Rodriguez J, Jacques-Berg W, Patel A J
MRC Collaborative Centre, National Institute for Medical Research, The Ridgeway, London, UK.
Neuroreport. 1991 Sep;2(9):517-20. doi: 10.1097/00001756-199109000-00005.
Stimulation of the quisqualate (QA) subtype of glutamate receptor increased the expression of phosphate activated glutaminase (needed for neurotransmitter glutamate synthesis) and the ability to release neurotransmitter glutamate in cultures of glutamatergic cerebellar granule neurons. In contrast, QA had no significant effects on the lactate dehydrogenase activity and amount of protein. The QA-mediated elevation in glutaminase activity was blocked by the ionotropic QA receptor antagonist CNQX and mimicked by the ionotropic QA receptor agonist AMPA, but not by the metatropic QA receptor agonist t-ACPD. The increase in Ca2+ influx essentially through activation of L-type channels, and not the mobilization of internal Ca2+ stores, was responsible for these QA receptor-mediated long-term changes in cerebellar granule neurons.
刺激谷氨酸受体的quisqualate(QA)亚型可增加磷酸激活谷氨酰胺酶(神经递质谷氨酸合成所需)的表达以及在谷氨酸能小脑颗粒神经元培养物中释放神经递质谷氨酸的能力。相比之下,QA对乳酸脱氢酶活性和蛋白量没有显著影响。QA介导的谷氨酰胺酶活性升高被离子型QA受体拮抗剂CNQX阻断,并被离子型QA受体激动剂AMPA模拟,但代谢型QA受体激动剂反式-ACPD则不能模拟。这些QA受体介导的小脑颗粒神经元的长期变化是由主要通过L型通道激活导致的Ca2+内流增加引起的,而非细胞内Ca2+储存的动员。