采用自发活动仪和观察翻正反射消失与否研究茶氨酸对戊巴巴比妥钠诱导的镇静催眠作用。结果显示:单用茶氨酸能剂量依赖性地抑制正常小鼠的自发活动,其半数抑制量为0.8518 g/kg;较小剂量(≤1.0 g/kg)茶氨酸能加强戊巴比妥钠(5 mg/kg)的抑制自发活动效应,而在2.0 g/kg时则引起自发活动反跳性的增加,呈现”U”型改变;单用茶氨酸5.0 g/kg并无催眠效应,但小于等于5.0 g/kg时茶氨酸加强戊巴比妥钠(25 mg/kg)的催眠作用,并呈明显的剂量依赖性。上述结果表明茶氨酸对戊巴比妥钠诱导的小鼠自发活动影响为双向改变(“U”改变);茶氨酸对戊巴比妥钠(25 mg/kg)的催眠效应呈剂量依赖性地加强作用,并未出现双向改变。
In the present study, the locomotor activities and disappearance of righting reflex on ICR mice were employed to evaluate effects of theanine on the sedative and hypnosis induced by pentobarbital sodium. Results showed that theanine alone decreased locomotor activity in dose-dependent manner and had no stimulant effect, 50% inhibition dose of locomotor activity was 0.8518 g/kg, low doses of theanine(≤1.0 g/kg) enhanced inhibition effect of locomotor activity induced by pentobarbital sodium(5 mg/kg), however, high dose (2.0 g/kg) of theanine reversed the inhibition, meanwhile, theanine enhanced hypnosis induced by pentobarbital sodium(25 mg/kg) in dose-dependent manner. It is concluded that theanine changed locomotor activity of mice induced by low dose of pentobarbital sodium(5 mg/kg) in dimensional change (“U” shape style), but not higher dose of pentobarbital sodium(25 mg/kg).
[1] 吕毅, 郭雯飞, 倪捷儿, 等. 茶氨酸的生理作用及合成[J]. 茶叶科学, 2003, 23(1): 1~5.
[2] Egashira N, Hayakawa K, Mishima K, et al. Neuroprotective effect of gamma-glutamylethylamide (theanine) on cerebral infarction in mice[J]. Neurosci Lett, 2004, 363(1): 58~61.
[3] Kakuda T, Yanase H, Utsunomiya K, et al. Protective effect of gamma-glutamylethylamide (theanine) on ischemic delayed neuronal death in gerbils[J]. Neurosci Lett, 2000, 289(3): 189~192.
[4] Nagasawa K, Aoki H, Yasuda E, et al. Possible involvement of group I mGluRs in neuroprotective effect of theanine[J]. Biochem Biophys Res Commun, 2004, 320(1): 116~122.
[5] Kakuda T, Nozawa A, Unno T, et al. Inhibiting effects of theanine on caffeine stimulation evaluated by EEG in the rats[J]. Biosci Biotech. Biochem, 2000, 64(2): 287~293.
[6] 王小雪, 邱隽, 宋宇, 等. 茶氨酸的抗疲劳作用研究[J]. 中国公共卫生, 2002, 18(3): 315~317.
[7] Taverna FA, Cameron BR, Wang LY, et al. Sensitivity of AMPA receptors to pentobarbital[J]. Eur J Pharmacol, 1994, 267(3): R3~5.
[8] Yamakura T, Sakimura K, Mishina M, et al. The sensitivity of AMPA-selective glutamate receptor channels to pentobarbital is determined by a single amino acid residue of the alpha 2 subunit[J]. FEBS-Lett, 1995, 374(3): 412~414.
[9] Kakuda T, Nozawa A, Sugimoto A, et al. Inhibition by theanine of binding of [3H]-AMPA, [3H]-kainite, and [3H]-MDL105519 to glutamate receptors[J]. Biosci Biotechnol Biochem, 2002, 66(12): 2683~2686.
[10] Menniti FS, Buchan AM, Chenard BL, et al. CP-465,022, a selective noncompetitive AMPA receptor antagonist, blocks AMPA receptors but is not neuroprotective in vivo[J]. Stroke, 2003, 34: 171~176.
[11] Imre G, Fokkema DS, Den Boer JA, et al. Dose-response characteristics of ketamine effect on locomotion, cognitive function and central neuronal Activity[J]. Brain Research Bull, 2006, 69: 338~345.
[12] Jentsch JD, Roth RH.The neuropsychopharmacology of phencyclidine: from NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia[J]. Neuropsychopharmacology, 1999, 20(3): 201~225.
[13] yokogoshi H, kobayashi M, et al. Effect of theanine, r-glutamylethylamide, on brain monoamines and striatal dopamine release in conscious rats[J]. Neurochem Res, 1998, 23(5): 667~673.