid, 3-hydroxykynurenine or 3-hydroxyanthranilic acid. Brain levels of 5-hydroxytryptamine and 5-hydroxyindole acetic acid were also unaffected. In contrast, all these measures were unchanged 15 h after a single nicotine dose (1.6 mg/kg). CONCLUSIONS: The acute studies indicate that head-shakes induced by DOI are indeed inhibited by nicotinic receptor agonists and suggest that this is not a consequence of an increase in kynurenine. While a role for kynurenine or its metabolites in increasing the head-shake rate after chronic nicotine cannot be excluded, alternative explanations included alterations in the expression or functional status of nicotinic receptor components and further work will be required to characterise this effect.

Animals↗
PubMed2000

Non-serotonergic potentiation by (-)-pindolol of DOI-induced forward locomotion in rats: possible involvement of beta-adrenoceptors?.

[1] We have previously shown that the beta-adrenergic/5-HT1 receptor partial agonist (-)-pindolol (2.0-32.0 micromol kg(-1)) enhances the increase in forward locomotion in rats produced by the 5-HT2 receptor agonist DOI (0.7 micromol kg(-1)) via net activation of post-synaptic 5-HT2 receptors. [2] It was found that neither the 5-HT1A receptor agonist and partial agonist, (+/-) 8-OH-DPAT (0.2-2.4 micromol kg(-1)) and (S)-(-)-UH-301, respectively, nor the 5-HT1A receptor antagonist WAY-100635 (0.09-1.5 micromol kg(-1)), substituted for (-)-pindolol in this in vivo behavioral model. [3] This also applies to the 5-HT1B receptor agonist and antagonist anpirtoline (0.3-4.0 micromol kg(-1)) and isamoltane (1.0-64.0 micromol kg(-1)), respectively. Neither of these compounds mimicked (-)-pindolol in its interactions with DOI. [4] The (-)-pindolol/DOI-induced increase in forward locomotion could be antagonized by the beta1 adrenoceptor antagonist betaxolol (24 micromol kg(-1)). [5] It is suggested that the intrinsic efficacy of (-)-pindolol at beta-adrenoceptors is an important aspect of its in vivo pharmacodynamic profile.

5-Hydroxytryptophan↗
PubMed1990

Automated continuous-flow colorimetric determination of glutathione peroxidase with dichloroindophenol.

Automation of the glutathione peroxidase enzyme assay has been problematical. Although such methods have been reported, they do not give equivalent results to the standard manual assay, wherein glutathione oxidation is coupled to NADPH oxidation via glutathione reductase. We report here the development of a fully automated, continuous-flow, colorimetric method for glutathione peroxidase assays in which glutathione oxidation is monitored by its effect on the reaction of glutathione with the colorimetric reagent 2,6-dichloroindophenol. This method has a linear response to glutathione peroxidase over an 800-fold range of enzyme concentrations. Results of assays done by this method in erythrocyte and plasma samples correlate well with the standard manual coupled assay (r = 0.997 and 0.923, respectively), with no evidence of systematic errors. The assay works equally well with hydrogen peroxide or cumene hydroperoxide as substrate and shows the same selectivity toward glutathione S-transferases as the standard coupled assay. The within-day repeatability and the between-day reproducibility were estimated as 1.1 to 6.4% and 1.3 to 7.1% (relative standard deviation), respectively. This method is suitable for enzyme determinations in whole blood, erythrocytes, plasma, and serum from rats, rabbits, monkeys, and humans.

2,6-Dichloroindophenol↗