1996 Fiscal Year Final Research Report Summary
Mechanisms of halothane action on glycinergic inhibitory synaptic transmission
| Project/Area Number |
07671659
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Osaka University |
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Principal Investigator |
TAKENOSHITA Makoto Osaka University Medical School, Lecturer, 医学部, 講師 (00144486)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIYA Ikuto Osaka University Medical School, Professor, 医学部, 教授 (80028505)
SHIBATA Masahiko Osaka University Medical School, Assistant Professor, 医学部, 助手 (50216016)
KAWAGUCHI Tetsu Osaka University Medical School, Assistant Professor, 医学部, 助手 (70214616)
UEYAMA Hiroshi Osaka University Medical School, Assistant Professor, 医学部, 助手 (10243205)
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| Project Period (FY) |
1995 – 1996
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| Keywords | halothane / inhalation anesthetic / mechanism of anesthesia / synaptic transmission / inhibitory synapse / glycine |
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| Research Abstract |
Introduction : The action of general anesthetics on the inhibitory synaptic transmission is controversial, both augmentation and suppression are reported. This ambiguity is due to the existence of the excitatory synapse in the middle of the conventional experiment to get the inhibitory response. Now, using the thin slice preparation, monosynaptic inhibitory transmission is available, allowing the measurement of unambiguous action of general anesthetics.
Method : Thin slices from the spinal cord of neonatal rats were prepared2, superfused with a Ringer solution containing 2muM CNQX and 10^-muM bicuculline, bubbled with 95% O2 + 5% CO2. Whole cell recordings were made from motoneurons (voltage clamped at -70mV). Nearby interneurons identified visually were stimulated to evoke monosynaptic inhibitory responses in motoneurons. Halothane was dissolved in the superfusing saline through a vaporizer (dial setting 2%) and applied for 10 min.
Result : The IPSC (inhibitory Post Synaptic Current) was suppressed by "2%" halothane and recovered. The amplitude of IPSC was 55(]SY.+-。[)23% (n=15), 48(]SY.+-。[)16% (n=8) (mean(]SY.+-。[)SD) of the control after 5 min or 10 min application of halothane, respectively. In some cells (4 out of 15), IPSC was slightly augmented at an early stage (1-2min) of halothane application. Microperfusion of glycine induced an inward current. The amplitude and the duration of this glycine-induced current was enhanced by 2% halothane, and returned to the control value after wash-out.
Conclusion : The present study showed that halothane enhances the postsynaptic event in the glycinergic inhibitory transmission. But using exactly the same preparation, we reported that halothane suppressed the overall monosynaptic inhibitory transmission evoked by electrical stimulation of the presynapse. These results indicate that halothane's main site of action in the glycinergic inhibitory transmission is presynapse.
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