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新生期谷氨酸钠及衰老对吗啡依赖形成的影响。

Effects of neonatal monosodium glutamate and aging on morphine dependence development.

作者信息

Koyuncuoğlu H, Aricioğlu F, Dizdar Y

机构信息

Istanbul Medical Faculty, Department of Pharmacology, Capa, Turkey.

出版信息

Pharmacol Biochem Behav. 1992 Oct;43(2):341-5. doi: 10.1016/0091-3057(92)90160-h.

DOI:10.1016/0091-3057(92)90160-h
PMID:1438475
Abstract

Administration of monosodium glutamate (MSG) to neonatal rats has been reported to destroy aspartatergic (ASPergic) and glutamatergic (GLUergic) neurons. Ageing has been shown to induce cell loss, a rather general CNS atrophy, and slowness in the CNS functions. On the other hand, it has been hypothesized that two of the main reasons for opiate dependence development are the blockade by opiates of the NMDA receptors and their associated upregulation and supersensitivity. Accordingly, the abstinence syndrome precipitating effect of naloxone (NL) has been assumed to be the consequences of the removal by NL of opiate from NMDA receptors without being able to prevent upregulated and supersensitive NMDA receptors from being stimulated stronger than normal. To investigate the role of the decrease in the number of NMDA receptors in the development of morphine (M) physical dependence, 4 g/kg MSG was SC injected into neonatal rats on days 2, 4, 6, 8 and 10 after birth. Their littermate controls SC received equimolar NaCl solution. Three or 14 months later, three pellets containing 75 mg base M were SC implanted into male rats treated neonatally with MSG or equimolar NaCl solution. Seventy-two hours after pellet implantation, all rats were injected with 2 mg/kg NL intraperitoneally. Some abstinence syndrome signs were counted or rated for 15 min immediately after NL injection and then statistically evaluated. The NL-precipitated abstinence syndrome was less intense in 3-month-old MSG-treated rats than in controls, most probably due to the decrease in the number of NMDA receptors in MSG-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

据报道,给新生大鼠注射味精(MSG)会破坏天冬氨酸能(ASPergic)和谷氨酸能(GLUergic)神经元。衰老已被证明会导致细胞丢失、相当普遍的中枢神经系统萎缩以及中枢神经系统功能迟缓。另一方面,有人提出阿片类药物依赖发展的两个主要原因是阿片类药物对NMDA受体的阻断及其相关的上调和超敏反应。因此,纳洛酮(NL)诱发戒断综合征的作用被认为是由于NL将阿片类药物从NMDA受体上移除,却无法阻止上调和超敏的NMDA受体受到比正常情况更强的刺激。为了研究NMDA受体数量减少在吗啡(M)身体依赖性发展中的作用,在新生大鼠出生后的第2、4、6、8和10天,皮下注射4 g/kg的味精。它们同窝的对照大鼠皮下注射等摩尔的NaCl溶液。3个月或14个月后,将含有75 mg碱基M的三个药 pellet 皮下植入新生时用味精或等摩尔NaCl溶液处理过的雄性大鼠体内。药 pellet 植入72小时后,所有大鼠腹腔注射2 mg/kg的NL。在NL注射后立即计数或评估15分钟内的一些戒断综合征体征,然后进行统计学分析。3个月大的经味精处理的大鼠中,NL诱发的戒断综合征比对照组轻,这很可能是由于经味精处理的大鼠中NMDA受体数量减少所致。(摘要截断于250字)

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