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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.

DOI:10.1016/0306-3623(94)00171-i
PMID:7713372
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。

相似文献

1
Premorbid behaviors produced by cocaine, ethanol and cocaethylene in the mouse.可卡因、乙醇和可口卡因在小鼠中产生的病前行为。
Gen Pharmacol. 1995 Jan;26(1):99-106. doi: 10.1016/0306-3623(94)00171-i.
2
The lethal effects of ethanol and cocaine and their combination in mice: implications for cocaethylene formation.乙醇和可卡因及其组合对小鼠的致死作用:对古柯乙烯形成的影响。
Pharmacol Biochem Behav. 1995 Sep;52(1):245-8. doi: 10.1016/0091-3057(95)00098-h.
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Comparative behavioral pharmacology and toxicology of cocaine and its ethanol-derived metabolite, cocaine ethyl-ester (cocaethylene).可卡因及其乙醇衍生代谢物可卡因乙酯(可口卡因)的比较行为药理学与毒理学
Life Sci. 1992;50(18):1351-61. doi: 10.1016/0024-3205(92)90286-x.
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Cocaethylene-induced kindling of seizure effects: cross-specificity with cocaine.可卡因乙烯醚诱发的癫痫发作效应的点燃:与可卡因的交叉特异性。
Pharmacol Biochem Behav. 1996 Jun;54(2):491-4. doi: 10.1016/0091-3057(95)02275-9.
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Protective effects of buprenorphine against amplified cocaine and ethanol lethality in mice: role of cocaethylene.丁丙诺啡对小鼠可卡因和乙醇致死性增强的保护作用:可卡因乙烯酯的作用
J Toxicol Sci. 1996 May;21(2):143-56. doi: 10.2131/jts.21.2_143.
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Cocaethylene is more potent than cocaine in mediating lethality.在介导致死性方面,可卡乙碱比可卡因更具效力。
Pharmacol Biochem Behav. 1991 Jun;39(2):531-3. doi: 10.1016/0091-3057(91)90222-n.
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Assessment of cocaethylene lethality in Long-Evans female and male rats.评估可卡因乙烯酯对长 Evans 雌性和雄性大鼠的致死性。
Neurotoxicol Teratol. 1998 Jul-Aug;20(4):459-63. doi: 10.1016/s0892-0362(97)00132-3.
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Role of cocaethylene in toxic symptoms due to repeated subcutaneous cocaine administration modified by oral doses of ethanol.可卡因乙烯醚在口服乙醇改变重复皮下注射可卡因所致中毒症状中的作用。
J Toxicol Sci. 1999 Aug;24(3):227-35. doi: 10.2131/jts.24.3_227.
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Role of brain cocaethylene levels in combined cocaine-ethanol lethality in mice.脑内可卡因乙烯酯水平在小鼠可卡因 - 乙醇联合致死性中的作用。
Nihon Arukoru Yakubutsu Igakkai Zasshi. 1996 Feb;31(1):95-109.
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Cocaethylene-induced lethality in mice is potentiated by alcohol.酒精会增强可卡因乙烯酯对小鼠的致死性。
Alcohol. 1995 Jul-Aug;12(4):383-5. doi: 10.1016/0741-8329(95)00022-j.

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Repeated administration of cocaethylene induces context-dependent sensitization to its locomotor effects.
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