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- W2019967505 abstract "1.1. There has been considerable research in the field of schizophrenia over the past few years with emphasis on the discovery of better drugs, particularly those with 5-HT2 antagonist activity.2.2. In an effort to enhance identification of such compounds and to further understand the contribution of 5-HT2 activity to the effects of antipsychotic drugs, a series of conventional, atypical and purported antipsychotic compounds were assessed as antagonists of DOI-induced behaviors in rats.3.3. DOI (l-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride) is an hallucinogen having high aIEnity and selectivity as an agonist at 5-HT2A/2C receptors. Over a 30-min period after injection, DOI (0.3 – 10.0 mg/kg; i.p.) produced dose-related behavioral effects including head-and-body shakes, forepaw tapping and skin-jerks. Effects of the antipsychotic drugs and other compounds (30 min pretreatment; i.p.) were examined against a fixed dose of DOI (3.0 mg/kg).4.4. In a dose-dependent manner, M100907 (MDL 100, 907), risperidone, haloperidol, clozapine, iloperidone, olanzapine, amperozide, remoxipride, ritanserin and the neurotensin agonist NT1 (NαleArg-Lys-Pro-Trp-Tle-Leu) antagonized each of the three behavioral effects of DOI. Drugs attenuating the head-and-body shakes were equally effective in blocking both forepaw tapping and skin-jerks indicating that these behaviors are mediated by similar mechanisms. The following compounds had either inconsistent or no effect on the DOI-induced behaviors: SB 200646A, citalopram, imipramine, fluoxetine, morphine, CP 99994, diazepam, ondansetron and SKF 97541.5.5. The data show that antipsychotic agents, as a drug class, effectively block the effects of DOI. These actions are selective, as a series of nine non-antipsychotic and centrally-acting drugs were generally inactive in the procedure." @default.
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- W2019967505 date "2012-03-01" @default.
- W2019967505 modified "2023-09-26" @default.
- W2019967505 title "P.1.002 Role of 5-HT2A-receptor and α2-adrenoceptor blockade in the asenapine-induced elevation of prefrontal cortical monoamine outflow" @default.
- W2019967505 doi "https://doi.org/10.1016/s0924-977x(12)70004-4" @default.
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