期刊
NEUROBIOLOGY OF DISEASE
卷 43, 期 3, 页码 588-597出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2011.05.007
关键词
Lithium-pilocarpine; GLUT1; GLUT3; MCT1; MCT2; In situ hybridization; Immunohistochemistry; Development; Temporal lobe epilepsy
资金
- Institut National de la Sante et de la Recherche Medicale
- Fondation pour la Recherche Medicale
- UNESCO
- NIH [HD30704, NS41405]
- Fonds National de la Recherche Suisse [31003A-125063]
- Swiss National Science Foundation (SNF) [31003A_125063] Funding Source: Swiss National Science Foundation (SNF)
The lithium-pilocarpine model mimics most features of human temporal lobe epilepsy. Following our prior studies of cerebral metabolic changes, here we explored the expression of transporters for glucose (GLUT1 and GLUT3) and monocarboxylates (Mal and MCT2) during and after status epilepticus (SE) induced by lithium-pilocarpine in PN10, PN21, and adult rats. In situ hybridization was used to study the expression of transporter mRNAs during the acute phase (1, 4, 12 and 24 h of SE), the latent phase, and the early and late chronic phases. During SE, GLUT1 expression was increased throughout the brain between 1 and 12 h of SE, more strongly in adult rats; GLUT3 increased only transiently, at 1 and 4 h of SE and mainly in PN10 rats; MCT1 was increased at all ages but 5-10-fold more in adult than in immature rats; MCT2 expression increased mainly in adult rats. At all ages, MCT1 and MCT2 up-regulation was limited to the circuit of seizures while GLUT1 and GLUT3 changes were more widespread. During the latent and chronic phases, the expression of nutrient transporters was normal in PN10 rats. In PN21 rats, GLUT1 was up-regulated in all brain regions. In contrast, in adult rats GLUT1 expression was down-regulated in the piriform cortex, hilus and CA1 as a result of extensive neuronal death. The changes in nutrient transporter expression reported here further support previous findings in other experimental models demonstrating rapid transcriptional responses to marked changes in cerebral energetic/glucose demand. (C) 2011 Elsevier Inc. All rights reserved.
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