Time-dependent changes in extracellular glutamate in the rat dorsolateral striatum following a single cocaine injection
Time-dependent changes in extracellular glutamate in the rat dorsolateral striatum following a single cocaine injection
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DOI：
10.1016/j.neuroscience.2005.02.020
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发表时间：
2005-01-01
期刊：
影响因子：
3.3
通讯作者：
Meshul, CK
中科院分区：
文献类型：
--
作者：
Mckee, NL;Meshul, CK
急性可卡因给药已被证明会改变背侧纹状体可塑性[Proc Natl Acad Sci USA 87 (1990) 6912； Brain Res Bull 30 (1993) 173]并产生长期的神经化学变化[Pharmacol Blochem Behav 27 (1987) 533]。迄今为止，急性可卡因对大鼠背外侧纹状体细胞外谷氨酸和神经末梢谷氨酸免疫标记的影响尚未见报道。为了研究可卡因诱导的细胞外谷氨酸变化，在接受单次注射载体或 15 mg/kg 可卡因后 1-14 天，在大鼠的背外侧纹状体中进行体内微透析。与对照组相比，在测量细胞外谷氨酸前一天注射可卡因的组中的细胞外谷氨酸含量有所增加。在微透析前三天注射可卡因的组细胞外谷氨酸水平降低。此外，在急性可卡因治疗后 14 天，细胞外谷氨酸仍然减弱。除钙后，可卡因治疗的大鼠纹状体谷氨酸减少，表明可卡因诱导的细胞外谷氨酸变化部分依赖于钙。使用免疫金电子显微镜测量经可卡因或媒介物急性治疗的相同大鼠的对侧纹状体中神经末梢谷氨酸免疫标记的密度。与对照组相比，在急性可卡因暴露后 1、2、3 或 14 天，所识别的产生不对称（兴奋性）突触接触的神经末梢内谷氨酸免疫标记的密度没有变化。因此，细胞外谷氨酸的这些变化并不是由突触小泡池内谷氨酸免疫标记的变化引起的。此外，在2小时前接受可卡因或在给予可卡因1周后停药的大鼠中，未发现谷氨酸免疫标记发生变化。结果表明，单次注射可卡因会在大鼠背外侧纹状体中产生细胞外谷氨酸的双相、时间依赖性变化。 (c) 2005 年由 Elsevier Ltd 代表 IBRO 出版。
Acute cocaine administration has been shown to alter dorsal striatal plasticity [Proc Natl Acad Sci USA 87 (1990) 6912; Brain Res Bull 30 (1993) 173] and produce long-term neurochemical changes [Pharmacol Blochem Behav 27 (1987) 533]. To date, the effects of acute cocaine on extracellular glutamate and nerve terminal glutamate immunolabeling in the rat dorsolateral striatum have not been reported. To investigate cocaine-induced changes in extracellular glutamate, in vivo microdialysis was carried out in the dorsolateral striatum of rats 1-14 days after receiving a single injection of either vehicle or 15 mg/kg cocaine. There was an increase in the group injected with cocaine I day prior to measuring extracellular glutamate as compared with the control group. The group injected with cocaine 3 days prior to the microdialysis session had decreased extracellular glutamate levels. Furthermore, extracellular glutamate remained attenuated 14 days after acute cocaine treatment. Striatal glutamate decreased in the cocaine-treated rats after calcium removal, suggesting that cocaine-induced changes in extracellular glutamate were partially calcium-dependent. The density of nerve terminal glutamate immunolabeling was measured using immunogold electron microscopy in the contralateral striatum of the same rats that had been acutely treated with cocaine or vehicle. There were no changes in the density of glutamate immunolabeling within identified nerve terminals making an asymmetrical (excitatory) synaptic contact 1, 2, 3, or 14 days after acute cocaine exposure as compared with the control groups. Hence, these alterations in extracellular glutamate did not result from changes in glutamate immunolabeling within the synaptic vesicle pool. In addition, no changes in glutamate immunolabeling were found in rats that received cocaine 2 h previously or were withdrawn after 1 week of cocaine administration. The results demonstrate that a single injection of cocaine produces biphasic, time-dependent changes in extracellular glutamate in the rat dorsolateral striatum. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.