ニューロンのエネルギー代謝におけるストレス耐性獲得機構 Energy metabolism in brain slices from rats pre-stressed by various means

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Author(s)

    • 西丸 直子 Nisimaru Naoko
    • 大分大・医・脳・神経機能統御講座(生理学) Division Physiol., Dept.Brain and Nerve Science, Facult. Med., Univ. Oita, Oita, Japan
    • 北野 敬明 Kitano Takaaki
    • 大分大・医・脳・神経機能統御講座(麻酔科学) Division Anesthesiol., Dept.Brain and Nerve Science, Facult. Med., Univ. Oita, Oita, Japan
    • 尾方 和枝 Ogata Kazue
    • 大分大・医・脳・神経機能統御講座(生理学) Division Physiol., Dept.Brain and Nerve Science, Facult. Med., Univ. Oita, Oita, Japan
    • 山田 和廣 Yamada Kazuhiro
    • 大分大・医・脳・神経機能統御講座(生理学) Division Physiol., Dept.Brain and Nerve Science, Facult. Med., Univ. Oita, Oita, Japan
    • 横井 功 Yokoi Isao
    • 大分大・医・脳・神経機能統御講座(生理学) Division Physiol., Dept.Brain and Nerve Science, Facult. Med., Univ. Oita, Oita, Japan

Abstract

We examined the possible role of lactate as an energy substrate by using <SUP>31</SUP>P-NMR in rat brain slices from pre-stressed rats. Preconditioned brain slices were obtained from rats, the brain of which had been made ischemic by occluding contralateral middle cerebral artery, from heat stroked rats (42-43°C,15 min.) or from rats pretreated with a low dose of 3-nitropropionic acid (3-NP) 48 hours before the preparation, respectively. Stimulation of the metabolism in brain slices was induced by changing the medium to a high-K solution (60 mM K<SUP>+</SUP>). Both glucose and lactate were able to support the recovery of high-energy phosphates (PCr etc.) levels in brain slices from control rats (7-10 weeks) following the high-K<SUP>+</SUP> stimulation at 25°C. After brain slices were treated with fluorocitrate (FC), a glial toxin, glucose was able, while lactate was unable, to support the recovery of PCr following the high-K<SUP>+</SUP> stimulation. In FC-treated brain slices obtained from pre-treated rats (ischemic, heat-stressed or pretreated with 3-NP), however, lactate supported the recovery of PCr substantially following the high-K<SUP>+</SUP> stimulation. These results suggest that neurons themselves are unable to take up and metabolize lactate, but after pre-conditioning neurons acquire the ability to take up and utilize lactate as an energy substrate. Even if the way of preconditioning is different, the same process may be involved in inducing similar changes in energy metabolism of the neuron. <b>[Jpn J Physiol 54 Suppl:S157 (2004)]</b>

We examined the possible role of lactate as an energy substrate by using <SUP>31</SUP>P-NMR in rat brain slices from pre-stressed rats. Preconditioned brain slices were obtained from rats, the brain of which had been made ischemic by occluding contralateral middle cerebral artery, from heat stroked rats (42-43°C,15 min.) or from rats pretreated with a low dose of 3-nitropropionic acid (3-NP) 48 hours before the preparation, respectively. Stimulation of the metabolism in brain slices was induced by changing the medium to a high-K solution (60 mM K<SUP>+</SUP>). Both glucose and lactate were able to support the recovery of high-energy phosphates (PCr etc.) levels in brain slices from control rats (7-10 weeks) following the high-K<SUP>+</SUP> stimulation at 25°C. After brain slices were treated with fluorocitrate (FC), a glial toxin, glucose was able, while lactate was unable, to support the recovery of PCr following the high-K<SUP>+</SUP> stimulation. In FC-treated brain slices obtained from pre-treated rats (ischemic, heat-stressed or pretreated with 3-NP), however, lactate supported the recovery of PCr substantially following the high-K<SUP>+</SUP> stimulation. These results suggest that neurons themselves are unable to take up and metabolize lactate, but after pre-conditioning neurons acquire the ability to take up and utilize lactate as an energy substrate. Even if the way of preconditioning is different, the same process may be involved in inducing similar changes in energy metabolism of the neuron. <b>[Jpn J Physiol 54 Suppl:S157 (2004)]</b>

Journal

  • Proceedings of Annual Meeting of the Physiological Society of Japan

    Proceedings of Annual Meeting of the Physiological Society of Japan 2004(0), S157-S157, 2004

    PHYSIOLOGICAL SOCIETY OF JAPAN

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