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Using three models of rats to analyse how vasopressin influences lactate production and it’s transporters in astrocytes under the condition of normoxia, hypoxia or reoxygenation, the authors proved that BDNF and iNOS/eNOS play an important role in supporting normal functions of neurons. Arginine vasopressin (AVP) can increase the expression of BDNF and iNOS/eNOS in astrocytes and NO can enhance the expression of monocarboxylate transporters (MCTs). Taken together, the authors show us that the expression of MCTs modulated by AVP may be regulated by NO through NF-kB. AVP attenuated the expression of MCTs in SHRSP/Izm and SHRpch1_18 astrocytes. AVP may influence post-ischemic neuronal recovery through this approach.


1. What’s the differences between SHRSP and SHR1-18?

2. What’s the function of MCT? And why did the authors choose MCT1 and MCT4?

3. How does the MCTs transport lactate from astrocytes to neurons?

4. How did the authors isolate the astrocyte from brain?

5. Why did the author choose 100nM AVP but not a more physiological concentration to treat astrocytes?

6. What’s the role of lactate in the physiology and pathophysiology of neuronal activity and what is the underlying mechanism?

7. How to control the hypoxia level at 1% O2 and what is the difference in its influence on cellular activity from that of physiologic levels  and 95% of O2?

8. What’s working mechanism in which the anti-epileptic drug valproate exerts seditive effect?




2017-12- 29 Literature Analysis

JKazuo Yamagata1*, Natsumi Takahashi1, Nozomi Akita1 and Toru Nabika2 . Arginine vasopressin altered the expression of monocarboxylate transporters in cultured astrocytes isolated from strokeprone spontaneously hypertensive rats and congenic SHRpch1_18 rats .Yamagata et al. Journal of Neuroinflammation (2017) 14:176 , Presented by Dongyang Li. Edited by Xiaoran Wang.

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