Voronina T A, Garibova T L
Biull Eksp Biol Med. 1980 Jul;89(7):41-3.
It has been shown that depakin, a GABA-ergic agonist, and alpha-methyl-DOPA that inhibits catecholamine synthesis are capable of removing the withdrawal syndrome (disturbed pavlovian behavior pattern and aggressiveness) occurring after discontinuance of long-term administration (30 days) of phenazepam to rats in a dose of 2 mg/kg. In contrast, bicucullin, a blocker of GABA-ergic receptors, thiosemicarbazide that inhibits GABA synthesis by the brain, disulfiram and 3,4-dioxyphenylalanine that increase dopamine and noradrenaline content in the barain aggravate the withdrawal syndrome after phenazepam is discontinued. The data obtained suggest a role of GABA-ergic and dopaminergic mechanisms in the emergence of the withdrawal syndrome after discontinuance of long-term administration of benzdiazepins.
已表明，γ-氨基丁酸能激动剂丙戊酸以及抑制儿茶酚胺合成的α-甲基多巴，能够消除大鼠以2毫克/千克的剂量长期（30天）服用芬那西泮后停药出现的戒断综合征（巴甫洛夫行为模式紊乱和攻击性）。相反，γ-氨基丁酸能受体阻滞剂荷包牡丹碱、抑制大脑γ-氨基丁酸合成的氨基硫脲、双硫仑以及增加大脑中多巴胺和去甲肾上腺素含量的3,4-二羟基苯丙氨酸，会在芬那西泮停药后加重戒断综合征。所获数据表明，γ-氨基丁酸能和多巴胺能机制在长期服用苯二氮䓬类药物停药后戒断综合征的出现中发挥作用。
