ドーパミンの放出を制御するための遠端軸索におけるアクションポテンシャル開始メカニズム

Changliang Liu¹, Xintong Cai¹, Andreas Ritzau-Jost²

¹Department of Neurobiology, Harvard Medical School, Boston, MA, USA.

Science (New York, N.Y.)

|March 24, 2022

まとめ

コリン神経はドーパミンのアクソンにアクションポテンシャルを誘発しドーパミンの放出と動きを制御しますこれは従来の統合経路から独立した神経信号伝達の新しいメカニズムを明らかにしています

科学分野:

神経科学
細胞生物学
神経生理学

背景:

ニューロンの伝達には通常, dendrites での信号統合と soma 近くのアクションポテンシャル生成が含まれます.
神経伝達物質の放出は,軸索の神経末端で起こります.

研究の目的:

ストライアトムのドーパミンアクソン活動におけるアセチルコリン放出ニューロンの役割を調査する.
somatodendritic 統合から独立した作用の可能性の開始と神経伝達物質の放出のメカニズムを明らかにする.

主な方法:

ニューロンの活動を監視するための線状体の電気生理学的記録
移動中のドーパミンとアセチルコレンの動態を観察するために,自由に動くマウスでの体内実験.
ニコチンアセチルコリン受容体の薬学的な阻害

主要な成果:

アセチルコリンを放出するニューロンは,遠隔ドーパミン軸索のアクションポテンシャルを誘発することが判明した.
ドーパミンの放出は局所的な信号域を超えて広がった.
ドーパミンとアセチルコレンの濃度は,自由に動くマウスの動き方向に合わせて変化した.
ニコチンアセチルコリン受容体の阻害はドーパミンの動態を乱し,運動行動に影響を与えました.

結論:

ドーパミンのアクソンにおける新種の内生性メカニズムが特定され,それは体内膜統合とは無関係であった.
このメカニズムは,軸索と体間のドーパミン信号の分離制御を可能にします.
ドーパミンのアクソン発射のホルモン調節は,運動の調節に重要な役割を果たします.

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