![]() (1984) and has subsequently been entered in several editions of the Diagnostic and Statistical Manual of Mental Disorders, including the most recent edition (DSM-5 American Psychiatric Association, 2013). The syndrome was first described by Rosenthal et al. In addition to depression, a significant subset of SAD patients display a multitude of ‘atypical’ secondary symptoms, including sleep disruption, fatigue, carbohydrate craving and weight gain ( Young et al., 1991). Seasonal affective disorder (SAD) is diagnosed based on a seasonally recurring pattern of depression that typically coincides with short photoperiods in fall or winter and subsequently abates each spring or summer ( Sandman et al., 2016 Sohn and Lam, 2005). However, although diurnal models make intuitive sense for the study of SAD and are more likely to mimic circadian disruption, their utility is currently hampered by a lack of genomic resources needed for the molecular interrogation of potential mechanisms. One exciting avenue of research involves the orexinergic system, which regulates functions that are disturbed in SAD, including sleep cycles, the reward system, feeding behavior, monoaminergic neurotransmission and hippocampal neurogenesis. Diurnal rodents show promise as models of SAD, as changes in affective-like behaviors are induced in response to short photoperiods or dim-light conditions, and symptoms can be ameliorated by brief exposure to intervals of bright light coincident with activity onset. Although circadian disruption is often invoked as a key contributor to SAD, a mechanistic understanding of how misalignment between endogenous circadian physiology and daily environmental rhythms affects mood is lacking. Here, we briefly review what is known regarding the etiology of SAD and then examine progress in developing appropriate diurnal rodent models. ![]() The need for diurnal models is most clear for seasonal affective disorder (SAD), a widespread recurrent depressive disorder that is linked to exposure to short photoperiods. Although most neuropsychiatric research is performed on nocturnal rodents, differences in how diurnal and nocturnal animals respond to changing photoperiods, combined with a possible link between circadian rhythm disruption and affective disorders, has led to a call for the development of diurnal animal models. The development of animal models is a critical step for exploring the underlying pathophysiological mechanisms of major affective disorders and for evaluating potential therapeutic approaches.
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