J Korean Neurol Assoc > Volume 14(1); 1996 > Article
Journal of the Korean Neurological Association 1996;14(1): 238-250.
백서 대뇌 피질에서 glutamate 자극에 의한 [3H]norepinephrine의 유리 기전
신병수, 송대원, 이상효, 서만욱, 김영현, 김기원*
전북대학교 의과대학 신졍과학교실 및 의과학연구소, 전북대학교 의과대학 약리학교실 및 의과연구소*
The Mechanism on the Glutamate-evoked Release of [3H) norepinephrine in Rat Cortex Slices
Byoung Soo Shin, M,D., Dae Won Song, M.D., Sang Hyo Lee, M.D., Man Wook Seo, M. D., Young Hyun Kim*, M.D.
Department of Neurology, College of Medicine, Institute for Medical Sciences Chonbuk National University
Abstract
Glutamate Is the predominant excitatory neurotransmitter in the mammalian CNS. To elucidate the influence of glutamate on the noradrenergic neurotransmission in rat cortex, we examined the effects of agents that act in several steps of neurotransmission on [3H]norepinephrine ([3H])NE) release evoked by glutamate. Glutamate (1 mM) evoked significant release of [3H]NE from rat cortex slices in the absence of Mg2+in the incubation media. This effect was attenuated by cromakalime (10 nM) and lemakalime (10 nM) , and the inhibitory effect of cromakalime was abolished by glipizide. Inhibitory effect of muscimol (30 uM) and baclofen (3 uM, 30 uM) was antagonized by biccuculine (3 uM), respectively. Nipecotic acid(10 uM), DABA(300 uM), and β-alanine(100 uM) attenuated the glutamate-induced release of [3H]NE. Dihydrokinate (300 uM) PDC (100 nM) increased the glutamate-induced release of [3H]NE. Ifenprodile (10 nM) and arcaine (1 uN), blockers of polyamine site, attenuated the release of ("H)NE. The stimulatory effect of spermine was abolished by arcaine. CPA(100 nM) and CPCA(100 nM), EHNA(30 uN) and NBTI(1 uN) attenuated the release of ("H)NE. Verapamil(S uN), nitredipine(10 uN), u- conotoxin (100 nM) and flunarizine (5 uM) attenuated the release of (3H)NE. Dantrolene(30 uM), KT-362(3 uM), and ryanodine(10 nM), attenuated the glutamate-induced release of [3H]NE. Glycine (10 uM) increased the release of [3H]NE. DCQX (30 uN) attenuated the release of [3H]NE. These results suggest that glutamate-evoked release of norepinephrine can be modulated by GABAergic, adenosinergic neurotransmitters, and by various drugs which modulate ion channel activities in rat cortex. Key Words ; glutamate, norepinephrine, cerebral cortex
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