期刊
JOURNAL OF NEUROSCIENCE
卷 27, 期 25, 页码 6823-6831出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0013-07.2007
关键词
methamphetamine; VGLUT1; basal ganglia; striatum; substantia nigra; glutamate
资金
- NIDA NIH HHS [DA07606, R01 DA007606] Funding Source: Medline
The vesicular glutamate ( GLU) transporter ( VGLUT1) is a critical component of glutamatergic neurons that regulates GLU release. Despite the likely role of GLU release in drug abuse pathology, there is no information that links VGLUT1 with drugs of abuse. This study provides the first evidence that methamphetamine ( METH) alters the dynamic regulation of striatal VGLUT1 function and expression through a polysynaptic pathway. METHincreases corticalVGLUT1mRNA, striatalVGLUT1protein in subcellular fractions, and theVmax of striatal vesicular GLU uptake. METH also increases glyceraldehyde- 3- phosphate dehydrogenase ( GAPDH) protein in the crude vesicle fraction. METH- induced increases in cortical VGLUT1 mRNA, as well as striatal VGLUT1 and GAPDH, are GABA(A) receptor- dependent because they are blocked by GABA(A) receptor antagonism in the substantia nigra. These results show that VGLUT1 can be dynamically regulated via a polysynaptic pathway to facilitate vesicular accumulation of GLU for subsequent release after METH.
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