Dopamine dysfunction might contribute to several aspects of SAD, including altered light responsivity at the level of the retina and both hypoarousal and overeating at the level

of the central nervous system. The D4 receptor gene is of great interest in this regard, in that the hypofunctional 7-repeat allele of DRD4 has been linked to both affective and appetitive Inhibitors,research,lifescience,medical symptoms in SAD. As discussed above, this same allele is an excellent candidate to study altered ERG responses in this population. The fact that this 7R allele has been positively selected for in recent human evolution85 adds an intriguing twist to this story given several evolutionary models of SAD.4-9 There Inhibitors,research,lifescience,medical are several other areas that hold great promise for future investigation. For example, in addition to examining the genetic basis of retinal ERG lower changes as alluded to above, there is a great need to study the role of the melanopsin system, and its genetic and phenotypic variants, in mediating the circadian changes seen in many SAD patients. As the genetic and molecular mechanisms underlying various clock genes becomes clearer, applying these findings to understand individual differences in circadian physiology

in SAD patients Inhibitors,research,lifescience,medical and matched controls should further improve our treatment of these patients. The use of genetic data to predict treatment http://www.selleckchem.com/products/Bosutinib.html response is Inhibitors,research,lifescience,medical largely unexplored to date. Ultimately, many features of SAD make it an ideal focus for pathophysiological studies, suggesting that many significant new findings will emerge from the next decade of Inhibitors,research,lifescience,medical work in this area. Selected abbreviations and acronyms 5-HTTLPR serotonin transporter gene repeat length polymorphism ERG electroretinography m-CCP meta-chlorophenyl-piperazine SAD seasonal affective disorder SCN suprachiasmatic nucleus
The role of the endogenous circadian System is to coordinate the body’s fonctions

with each other and with the external environment.1 This includes the integration of sensory information and environmental time eues, and of the organismes physiological and psychological states. When the harmony of this integrative fonction is Anacetrapib perturbed, as could be the case with several mental disorders, disturbances of mood, a disrupted sleepwake cycle, and changes in levels and/or timing of hormones can occur. Whether these changes precede, follow, or are epiphenonrenal to the mental disorders is often difficult to determine with certainty, although several lines of evidence support a role of the endogenous circadian system in the pathophysiology of these disorders.