• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Effect of volatile anesthetics on Cultured Neuron of Lymnaea stagnalis

Research Project

Project/Area Number 11671510
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Anesthesiology/Resuscitation studies
Research InstitutionMiyazaki 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)
KeywordsLymnaea 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.

Report

(3 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report

URL: 

Published: 1999-04-01   Modified: 2016-04-21  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi