Project/Area Number |
11671510
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | Miyazaki Medical College |
Principal Investigator |
KASABA Toshiharu Miyazaki Medical College, Department of Anesthesiology, Associate Professor, 医学部, 助教授 (80145599)
|
Co-Investigator(Kenkyū-buntansha) |
ONIZUKA Shin Miyazaki Medical College, Department of Anesthesiology, Instructor, 医学部, 助手 (20264393)
HAMAKAWA Toshiro Miyazaki Medical College, Department of Anesthesiology, Assistant Professor, 医学部, 講師 (50253836)
成尾 浩明 宮崎医科大学, 医学部, 助手 (10274797)
|
Project Period (FY) |
1999 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | Lymnaea stagnalis / Respiration / Volatile anesthetics / Sevoflurane / calcium concentration / Lymnaea stagnalils / シナプス |
Research Abstract |
The cellular and synaptic mechanisms by which general anesthetics affect cell-cell communications in the nervous system remain poorly defined. Inhibitory synapses were reconstructed in cell culture, between the somata of two functionally well-characterized neurons, right pedal 1 (RPeD1) and visceral dorsal 4 (VD4). Clinically relevant concentrations of sevoflurane (1-4%) were tested for their effects on synaptic transmission and the intrinsic membrane properties of soma-soma paired cells. RPeD1-induced inhibitory postosynaptic potentials in VD4 were completely and reversibly blocked by sevoflurane (4%). Sevoflurane also suppressed action potentials in both RPeD1 and VD4 cells. To clear the mechanism in [Ca^<2+>]i produced by clinically relevant concentration of volatile anesthetics, we measured [Ca^<2+>]i and intracellular recording simultaneously using a cultured neuron of Lymnaea stagnalis. The RPeD1 neurons were dissected from snails. Anesthetic-induced change in [Ca^<2+>]i were measured with fura-2 fluorescence spectroscopy. The concentration of 1% and 4% were evaluated. To neglect the action potential, we hyperpolarized the membrane potential 10mV and the same measurements were repeated. Sevoflurane 1% increased [Ca^<2+>]i from 325±7 (nM±SD) to 350±8, with the increasing of the number of action potentials to 30±12 (/min±SD) in RPeD1 neurons. Sevoflurane 4%, first increased [Ca^<2+>]i from 330±41 to 380±35 with the increasing to 50±5, in which [Ca^<2+>]i decreased gradually and the number of action potentials decreased to 0 rapidly. Sevoflurane, without activation, increase [Ca2+]i from 320±32 to 332±32 in 1%, and no change from 332±19 to 341±17 in 4%. We concluded that low concentration of sevoflurane increase [Ca^<2+>]i both with and without the activation of the RPeD1 neuron of Lymnaea stagnalis, while high concentration of sevoflurane d [Ca^<2+>]i from the increasing level.
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