• Top page
  • Timetable
  • Per session
  • Per presentation
  • How to
  • Meeting Planner



Parkinson's Disease and Related Disorders

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Mechanism of nicotine for induction of tremor

  • P3-301
  • 清水 佐紀 / Saki Shimizu:1 國澤 直史 / Naofumi Kunisawa:1 水口 裕登 / Yuto Mizuguchi:1 奥村 貴裕 / Takahiro Okumura:1 徳留 健太郎 / Kentaro Tokudome:1 大高 美幸 / Miyuki Ohtaka:1 近持 壽郎 / Hisao Chikamochi:1 高久保 佑一 / Yuichi Takakubo:1 芹川 忠夫 / Tadao Serikawa:1 大野 行弘 / Yukihiro Ohno:1 
  • 1:大阪薬大・薬・薬品作用解析 / Lab Pharmacol, Osaka Univ Pharm Sci, Osaka, Japan 

Nicotine affects various biological processes including psycho-emotional, autonomic and motor functions, and elicits movement/motor disorders such as tremor and convulsions. However, the mechanisms of nicotine-induced movement/motor disorders are not fully understood. Here, we conducted behavioral and pharmacology studies to clarify the mechanisms of nicotine-induced tremor. Male ddY mice were treated with nicotine (0.5-4 mg/kg, i.p.) and nicotine-induced motor symptoms was evaluated using 6-ranked scores (0: no effect, 1: mild head- and/or tail-tremors and straub tail, 2: intensive tremors including body trunk, 3: any combination of severe tremors and wild running and loss of righting response, 4: clonic seizure, 5: tonic seizure). In addition, brain samples of mice were obtained 2 hours after the nicotine injection and subjected to Fos-immunohistochemistry. Electrical lesion studies were also performed. Nicotine elicited straub tail and tremor at low doses (0.5-2 mg/kg), and wild-running, clonic and/or tonic-clonic seizures at higher doses (3-4 mg/kg). Tremorgenic dose (1 mg/kg) of nicotine significantly and region-specifically elevated Fos expression in the piriform cortex (Pir), medial habenular nucleus (MHb), inferior olive (IO) and solitary nucleus (Sol). Nicotine-induced tremor was significantly suppressed by the non-selective nicotinic acetylcholine (nACh) antagonist mecamylamine and the α7 nACh antagonist methyllycaconitine, but was unaffected by the α4 nACh antagonist dihydro-β-erythroidine. In addition, nicotine-elevated Fos expression in above brain regions were inhibited by mecamylamine and methyllycaconitine whereas dihydro-β-erythroidine failed to reverse the Fos expression in the Pir and IO. Furthermore, electrical lesioning of IO regions in rats significantly inhibited nicotine-induced tremor. These results suggest that tremor induction by nicotine is brought about by neural excitation of IO mediated by α7 nACh receptors.

Copyright © Neuroscience2014. All Right Reserved.