Amphetamine induces β-adrenergic receptor supersensitivity
Amphetamine induces β-adrenergic receptor supersensitivity
复制标题
安非他明诱导β-肾上腺素能受体超敏反应
作者：
S. Banerjee;V. Sharma;L. S. Kung;S. K. Chanda
安非他明和儿茶酚胺在周围交感神经系统和大脑中的相互作用已被广泛研究。据报道，安非他明在受体位点模仿儿茶酚胺1 - 3，抑制单胺氧化酶4，破坏儿茶酚胺的再摄取机制5，并直接将儿茶酚胺释放到突触间隙6。虽然现有文献的共识表明，d-安非他明通过增加儿茶酚胺的释放和阻断儿茶酚胺的再摄取间接刺激儿茶酚胺突触后受体7,8，但多巴胺、去甲肾上腺素或两者对d-安非他明的中枢作用是否重要的问题仍有争议7,8。最近，α-肾上腺素能9，β-肾上腺素能10 - 13和多巴胺能14,15受体在脑组织中通过测量放射性标记配体与特定受体位点的结合已成功鉴定。这些方法的可用性使得研究急性和慢性精神药物对脑组织突触后儿茶酚胺能受体的影响成为可能13,16。我们报告了急性和慢性服用d-安非他明对大鼠脑突触后β-肾上腺素能受体的影响。
THE interactions of amphetamines and catecholamines in the peripheral sympathetic nervous system and in the brain have been widely studied. Amphetamines have been reported to mimic catecholamines at their receptor sites1–3, inhibit monoamine oxidase4, impair reuptake mechanism for the catecholamines5 and to directly release catecholamines into the synaptic cleft6. Although the consensus of the available literature indicates that d-amphetamine indirectly stimulates catecholamine postsynaptic receptors by increasing the release and blocking the reuptake of catecholamines7,8, the question whether dopamine, noradrenaline or both, are of importance for the central actions of d-amphetamine is controversial7,8. Recently, α-adrenergic9, β-adrenergic10–13 and dopaminergic14,15 receptors in brain tissue have been successfully identified by measuring the binding of radiolabelled ligands to specific receptor sites. Availability of such methods has permitted the examination of the effects of acute and chronic administration of psychotropic drugs on the postsynaptic catecholaminergic receptors in brain tissue13,16. We report here the effects of acute and chronic administration of d-amphetamine on the postsynaptic β-adrenergic receptors in rat brain.