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• W2108604025 abstract "Brain tryptophan concentrations are increased by various stressful treatments, an effect that can be prevented by β-adrenoceptor antagonists. This study aimed to determine the β-adrenergic subtype responsible for the tryptophan response. Male CD-1 mice received intraperitoneal injections of nonselective and subtype-selective β-adrenergic antagonists 20 min before subtype-selective β-agonists. Selected brain regions were dissected for analysis of tryptophan content by high-performance liquid chromatography with electrochemical detection. The β₂-selective agonist clenbuterol (0.3 mg/kg) induced increases in brain tryptophan that reached a peak (∼60%) 1 h following injection and small but statistically significant increases (∼20%) in 5-hydroxyindoleacetic acid: serotonin ratios 2 h following injection. The β₁-selective agonist dobutamine (10 mg/kg) produced less robust increases (∼40%) in brain tryptophan, whereas the β₃-selective agonists BRL 37344 (0.2 mg/kg (±)-(<i>R</i>*,<i>R</i>*)-[4-[2-[[2-(3-chlorophenyl)-2-hydroxyethyl]amino)propyl] phenoxy]acetic acid sodium)) and CL 316243 [0.1 mg/kg disodium 5-[(2<i>R</i>)-2-([(2<i>R</i>)-2-(3-chlorophenyl)-2-hydroxyethyl]amino)propyl]-1,3-benzodioxole-2,2-dicarboxylate)] resulted in larger increases (80 to 100%). Pretreatment with the β₂-selective antagonist ICI 118551 (0.5 mg/kg (±)-1-[2,3-(dihydro-7-methyl-1<i>H</i>-inden-4-yl)oxyl]-3-[(1-methylethyl)amino]-2-butanol) attenuated the increases in tryptophan induced by both clenbuterol (0.1 mg/kg) and dobutamine (10 mg/kg). Pretreatment with the β_1/2-selective antagonist propranolol (2.5 mg/kg), the β₃-selective antagonist SR 59230A [1.5, 2.5, 5, or 20 mg/kg (3-(2-ethylphenoxy)-1[1<i>S</i>)-1,2,3,4-tertahydronaphth-1-yl-amino]-(2<i>S</i>)-2-propanol oxalate)], or ICI 118551 (0.5 mg/kg) did not prevent the BRL 37344-induced increase in brain tryptophan, whereas the β_1/2/3-antagonist bupranolol (10 mg/kg) attenuated it. CL 316243 had no effect on brain tryptophan in β₃-receptor knockout mice, whereas clenbuterol increased brain tryptophan, indicating that β-adrenergic modulation of brain tryptophan occurs in the absence of β₃-receptors. We conclude that activation of either β₂- or β₃-adrenergic receptors, but not β₁-adrenergic receptors, increases mouse brain tryptophan content." @default.
• W2108604025 created "2016-06-24" @default.
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• W2108604025 date "2003-01-24" @default.
• W2108604025 modified "2023-09-27" @default.
• W2108604025 title "Activation of β₂- and β₃-Adrenergic Receptors Increases Brain Tryptophan" @default.
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• W2108604025 doi "https://doi.org/10.1124/jpet.102.048249" @default.
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