Upregulation of Striatal Metabotropic Glutamate Receptor Subtype 1 (mGluR1) in Rats with Excessive Glutamate Release Induced by N-Acetylcysteine

Author(s):  
Tomoteru Yamasaki ◽  
Maki Okada ◽  
Atsuto Hiraishi ◽  
Wakana Mori ◽  
Yiding Zhang ◽  
...  
2018 ◽  
Vol 17 ◽  
pp. 153601211878863 ◽  
Author(s):  
Lauren Kosten ◽  
Jeroen Verhaeghe ◽  
Leonie wyffels ◽  
Sigrid Stroobants ◽  
Steven Staelens

Detecting changes in metabotropic glutamate receptor 5 (mGluR5) availability through molecular imaging with the positron emission tomography (PET) tracer [11C]ABP688 is valuable for studying dysfunctional glutamate transmission associated with neuropsychiatric disorders. Using an infusion protocol in rats, we visualized the acute effect of subanesthetic doses of ketamine on mGluR5 in rat brain. Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist known to increase glutamate release. Imaging was performed with a high-affinity PET ligand [11C]ABP688, a negative allosteric modulator of mGluR5. Binding did not change significantly from baseline to ketamine in any region, thereby confirming previous literature with other NMDA receptor antagonists in rodents. Hence, in rats, we could not reproduce the findings in a human setup showing significant decreases in the [11C]ABP688 binding after a ketamine bolus followed by ketamine infusion. Species differences may have contributed to the different findings in the present study of rats. In conclusion, we could not confirm in rats that endogenous glutamate increases by ketamine infusion are reflected in [11C]ABP688 binding decreases as was previously shown for humans.


2018 ◽  
Vol 19 (8) ◽  
pp. 907-915 ◽  
Author(s):  
Jaya Kumar ◽  
Zalina Ismail ◽  
Nurul Hazwani Hatta ◽  
Najwa Baharuddin ◽  
Hermizi Hapidin ◽  
...  

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