Glucose/Oxygen Deprivation Induces Release of [3H]5-hydroxytryptamine Associated with Synapsin 1 Expression in Rat Hippocampal Slices

• 영문명: Glucose/Oxygen Deprivation Induces Release of [³H]5-hydroxytryptamine Associated with Synapsin 1 Expression in Rat Hippocampal Slices
• 발행기관: 대한생리학회-대한약리학회
• 저자명: EunMi Park Sang Hui Chu KyungEun Lee
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제4권 제5호, 347~353쪽, 전체 7쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2000.01.01

영문 초록

It has been well documented that a massive release of not only glutamate but also other neurotransmitters may modulate the final responses of nerve cells to the ischemic neuronal injury. But there is no information regarding whether the release of monoamines is directly associated with synaptic vesicular proteins under ischemia. In the present study, it was investigated whether synapsin 1, syntaxin and SNAP-25 are involved in the release of 5-hydroxytryptamine ([³H]5-HT) in glucose/oxygen deprived (GOD) rat hippocampal slices. And, the effect of NMDA receptor using DL-2-amino-5-phosphonovaleric acid (APV) on ischemia- induced release of 5-HT and the changes of the above proteins were also investigated. GOD for 20 minutes enhanced release of [³H]5-HT, which was in part blocked by the NMDA receptor antagonist, APV. The augmented expression of synapsin 1 during GOD for 20 minutes, which was also in part prevented by APV. In contrast, the expression of syntaxin and SNAP-25 were not altered during GOD. These results suggest that ischemic insult induces release of [³H]5-HT associated with synapsin 1, synaptic vesicular protein, via activation of NMDA receptor in part.

키워드

Hippocampal slices Glucose/oxygen deprivation 5-Hydroxytryptamine Synapsin Syntaxin SNAP-25