Pentylentetrazole-induced loss of blood-brain barrier integrity involves excess nitric oxide generation by neuronal nitric oxide synthase.
作者： Sonoko Danjo , Yasuhiro Ishihara , Masatomo Watanabe , Yu Nakamura , Kouichi Itoh
DOI: 10.1016/J.BRAINRES.2013.06.043
关键词: Cerebral cortex 、 Hippocampus 、 Chemistry 、 Neuroscience 、 Pharmacology 、 NMDA receptor 、 gamma-Aminobutyric acid 、 AMPA receptor 、 Glutamatergic 、 Blood–brain barrier 、 Nitric oxide
摘要: Dysfunction of the blood–brain barrier (BBB) is one major pathophysiological consequences epilepsy. The increase in permeability caused by BBB failure thought to contribute development epileptic outcomes. We developed a method which can be demonstrated gadolinium-enhanced T1 weighted imaging (GdET1WI). present study examined changes mice with generalized convulsive seizures (GCS) induced acute pentylentetrazole (PTZ) injection. At 15 min after PTZ-induced GCS, temporarily leaks BBB-impermeable contrast agent into parenchyma diencephalon, hippocampus and cerebral cortex mice, loss integrity was gradually recovered 24 h. temporary critical link glutamatergic activities that occur following injection PTZ. PTZ activates pathway via NMDA receptor, then nitric oxide (NO) generated receptor-coupled neuronal NO synthase (nNOS). To examine influence nNOS-derived on increases permeability,
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