ID 113066
Title Alternative
Triphenyltin and intra-axonal Ca2+ mobilization
Author
Noma, Kazuki Kumamoto University
Kurauchi, Yuki Kumamoto University
Katsuki, Hiroshi Kumamoto University
Akaike, Norio Kumamoto University|Kumamoto Kinoh Hospital|Kitamoto Hospital
Keywords
Triphenyltin
Glycinergic spontaneous transmission
Intra-axonal Ca stores
Synaptic button preparation
Content Type
Journal Article
Description
Triphenyltin (TPT) is an organotin compound causing environmental hazard to many wild creatures. Our previous findings show that TPT increases of the frequency of spontaneous glycinergic inhibitory postsynaptic currents (sIPSCs) in rat spinal neurons without changing the amplitude and 1/e decay time. In our study, the effects of 2-aminoethoxydiphenyl borate (2-APB), dantrolene sodium, and thapsigargin on sIPSC frequency were examined to reveal the contribution of intra-axonal Ca2+ mobilization by adding TPT. 2-APB considerably attenuated the TPT-induced facilitation of sIPSC frequency while dantrolene almost completely masked the TPT effects, suggesting that the TPT-induced synaptic facilitation results from the activation of both IP3 and ryanodine receptors on endoplasmic reticulum (ER) membrane, though inositol triphosphate (IP3) receptor is less sensitive to TPT. Thapsigargin itself significantly increased the sIPSC frequency without affecting the current amplitude and decay time. Successive addition of TPT could not further increase the sIPSC frequency in the presence of thapsigargin, indicating that thapsigargin completely masked the facilitatory action of TPT. Results suggest that TPT activates the IP3 and ryanodine receptors while TPT inhibits the Ca2+-pump of ER membranes, resulting in the elevation of intra-axonal Ca2+ levels, leading to the increase of spontaneous glycine release from synaptic vesicles.
Journal Title
Toxicology in Vitro
ISSN
08872333
NCID
AA10678594
AA11540107
Publisher
Elsevier
Volume
55
Start Page
11
End Page
14
Published Date
2018-11-12
Remark
論文本文は2019-11-12以降公開予定
Rights
© 2018. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
language
eng
TextVersion
その他
departments
Bioscience and Bioindustry