INTERACTION OF GABAERGIC AND BETA-NORADRENERGIC DRUGS IN THE REGULATION OF MEMORY STORAGE
INTERACTION OF GABAERGIC AND BETA-NORADRENERGIC DRUGS IN THE REGULATION OF MEMORY STORAGE
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DOI：
10.1016/s0163-1047(05)80068-8
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发表时间：
1994-03-01
期刊：
影响因子：
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通讯作者：
MCGAUGH, JL
中科院分区：
文献类型：
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作者：
INTROINICOLLISON, IB;CASTELLANO, C;MCGAUGH, JL
这些实验研究了影响去甲肾上腺素能和GABA能系统的药物的相互作用，训练后给药，影响抑制性回避反应的保留。在抑制性回避任务中训练雄性CD 1小鼠（23-28 g），在训练后立即ip注射单独或同时施用的盐水或GABA能和肾上腺素能药物。48小时后测试保留。与大量先前证据一致，GABA能拮抗剂荷包牡丹碱（0.3、1.0或3.0 mg/kg）产生剂量依赖性（倒U）保留增强，GABA能激动剂蝇蕈醇（1.0 mg/kg）损害保留。荷包牡丹碱的保留增强作用被阻断，同时给予β-去甲肾上腺素受体拮抗剂普萘洛尔（2.0 mg/kg）。同样与先前的证据一致，β-肾上腺素受体激动剂克仑特罗（0.030，0.100或0.300 mg/kg，ip）产生剂量依赖性（倒U）的保留增强。克仑特罗还阻断蝇蕈醇（1.0 mg/kg）的保留损害作用。此外，普萘洛尔（2.0 mg/kg）加强蝇蕈醇（1.0或3.0 mg/kg，ip）的保留损害作用。这些发现支持GABA能系统通过与β-去甲肾上腺素能机制相互作用来调节记忆的观点。(C)1994年出版社出版。
These experiments examined the interaction of drugs affecting noradrenergic and GABAergic systems, administered post-training, in influencing retention of an inhibitory avoidance response. Male CD1 mice (23-28 g) were trained in an inhibitory avoidance task, given immediate post-training ip injections of saline or GABAergic and adrenergic drugs administered either alone or concurrently. Retention was tested 48 h later. In agreement with extensive previous evidence, the GABAergic antagonist bicuculline (0.3, 1.0, or 3.0 mg/kg) produced dose-dependent (inverted-U) enhancement of retention and the GABAergic agonist muscimol (1.0 mg/kg) impaired retention. The retention-enhancing effects of bicuculline were blocked by concurrent administration of the beta-noradrenoceptor antagonist propranolol (2.0 mg/kg). Also in agreement with previous evidence, the beta-adrenoceptor agonist clenbuterol (0.030, 0.100, or 0.300 mg/kg, ip) produced dose-dependent (inverted-U) enhancement of retention. Clenbuterol also blocked the retention-impairing effects of muscimol (1.0 mg/kg). In addition, propranolol (2.0 mg/kg) potentiated the retention impairing effects of muscimol (1.0 or 3.0 mg/kg, ip). These findings support the view that GABAergic systems modulate memory through an interaction with beta-noradrenergic mechanisms. (C) 1994 Academic Press, Inc.