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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >REM sleep deprivation-induced noradrenaline stimulates neuronal and inhibits glial Na-K ATPase in rat brain: in vivo and in vitro studies.
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REM sleep deprivation-induced noradrenaline stimulates neuronal and inhibits glial Na-K ATPase in rat brain: in vivo and in vitro studies.

机译：REM睡眠剥夺诱导的去甲肾上腺素刺激大鼠脑神经元并抑制神经胶质Na-K ATPase：体内和体外研究。

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摘要

Increased noradrenaline, induced by rapid eye movement (REM) sleep deprivation, stimulates Na-K ATPase activity in the rat brain. The brain contains neurons as well as glia and both possess Na-K ATPase, however, it was not known if REM sleep deprivation affects the enzyme in both types of cells identically. Rats were REM sleep deprived by the flowerpot method and free moving, large platform and recovery controls were carried out. Na-K ATPase activity was measured in membranes prepared from whole brain as well as from neuronal and glial fractions separated from REM sleep-deprived and control rats. The effects of noradrenaline (NA) in different fractions were studied with or without in vivo i.p. treatment of prazosin, an alpha1-adrenpceptor antagonist, as well as in vitro membranes prepared from neurons and glia separated from normal rat brain. Further, to confirm the findings, membranes were prepared from neuro2a and C6 cell lines treated with NA in the presence and absence of prazosin and Na-K ATPase activity was estimated. The results showed that neuron and neuro2a as well as glia and C6 possess comparable Na-K ATPase activity. After REM sleep deprivation the neuronal Na-K ATPase activity increased, while the glial enzyme activity decreased and these changes were mediated by NA acting on alpha1-adrenoceptor; comparable results were obtained by treating the neuro2a and C6 cell lines with NA. The opposite actions of NA on neuronal and glial Na-K ATPase activity probably help maintain neuronal homeostasis.
机译：快速眼动（REM）睡眠剥夺引起的去甲肾上腺素升高会刺激大鼠脑中的Na-K ATPase活性。大脑既有神经元又有神经胶质，都具有Na-K ATPase，但是，REM睡眠剥夺是否会同时影响两种细胞中的酶，这一点尚不清楚。通过花盆法剥夺大鼠的REM睡眠，并进行自由移动，大平台和恢复控制。 Na-K ATPase活性在从全脑以及从REM睡眠不足和对照组大鼠中分离的神经元和神经胶质级分制备的膜中进行测量。有或没有体内腹膜内注射均研究了去甲肾上腺素（NA）在不同部位的作用。 α1肾上腺素受体拮抗剂prazosin的治疗，以及从正常大鼠大脑分离的神经元和神经胶质制备的体外膜。此外，为证实这一发现，在存在和不存在哌唑嗪的情况下，由用NA处理的Neuro2a和C6细胞系制备膜，并评估Na-K ATPase活性。结果表明，神经元和神经2a以及神经胶质和C6具有相当的Na-K ATPase活性。 REM睡眠剥夺后，神经元Na-K ATPase活性增加，而神经胶质酶活性下降，而这些变化是由NA对α1-肾上腺素受体的作用介导的。通过用NA处理Neuro2a和C6细胞系可获得可比的结果。 NA对神经元和神经胶质Na-K ATPase活性的相反作用可能有助于维持神经元稳态。

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