Argiolas A, Melis M R
Bernard B. Brodie Department of Neuroscience, University of Cagliari and Center for Neuropharmacology, National Research Council, Italy.
Eur J Pharmacol. 1998 Feb 5;343(1):1-16. doi: 10.1016/s0014-2999(97)01538-0.
Yawning is a phylogenetically old, stereotyped event that occurs alone or associated with stretching and/or penile erection in humans and in animals from reptiles to birds and mammals under different conditions. Although its physiological function is still unknown, yawning is under the control of several neurotransmitters and neuropeptides at the central level as this short overview of the literature on the neurochemistry of yawning shows. Among these substances, the best known are dopamine, excitatory amino acids, acetylcholine, serotonin, nitric oxide, adrenocorticotropic hormone-related peptides and oxytocin, that facilitate yawning and opioid peptides that inhibit this behavioral response. Some of the above compounds interact in the paraventricular nucleus of the hypothalamus to control yawning. This hypothalamic nucleus contains the cell bodies of oxytocinergic neurons projecting to extra-hypothalamic brain areas that play a key role in the expression of this behavioral event. When activated by dopamine, excitatory amino acids and oxytocin itself, these neurons facilitate yawning by releasing oxytocin at sites distant form the paraventricular nucleus, i.e. the hippocampus, the pons and/or the medulla oblongata. Conversely, activation of these neurons by dopamine, oxytocin or excitatory amino acids, is antagonized by opioid peptides, that, in turn, prevent the yawning response. The activation and inhibition, respectively of these oxytocinergic neurons is related to a concomitant increase and decrease, respectively, of paraventricular nitric oxide synthase activity. However, other neuronal systems in addition to the central paraventricular oxytocinergic neurons are involved in the control of yawning, since they do not seem to be involved in the expression of yawning induced by the stimulation of acetylcholine or serotoninergic receptors, nor by adrenocorticotropic hormone (ACTH) and related peptides. Nitric oxide is also involved in the induction of yawning by the latter compounds and neuronal links, for instance between dopamine and acetylcholine and dopamine and serotonin, seem to be involved in the yawning response. Finally, other neurotransmitters, i.e. gamma-aminobutyric acid (GABA) and noradrenaline, and neuropeptides, i.e. neurotensin and luteinizing hormone-releasing hormone (LH-RH), influence this behavioral response. In conclusion, in spite of some recent progress, little is known of, and more has to be done to identify, the neurochemical mechanisms underlying yawning at the central level.
打哈欠是一种在系统发育上古老且模式化的行为，在不同条件下，人类以及从爬行动物到鸟类和哺乳动物的动物中，打哈欠可单独出现，或与伸展和/或阴茎勃起相关联。尽管其生理功能仍然未知，但正如这篇关于打哈欠神经化学的文献简短综述所示，打哈欠在中枢水平受多种神经递质和神经肽的控制。在这些物质中，最知名的是多巴胺、兴奋性氨基酸、乙酰胆碱、血清素、一氧化氮、促肾上腺皮质激素相关肽和催产素，它们促进打哈欠，而阿片肽则抑制这种行为反应。上述一些化合物在下丘脑室旁核相互作用以控制打哈欠。这个下丘脑核包含投射到下丘脑外脑区的催产素能神经元的细胞体，这些脑区在这种行为的表达中起关键作用。当被多巴胺、兴奋性氨基酸和催产素自身激活时，这些神经元通过在远离室旁核的部位，即海马体、脑桥和/或延髓释放催产素来促进打哈欠。相反，多巴胺、催产素或兴奋性氨基酸对这些神经元的激活会被阿片肽拮抗，而阿片肽反过来会阻止打哈欠反应。这些催产素能神经元的激活和抑制分别与室旁一氧化氮合酶活性的相应增加和减少有关。然而，除了中枢室旁催产素能神经元外，其他神经元系统也参与打哈欠的控制，因为它们似乎不参与由乙酰胆碱或血清素能受体刺激、促肾上腺皮质激素（ACTH）及相关肽诱导的打哈欠的表达。一氧化氮也参与后一类化合物诱导的打哈欠，并且神经元联系，例如多巴胺与乙酰胆碱之间以及多巴胺与血清素之间的联系，似乎也参与打哈欠反应。最后，其他神经递质，即γ-氨基丁酸（GABA）和去甲肾上腺素，以及神经肽，即神经降压素和促黄体生成素释放激素（LH-RH），也会影响这种行为反应。总之，尽管最近有一些进展，但对于中枢水平上打哈欠背后的神经化学机制仍知之甚少，还有更多工作有待开展以确定这些机制。
