オピオイドは,阻害性シナプスの長期的な増強を阻害します
Fereshteh S Nugent1, Esther C Penick, Julie A Kauer
1Brown University, Department of Molecular Pharmacology, Physiology and Biotechnology, Providence, Rhode Island 02912, USA.
Nature
|April 27, 2007
まとめ
研究者らは,脳のシナプス性可塑性の新しい形態を発見した.
科学分野:
- 神経科学は神経科学である.
- シナプスの可塑性
- 神経薬理学神経薬理学について
背景:
- シナプスの可塑性,シナプスの強さの変化が,学習と中毒の基礎となっている.
- 阻害性GABA (ガンマアミノバター酸) を放出するシナプスの可塑性はあまり理解されていません.
- ベントラル・テグメンタル領域は,薬物中毒の発達に極めて重要です.
研究 の 目的:
- ドーパミンニューロンへのGABA (((A)) 媒介のシナプス伝達 (LTP (((GABA)) の長期的な増強を調査する.
- この新しい形のシナプス可塑性の基礎となるメカニズムを探求する.
- モルヒネがLTPに及ぼす影響を調べるために (GABA).
主な方法:
- ネズミの脳断片における電気生理学的記録.
- NMDA受容体の活性化を必要とする研究されたヘテロシナプス性可塑性.
- 逆行シグナリング分子として窒素酸化物を利用した.
主要な成果:
- ドーパミンニューロンにLTP ((GABA) を同定した.
- LTP (GABA) は,NMDA受容体誘発の酸化窒素によって媒介されるヘテロシナプスであることが実証されました.
- モルヒンの暴露は,in vitroとin vivoの両方で,LTPを防ぐことが示されました.
結論:
- LTP ((GABA)) のオピオイド誘発性神経適応は,依存症に寄与する可能性があります.
- 新しいメカニズムは,ドーパミンニューロンからGABA端末への酸化窒素のシグナル伝達を含む.
- GABA (A) 受容体を標的とする治療戦略は有益である可能性があります.
関連する概念動画
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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