演題詳細
Poster
運動課題遂行中のサルにおける淡蒼球ニューロン活動のグルタミン酸およびGABA作動性調節
Glutamatergic and GABAergic Control of Monkey Pallidal Activity during Performance of a Motor Task
- P1-141
- 金子 将也 / Nobuya Kaneko:1 畑中 伸彦 / Nobuhiko Hatanaka:1 高良 沙幸 / Sayuki Takara:1,2 高田 昌彦 / Masahiko Takada:3 南部 篤 / Atsushi Nambu:1
- 1:生理研統合生理生体システム / Div of System Neurophysiol, NIPS, Okazaki, Japan 2:理研ライフサイエンス技術基盤研セ生体機能評価研究チーム / Bio-function Imaging Team, Center for Life Science Technologies, RIKEN, Kobe, Japan 3:京都大 霊長研統合脳システム / Systems Neurosci Sec, Primate Res Inst, Kyoto Univ, Inuyama, Japan
Neurons in the internal (GPi) and external (GPe) segments of the globus pallidus receive excitatory glutamatergic inputs from the subthalamic nucleus and inhibitory GABAergic input from the striatum. However, it is still unclear how such excitatory and inhibitory inputs modulate the activity of GPi/GPe neurons during motor behavior. To address this issue, we identified GPi/GPe neurons that responded to stimulation of the primary motor cortex and the supplementary motor area in macaque monkeys, and recorded their activity during the performance of a reaching task with delay. Then, CPP+NBQX (NMDA or AMPA/kainate receptor antagonist, respectively) and/or gabazine (GABAA receptor antagonist) were injected in the vicinity of GPi/GPe neurons under recordings. The following results were obtained: 1) Both glutamatergic and GABAergic inputs contributed to GPi/GPe neuron activity related to reaching movement, and the extent of their contributions was different among neurons; 2) Phasic changes in glutamatergic and GABAergic inputs preceded the movement onset in more than half of the GPi/GPe neurons recorded; 3) Such phasic changes were dependent on the direction of reaching movement; 4) In addition to incremental glutamatergic and decremental GABAergic components, decremental glutamatergic and incremental GABAergic components were detected, although their contributions were small. They were considered to be caused by disfacilitatory and disinhibitory mechanisms; and 5) Sustained glutamatergic input was observed in the GPi during the delay period. The overall data clearly indicate that both the glutamatergic and the GABAergic inputs transfer specific neural information about motor behavior to the GPi/GPe at a similar timing and contribute to GPi/GPe neuron activity. The identified changes in GPi/GPe neuron activity during reaching movement may be ascribable to competition between the glutamatergic and the GABAergic input.