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可卡因、乙醇和可口卡因在小鼠中产生的病前行为。

Premorbid behaviors produced by cocaine, ethanol and cocaethylene in the mouse.

作者信息

Meehan S M, Schechter M D

机构信息

Department of Pharmacology, Northeastern Ohio Universities, College of Medicine, Rootstown 44266-0095, USA.

出版信息

Gen Pharmacol. 1995 Jan;26(1):99-106. doi: 10.1016/0306-3623(94)00171-i.

Abstract
  1. The premorbid behaviors produced by the administration of cocaine, ethanol, their combination, as well as a metabolite produced by their co-administration, viz. cocaethylene, were defined, determined and quantified in the HS strain of mice. 2. The LD50 for ethanol was 9.71 g/kg in males and 9.45 g/kg in females, whereas the LD50 values in male and female mice for cocaine were 101.55 and 90.00 mg/kg, respectively. 3. The data indicate that clonic-tonic seizures continued into status epilepticus after cocaine administration and prior to cocaine-induced lethality. In contrast, administration of the cocaine-ethanol metabolite cocaethylene produced status epilepticus without producing clonic-tonic seizures yet still resulted in lethality. 4. Thus, both cocaine and cocaethylene may produce their lethal effects in mice through neuro-regulatory mechanisms mediating protracted seizure induction.
摘要
  1. 在HS品系小鼠中定义、确定并量化了给予可卡因、乙醇、它们的组合以及它们共同给药产生的一种代谢物(即可卡乙碱)所产生的病前行为。2. 乙醇对雄性小鼠的半数致死量为9.71 g/kg,对雌性小鼠为9.45 g/kg,而可卡因对雄性和雌性小鼠的半数致死量分别为101.55和90.00 mg/kg。3. 数据表明,在给予可卡因后且在可卡因诱导的致死性出现之前,阵挛 - 强直发作会持续发展为癫痫持续状态。相比之下,给予可卡因 - 乙醇代谢物可卡因乙碱会产生癫痫持续状态,但不会产生阵挛 - 强直发作,不过仍会导致死亡。4. 因此,可卡因和可卡因乙碱可能通过介导持续性癫痫发作诱导的神经调节机制在小鼠中产生致死作用。

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