| Co-Investigator(Kenkyū-buntansha) |
OHKAWA Hirobumi University Hospital, Hirosaki University Instructor, 医学部・附属病院, 助手 (40322953)
MIHOKO Kudo School of Medicine, Hirosaki University Instructor, 医学部, 助手 (30003411)
KUSHIKATA Tetsuya University Hospital, Hirosaki University Instructor, 医学部・附属病院, 助手 (80250603)
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| Research Abstract |
[In Vitro] We used model of K^+-evoked neurotransmitter (noradrebaline [NA], dopamine and glutamate) release from rat brain slices to study effects of iv anesthetic agents on voltage sensitive Ca^<2+> channels (VSCCs). First, we found that the release is mediated mainly via P/Q-VSCCs. Second, iv anesthetic agents except ketamine significantly inhibit the release in a concentration dependent manner. Thus, these anesthetic agents may inhibit VSCC.However, bicuculline, a GABA_A receptor antagonist, reversed the inhibitory effects of iv anesthetic agents. Therefore, it is likely that activation of GABA_A receptors by these anesthetic agents may reduce VSCC activities.
[In Vivo] Using microdialysis method, we studied effects general anesthetic agents on NA release from several brain regions. We found that anesthetics inhibiting NMDA receptor increase NA release, whereas anesthetics activating GABA_A receptor reduce the release. Isoflurane that has both characters decreases the release in the cerebrocortex and increases in the preoptic area of anterior hypothalamus. As sleep-inducing NAergic neurons exist, increase in NA release by NMDA antagonist like anesthetics may contribute to activating sleep-inducing NAergic neurons. In contrast, decrease in NA release by GABA_A agonist like anesthetics may induces inhibition of wakefulness-inducing NAergic neurons.
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