褪黑激素(N-乙酰基-5甲氧基雷公藤胺)是在光周期的黑暗阶段由松果体分泌的吲哚胺。它的主要功能是使不同的身体节律与暗光周期同步。褪黑激素的研究自发现以来已取得显著进展,我们现在知道它在各种生理过程中具有相当大的意义,包括豁免权,老化,和繁殖。此外,近年来,褪黑激素的药理学可能性的证据有所增加。吲哚胺,另一方面,对啮齿类动物有抗抑郁作用,这可能是由CaMKII的激活介导的,也与神经可塑性过程的调节有关,包括神经发生,突触维持,和长期增强。值得注意的是,重度抑郁症患者血浆中循环褪黑素水平降低。这篇综述提供了褪黑激素在临床前模型中抗抑郁样作用的证据。以及CaMKII参与这些行动。CaMKII在认知和记忆过程中的作用,在抑郁状态下改变,是综述的一部分,褪黑激素在这些过程中的作用也进行了综述。此外,还描述了CaMKII对结构和突触可塑性的参与以及褪黑激素的影响。最后,本文还介绍了褪黑激素与其他抗抑郁剂如氯胺酮联合用于神经可塑性的优点.证据支持CaMKII被褪黑激素激活,下游褪黑激素受体,可能是褪黑激素与其他抗抑郁药协同作用的共同效应。意义陈述这篇综述汇编了支持褪黑激素通过钙调蛋白激酶II刺激下游褪黑激素受体在小鼠中引起抗抑郁样作用的证据,以及这种酶参与神经可塑性,记忆,和认知。最后,我们描述了褪黑激素与氯胺酮联合使用抗抑郁药样作用的有效性的证据。
Melatonin (N-acetyl-5-methoxytryptamine) is an indoleamine secreted by the pineal gland during the dark phase of the photoperiod. Its main function is the synchronization of different body rhythms with the dark-light cycle. Research on melatonin has significantly advanced since its discovery and we now know that it has considerable significance in various physiological processes, including immunity, aging, and reproduction. Moreover, in recent years evidence of the pharmacological possibilities of melatonin has increased. Indoleamine, on the other hand, has antidepressant-like effects in rodents, which may be mediated by the activation of calcium-calmodulin-dependent kinase II (CaMKII) and are also related to the regulation of neuroplasticity processes, including neurogenesis, synaptic maintenance, and long-term potentiation. Remarkably, patients with major depression show decreased levels of circulating melatonin in plasma. This review presents evidence of the antidepressant-like effects of melatonin in preclinical models and the participation of CaMKII in these actions. CaMKII\'s role in cognition and memory processes, which are altered in depressive states, are part of the review, and the effects of melatonin in these processes are also reviewed. Furthermore, participation of CaMKII on structural and synaptic plasticity and the effects of melatonin are also described. Finally, the advantages of using melatonin in combination with other antidepressants such as ketamine for neuroplasticity are described. Evidence supports that CaMKII is activated by melatonin and downstream melatonin receptors and may be the common effector in the synergistic effects of melatonin with other antidepressants. SIGNIFICANCE STATEMENT: This review compiled evidence supporting that melatonin causes antidepressant-like effects in mice through calmodulin kinase II stimulation of downstream melatonin receptors as well as the participation of this enzyme in neuroplasticity, memory, and cognition. Finally, we describe evidence about the effectiveness of antidepressant-like effects of melatonin in combination with ketamine.