Kumar Velayudhan Mohan
Department of Physiology, All India Institute of Medical Sciences, 110029 New Delhi, India.
J Chem Neuroanat. 2003 Oct;26(2):87-93. doi: 10.1016/s0891-0618(03)00003-6.
The preoptic area (POA) has noradrenergic (NE) terminals, and this area controls sleep apart from body temperature and reproduction. The destruction of catecholaminergic (CA) terminals in the POA produced a decrease in sleep in rats. This effect was shown to be due to the destruction of NE and not dopaminergic terminals. The rats, which were hyperthermic after the destruction of CA fibers in the POA, preferred a lower ambient temperature. Though they were unable to have normal amount of sleep after lesion, it did not affect their behavioral thermoregulation. Acute total sleep deprivation for 48 h led to a significant decrease in noradrenaline, increase in the level of metabolites of monoamines, and an enhancement in the number of dendritic spines at the medial preoptic area (mPOA). Enhanced sleep pressure during sleep deprivation could have led to a higher release of noradrenaline, and an increase in dendritic spines in the mPOA. Arousal was produced by application of noradrenaline at the mPOA, whereas the alpha antagonists produced sleep in free-moving rats. This was in contrast to the increased wakefulness produced by the destruction of NE terminals. As wakefulness and sleep, respectively, were induced on local application of alpha-2 antagonist and agonists, it was suspected that the noradrenaline and alpha antagonists might have acted on the alpha-2 receptors, which are predominantly present on the pre-synaptic terminals. Sleep produced by noradrenaline, which was locally applied at the mPOA, after destroying the NE terminals, further confirmed this possibility. Hypothermia and sexual arousal produced by application of alpha- and beta-adrenergic agonists at the mPOA would have contributed towards the wakefulness induced by these drugs in normal rats. Thus, the available evidence shows that the NE fibers in the POA are involved in the induction of sleep.
视前区（POA）有去甲肾上腺素能（NE）终末，该区域除了控制体温和生殖外，还控制睡眠。视前区儿茶酚胺能（CA）终末的破坏导致大鼠睡眠减少。已证明这种作用是由于NE终末而非多巴胺能终末的破坏。视前区CA纤维破坏后体温过高的大鼠更喜欢较低的环境温度。尽管它们在损伤后无法获得正常量的睡眠，但这并不影响它们的行为体温调节。急性完全睡眠剥夺48小时导致去甲肾上腺素显著减少、单胺代谢产物水平升高以及内侧视前区（mPOA）树突棘数量增加。睡眠剥夺期间增强的睡眠压力可能导致去甲肾上腺素释放增加以及mPOA中树突棘增加。在mPOA应用去甲肾上腺素会引起觉醒，而α拮抗剂会使自由活动的大鼠入睡。这与NE终末破坏导致的觉醒增加形成对比。由于局部应用α-2拮抗剂和激动剂分别诱导了觉醒和睡眠，因此怀疑去甲肾上腺素和α拮抗剂可能作用于主要存在于突触前终末的α-2受体。在破坏NE终末后，在mPOA局部应用去甲肾上腺素产生的睡眠进一步证实了这种可能性。在mPOA应用α和β肾上腺素能激动剂产生的体温过低和性觉醒可能促成了这些药物在正常大鼠中诱导的觉醒。因此，现有证据表明视前区的NE纤维参与睡眠的诱导。
