Circadian rhythms are endogenous and self-sustaining in all animals and plants. These rhythms are present in the absence of environmental cues such as light, temperature, and social cues. In the absence of cues, animals run freely in constant darkness due to programmed genetic interactions. Some of the genes involved in this process are Per, Clock and Cry. The expressions of these genes are tightly regulated at the molecular level by proteins that bind to promoters and repressors to create a rhythm throughout the day. For example, bmal and clock bind to the ebox region to produce the cry and mper proteins (Hong and Chong, 2007). These proteins are concentration dependent, meaning that a high level binds to the repressor region to prevent further transcription. Such oscillations operate on a nearly 24-hour cycle in animals and plants. These processes occur without any environmental cues. In case environmental cues are introduced to animals, they tend to synchronize the internal clock with external signals. One such example of synchronization is shown in dorsophilia which increases Tim protein at night and the presence of external light decreases Tim protein production. This results in a phase delay in dorsophilia (Leuloup and Goldbeter, 2001). The idea of ​​phase advance and delay was first proposed by Aschoff and Pittendrigh (1960), but later genetic studies showed that the exact genes involved in phase delay and advance occur in due to over or underproduction of proteins as described in dorsophilia studies. Numerous knockout studies have shown that disrupting genes involved in circadian rhythm created arrhythmicity in animals. Low-Zeddies and Takahashi (2001) created clock mutants that were arrhythmic when exposed to darkness. The period of clock mutants was longer than that of wild-type mice. The mutant also showed higher time phase shifts and lower circadian amplitude. Although clock expression has been important for understanding rhythm, initial information from the retinohypothalamic tract to the nucleus or ventrolateral region of the SCN has been the focus of recent studies. It is well known that information from the ventrolateral region of the SCN communicates with other regions of the SCN. Buhr and Yoo (2010) show that a ventrolateral and dorsomedial neuronal connection exists and that this connection plays a role in the circadian rhythm. Their data show that tetrodoxin can compensate for SCN temperature due to signal inhibition from core to shell regions. Similarly, vasoactive intestinal peptide and histidine iso-leucine peptide are expressed in the SCN when light information originates from the retinohypothalamic tract..