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 clues, animals run free in constant darkness due to programmed genetic interactions. Some of the genes involved in these processes 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 cry and mper proteins (Hong and Chong, 2007). These proteins are concentration dependent, meaning they bind at a high level to the repressor region to prevent further transcription. Such oscillations operate on a cycle close to 24 hours in animals and plants. These processes occur without any environmental cues. When environmental cues are introduced to animals, they tend to synchronize their internal clock with external signals. One such example of synchronization is shown in Dorsophilia which increases Tim protein during the night and the presence of external light decreases the production of Tim protein. 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 subsequent genetic studies have shown that the exact genes involved in phase delay and advance occur due to overproduction or insufficient protein as described in the Dorsophilia studies. Many knock-out studies have shown that altering genes involved in the circadian rhythm created arrhythmia in animals. Low-Zeddies and Takahashi (2001), created clock mutants that were arrhythmic when exposed to dark conditions. The period of the clock mutants was longer than in wild-type mice. The mutant also showed higher hours of phase shift 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 primary focus of recent studies. It is widely known that information from the ventrolateral region of the SCN communicates with other regions of the SCN. Buhr and Yoo (2010), show that there is a ventrolateral and dorsal medial neuronal connection and this connection plays a role in the circadian rhythm. Their data show that tetrodoxin can compensate for SCN temperature due to inhibition of signaling from core-to-shell regions. Similarly, vasoactive intestinal peptide and histidine peptide iso-leucine are expressed in the SCN when light information travels from the retinohypothalamic tract.