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Original Article

The role of glutamate transporter-1 in the acquisition of brain ischaemic tolerance in rats induced by electro-acupuncture pre-treatment

, , , , , , , & show all
Pages 396-402 | Received 17 May 2013, Accepted 18 Feb 2014, Published online: 11 Feb 2015
 

Abstract

Objective: To investigate whether electro-acupuncture can serve as a method of inducing brain ischaemic tolerance (BIT) by encouraging the expression of glutamate transporter-1 (GLT-1) and suppressing the release of glutamate (Glu).

Methods: Sprague-Dawley (SD) rats were divided into sham, ischaemia and EA groups. EA was performed on dazhui and baihui acupoints and the rat cerebral ischaemia model was achieved by occluding the middle cerebral artery (MCA) for 2 hours, followed by reperfusion. Dialysate was collected from the striatum in vivo to detect the concentration of Glu and the expression of Glutamate Transporter-1 (GLT-1) was examined. The changes of neurological deficit scores were evaluated at 24 hours after reperfusion, while the infarct volumes of brains were then measured with 2,3,5-triphenyltetrazolium chloride (TTC) staining.

Results: Compared with the ischaemia group, the concentration of Glu decreased and the expression of GLT-1 increased at most of the detective time points in the EA group; the neurological deficit scores were lower and the infarct volumes were smaller in the EA group.

Conclusion: EA can up-regulate the expression of GLT-1 and inhibit the excessive release of Glu in the striatum in the process of subsequent ischaemic-reperfusion brain injury, which may be one of the mechanisms of inducing BIT and, thus, be neuroprotective for early ischaemic brain injury.

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Erratum

Declaration of interest

The present study was supported by the Chinese National Nature Science Foundation (81472150; 81472151) and 12th Five-year Plan supporting project of Ministry of Science and Technology of the People’s Republic of China (NO: 2013BAI10B03). The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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