Effect of lidocaine on intracellular calcium dynamics of superiol cervical garglia

2003 Fiscal Year Final Research Report Summary

• Project/Area Number: 13671975
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: 病態科学系歯学(含放射線系歯学)
• Research Institution: Iwate Medical University
• Principal Investigator: JOH Shigeharu Iwate Medical University, School of Dentistry, Professor, 歯学部, 教授 (20154411)
• Co-Investigator(Kenkyū-buntansha): SHINOHE Yutaka Iwate Medical University, School of Dentistry, Research Associate, 歯学部, 助手 (30347885) ; SATO Kenichi Iwate Medical University, School of Dentistry, Lecturer, 歯学部, 講師 (90265174) ; SATO Masahito Iwate Medical University, School of Dentistry, Associate Professor, 歯学部, 助教授 (60215845)
• Project Period (FY): 2001 – 2003
• Keywords: Superior ceryical ganglia / sciatic nerve / Intracellular calcium / Canfocal microscopy

Research Abstract

Adenosine-5'-triphosphate (ATP) which is released from neuronal and non-neuronal tissues interacts with cell surface receptors to produce a broad range of physiological responses. The present study addressed the issue of whether the cells of the superior cervical ganglia (SCG) respond to ATP. To this end, the dynamics. of the intracellular calcium ion concentration ([Ca^<2+>]_i) of neurons and satellite cells in intact SCG was analyzed by laser scanning confocal microscopy. ATP produced an increase of [Ca^<2+>]_i in both neurons and satellite cells; initially, ATP elicited increase in satellite cells, subsequently, a [Ca^<2+>]_i change in neurons was observed. P1 purinoceptor agonists had no effect on this process, but P2 purinoceptor agonists induced [Ca^<2+>]_i increase and suramin totally inhibited ATP-induced [Ca^<2+>]_i dynamics in both neurons and satellite cells.
In satellite cells, Ca^<2+> blockers and the removal of extracellular Ca, but not thapsigargin-pretreatment, abolished ATP-induced [Ca^<2+>]_i dynamics. In contrast, thapsigargin-pretreatment abolished ATP-induced [Ca^<2+>]_i dynamics in neurons. Reactive blue-2 inhibited the ATP-induced reaction on neurons alone. Uridine-5'-triphosphate caused a [Ca^<2+>]_i increase in neurons and α,β-methylene ATP caused a [Ca^<2+>]_i increase in satellite cells.
We concluded that neurons respond to extracellular ATP mainly via P2Y purinoceptors and that satellite cells respond via P2X purinoceptors.
ATP induced a [Ca^<2+>]_i increase of perineurial cells. Ca2+ channel blockers and removing of extracellular Ca2+, but not thapsigargin pretreatment, abolished ATP-induced [Ca2+]i dynamics. This indicated that the [Ca2+]i increase was due to an influx of extracellular Ca2+. Adenosine-5'-diphosphate also elicited an increase of [Ca2+]i, but P1 receptor agonists had few effects on [Ca2+]i dynamics. Suramin totally inhibited ATP-induced [Ca2+]i dynamics, but reactive blue 2 did not. Uridine-5'-triphosphate induced no significant change in [Ca2+]i, but alpha, beta-methylene ATP caused a [Ca2+]i increase. In conclusion, perineurial cells respond to extracellular ATP mainly via P2X receptors.