Alterations of melatonin receptors MT1 and MT2 in the hypothalamic suprachiasmatic nucleus during depression

Jan 30, 2013Journal of affective disorders

Changes in Melatonin Receptors in the Brain’s Internal Clock Area During Depression

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Abstract

Melatonin receptor 1 (MT1) cells were found to be increased in the central suprachiasmatic nucleus (SCN) of 14 depressed patients compared to matched controls.

MT2 receptor immunoreactivity was localized to the SCN, supraoptic nucleus, and paraventricular nucleus.
The number of MT1-immunoreactive cells was increased in the SCN of depressed patients, while the number of MT2-immunoreactive cells did not change.
A negative correlation exists between the number of MT1-immunoreactive cells and age at onset of depression.
A positive correlation was observed between the number of MT1-immunoreactive cells and the duration of the disease.
MT1 receptor increases in the SCN may be associated with circadian disorders in depression.

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BACKGROUND: The pineal hormone melatonin regulates circadian rhythms, largely by feedback on the central biological clock of the brain, the hypothalamic suprachiasmatic nucleus (SCN). This feedback is mediated by the melatonin receptors, melatonin receptor 1 (MT1) and melatonin receptor 2 (MT2). The circadian system may play a role in the pathophysiology of mood disorders, and indeed, melatonin-receptor agonists are considered a potential therapy for depression.

METHOD: In order to investigate melatonin receptors in the SCN during depression, and their relationship to the major neuropeptides in the SCN, vasopressin (AVP) and vasoactive intestinal peptide (VIP), we studied the SCN in 14 depressed patients (five major depression and nine bipolar disorder) and 14 matched controls by immunocytochemistry.

RESULTS: We show here that hypothalamic MT2 receptor immunoreactivity was limited to SCN, the supraoptic nucleus and paraventricular nucleus. We found that numbers of MT1-immunoreactive (MT1-ir) cells and AVP and/or VIP-ir cells were increased in the central SCN in depression, but numbers of MT2-ir cells were not altered. Moreover, the number of MT1-ir cells, but not MT2-ir cells was negatively correlated with age at onset of depression, while positively correlated with disease duration. CONCLUSION AND LIMITATIONS: Although every post-mortem study has limitations, MT1 receptors appeared specifically increased in the SCN of depressed patients, and may increase during the course of the disease. These changes may be involved in the circadian disorders and contribute to the efficacy of MT agonists or melatonin in depression. Moreover, we suggest that melatonin receptor agonists for depression should be targeted towards the MT1 receptor selectively.

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Alterations of melatonin receptors MT1 and MT2 in the hypothalamic suprachiasmatic nucleus during depression

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