作者: Takako Takemiya , Kanato Yamagata
DOI: 10.3390/IJMS14048345
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摘要: Neurons interact closely with astrocytes via glutamate; this neuron-glia circuit may play a pivotal role in synaptic transmission. On the other hand, contact vascular endothelial cells their end-feet. It is becoming obvious that non-neuronal critical regulating neuronal activity brain. We find kainic acid (KA) administration induces expression of microsomal prostaglandin E synthase-1 (mPGES-1) venous and E2 (PGE2) receptor (EP)-3 on astrocytes. Endothelial mPGES-1 exacerbates KA-induced damage vivo experiments. In vitro experiments, produces PGE2, which enhances astrocytic Ca2+ levels EP3 increases Ca2+-dependent glutamate release, thus aggravating injury. This novel endothelium-astrocyte-neuron signaling pathway be crucial for driving after repetitive seizures could new therapeutic target epilepsy brain disorders.