2012年5月
Effect of Xenon on Excitatory and Inhibitory Transmission in Rat Spinal Ventral Horn Neurons
ANESTHESIOLOGY
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回数 : 145
- ,
- ,
- ,
- 巻
- 116
- 号
- 5
- 開始ページ
- 1025
- 終了ページ
- 1034
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1097/ALN.0b013e31825037a1
- 出版者・発行元
- LIPPINCOTT WILLIAMS & WILKINS
Background: The minimum alveolar concentration is determined in the spinal cord rather than in the brain. Xenon inhibits glutamatergic excitatory synaptic transmission in the dorsal horn neurons. However, its actions in the ventral horn neurons have not been investigated.
Methods: The effects of 50 or 75% xenon on excitatory and inhibitory synaptic transmission were examined in the spinal lamina IX neurons of neonatal rats by using a whole cell patch clamp technique.
Results: Fifty percent xenon inhibited the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid-induced currents (amplitudes = 72 +/- 9% and integrated area = 73 +/- 13% of the control values), and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid receptor-mediated electrically evoked excitatory postsynaptic currents (amplitudes = 69 +/- 13% of the control values). Seventy-five percent xenon similarly inhibited alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid-induced currents. However, xenon had no effect on the N-methyl-D-aspartate-induced currents or N-methyl-D-aspartate receptor-mediated electrically evoked excitatory postsynaptic currents. Xenon decreased the amplitude, but not the frequency, of miniature excitatory postsynaptic currents. There were no discernible effects on the currents induced by gamma-aminobutyric acid or glycine or on miniature inhibitory postsynaptic currents.
Conclusions: Xenon inhibits alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid receptor-mediated glutamatergic excitatory transmission in the spinal lamina IX neurons via a postsynaptic mechanism. In contrast, there are no substantial effects on N-methyl-D-aspartate receptor-mediated or inhibitory synaptic transmission. The suppressive effects on excitatory synaptic transmission in the ventral horn neurons partly account for the mechanism behind xenon's ability to produce immobility in response to noxious stimuli and to determine the minimum alveolar concentration.
Methods: The effects of 50 or 75% xenon on excitatory and inhibitory synaptic transmission were examined in the spinal lamina IX neurons of neonatal rats by using a whole cell patch clamp technique.
Results: Fifty percent xenon inhibited the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid-induced currents (amplitudes = 72 +/- 9% and integrated area = 73 +/- 13% of the control values), and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid receptor-mediated electrically evoked excitatory postsynaptic currents (amplitudes = 69 +/- 13% of the control values). Seventy-five percent xenon similarly inhibited alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid-induced currents. However, xenon had no effect on the N-methyl-D-aspartate-induced currents or N-methyl-D-aspartate receptor-mediated electrically evoked excitatory postsynaptic currents. Xenon decreased the amplitude, but not the frequency, of miniature excitatory postsynaptic currents. There were no discernible effects on the currents induced by gamma-aminobutyric acid or glycine or on miniature inhibitory postsynaptic currents.
Conclusions: Xenon inhibits alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid receptor-mediated glutamatergic excitatory transmission in the spinal lamina IX neurons via a postsynaptic mechanism. In contrast, there are no substantial effects on N-methyl-D-aspartate receptor-mediated or inhibitory synaptic transmission. The suppressive effects on excitatory synaptic transmission in the ventral horn neurons partly account for the mechanism behind xenon's ability to produce immobility in response to noxious stimuli and to determine the minimum alveolar concentration.
- リンク情報
- ID情報
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- DOI : 10.1097/ALN.0b013e31825037a1
- ISSN : 0003-3022
- PubMed ID : 22411062
- Web of Science ID : WOS:000303199600010