Department of Physiology & Pharmacology, Oregon Health & Science University, Portland, Oregon, USA.
Synapse. 2010 Jun;64(6):445-8. doi: 10.1002/syn.20749.
A single injection of cocaine increases extracellular glutamate in the rat dorsolateral striatum 1 day after the acute cocaine was administered (McKee and Meshul, 2005). However, the nuclei that facilitate this increase in striatal glutamate remain unknown. We hypothesized that the cocaine-induced increase in striatal glutamate was produced by activation of the ventromedial (VM) nucleus of the thalamus via the thalamo-corticostriatal or thalamostriatal pathways. First, rats received an electrolytic lesion of the VM. One day after a single cocaine or vehicle injection, extracellular glutamate was measured in the dorsolateral striatum using in vivo microdialysis. The motor thalamus lesion blocked the cocaine-induced increase in striatal glutamate and reduced extracellular glutamate to the level of the vehicle-treated group. This study shows a critical role for the VM nucleus of the thalamus in mediating the effects of cocaine on extracellular glutamate levels in the rat dorsolateral striatum.
单次注射可卡因可在急性可卡因给药后 1 天增加大鼠背外侧纹状体中的细胞外谷氨酸（McKee 和 Meshul，2005）。然而，促进纹状体谷氨酸增加的核仍不清楚。我们假设，通过丘脑皮质纹状体或丘脑纹状体通路，可卡因诱导的纹状体谷氨酸增加是由腹内侧（VM）核的激活产生的。首先，大鼠接受 VM 的电解损伤。单次可卡因或载体注射后 1 天，使用活体微透析测量背外侧纹状体中的细胞外谷氨酸。运动丘脑损伤阻断了可卡因引起的纹状体谷氨酸增加，并将细胞外谷氨酸降低至载体处理组的水平。这项研究表明，丘脑的 VM 核在介导可卡因对大鼠背外侧纹状体细胞外谷氨酸水平的影响方面起着关键作用。
