Cocaine, in contrast to D-amphetamine, does not cause axonal terminal degeneration in neostriatum and agranular frontal cortex of Long-Evans rats.
Cocaine, in contrast to D-amphetamine, does not cause axonal terminal degeneration in neostriatum and agranular frontal cortex of Long-Evans rats.
复制标题
与 D-苯丙胺相比，可卡因不会引起 Long-Evans 大鼠新纹状体和无颗粒额叶皮层的轴突变性。
DOI：
10.1016/0024-3205(88)90307-4
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发表时间：
1988
期刊：
影响因子：
6.1
通讯作者：
Groves,PM
中科院分区：
文献类型：
--
作者：
Ryan,LJ;Martone,ME;Linder,JC;Groves,PM
Continuous three day administration via implanted minipumps of cocaine hydrochloride (50–450 mg/kg/day, sc and 100–250 mg/kg/day, iv) did not produce axonal degeneration in frontal agranular cortex or neostriatum that was detectable by Fink-Heimer silver staining or tyrosine hydroxylase immunolabeling. This is in contrast to the extensive axonal degeneration detectable in these regions following d-amphetamine sulfate (10–60 mg/kg/day) administered following an identical protocol. Doses of cocaine and amphetamine were equated using three measures: 1) weight loss, 2) lethality and 3) behavioral activation. Thus, cocaine resembles other catecholamine reuptake blockers and does not cause the neurodegenerative changes characteristic of other abused drugs that interact with the brain's dopamine systems.
