Melatonin Modulates Serotonin and Norepinephrine Activity in the Midbrain

The article below finds a connection between serotonin and norepinephrine activity in mouse midbrain and exposure to longer versus shorter daylight periods. That the effect is most likely via melatonin is confirmed by the effect disappearing when melatonin receptors are blocked in the midbrain. Since depression is also modulated via serotonin and norepinephrne, this suggests that seasonal affective disorder in humans may be acquired via decreases in melatonin activity at the midbrain level.



Photoperiod Programs Dorsal Raphe Serotonergic Neurons and Affective Behaviors

Noah H. Green, Chad R. Jackson, Hideki Iwamoto, Michael C. Tackenberg, Douglas G. McMahon

Publication stage: In Press Corrected Proof



•Summer-like long photoperiods increase serotonin neuron excitability and firing

•Long photoperiods increase serotonin and norepinephrine levels in the midbrain

•Long photoperiods during development induce lasting increases in firing rate

•Knockout of the MT1 receptor negates the observed photoperiodic changes


The serotonergic raphe nuclei of the midbrain are principal centers from which serotonin neurons project to innervate cortical and sub-cortical structures. The dorsal raphe nuclei receive light input from the circadian visual system [ 1 ] and indirect input from the biological clock nuclei [ 2, 3 ]. Dysregulation of serotonin neurotransmission is implicated in neurobehavioral disorders, such as depression and anxiety [ 4 ], and alterations in the serotonergic phenotype of raphe neurons have dramatic effects on affective behaviors in rodents [ 5 ]. Here, we demonstrate that day length (photoperiod) during development induces enduring changes in mouse dorsal raphe serotonin neurons—programming their firing rate, responsiveness to noradrenergic stimulation, intrinsic electrical properties, serotonin and norepinephrine content in the midbrain, and depression/anxiety-related behavior in a melatonin receptor 1 (MT1)-dependent manner. Our results establish mechanisms by which seasonal photoperiods may dramatically and persistently alter the function of serotonin neurons.

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