Chronic morphine treatment increases the expression of vesicular glutamate transporter 1 in the mouse spinal cord.
Chronic morphine treatment increases the expression of vesicular glutamate transporter 1 in the mouse spinal cord.
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DOI：
10.1016/j.ejphar.2006.01.033
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发表时间：
2006-03
影响因子：
5
通讯作者：
Masami Suzuki;M. Narita;Michiko Narita;Tsutomu Suzuki
中科院分区：
文献类型：
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作者：
Masami Suzuki;M. Narita;Michiko Narita;Tsutomu Suzuki
长期暴露于吗啡导致对吗啡诱导的抗痛觉耐受性。本研究发现，吗啡耐受小鼠囊泡谷氨酸转运蛋白1和突触囊泡特异性小G蛋白Rab3A的蛋白水平显著升高，但囊泡谷氨酸转运蛋白2和囊泡γ-氨基丁酸转运蛋白水平无显著升高。这些发现表明，反复使用吗啡可以增强脊髓中的兴奋性突触传递，进而抑制吗啡诱导的抗痛觉作用。
Long-term exposure to morphine results in tolerance to morphine-induced antinociception. Here, we found that mice tolerant to morphine exhibited the significant increase in the protein levels of the vesicular glutamate transporter 1 and the synaptic vesicle-specific small G protein Rab3A, but not vesicular glutamate transporter 2 and vesicular γ-aminobutyric acid transporter. These findings suggest that repeated treatment with morphine enhances excitatory synaptic transmission in the spinal cord, and in turn suppresses the morphine-induced antinociception.