Mammalian sleep patterns are driven by genetic regulation

According to Cirelli (2009) who is the proponent this hypothesis; he supposes that there are mammalian genes whose presence in mammals’ genetic makeup induces sleep by prolonging general sleep patterns while others reduce the sleeping periods considerably. One example is the ion exchange channels. In ion exchange channels, two genes have been identified in mammals such as rats and mice; and these genes have been found to regulate sleep patterns through mutagenesis.

These two genes are shaker and sleepless. In the experiment done, mice that were regulated with the shaker gene reduced their sleep patterns from the normal nine hours to three hours per day. Under sleepless gene expression, the mice exhibited similar change in sleep patterns from the normal nine hours to three hours in a day. This shows that the genetic makeup of mammals has an influence on expression of mammalian sleep patterns, which supports this second hypothesis (Cirelli 2009).

In Circadian regulation, there is an interaction of the circadian genes and this determines the circadian rhythmicity. There have been several experiments to test the effect of these genes on sleep. In mice, the two circadian genes namely cryptochrome 1 and cryptochrome 2 were shown to have an impact on the sleep patterns. According to Cirelli (2009) these two genes are associated with higher non-rapid eye movement sleep, which makes mice to sleep more and in the event increasing their sleeping periods. Cirelli (2009) still indicates that there are other genes such as ARNT – like protein 1, prokineticin 2, and neuronal PAS domain protein 2, which are responsible for the different sleep patterns in mammals and are specifically responsible for causing longer sleep patterns in these animals (Cirelli 2009). These corroborating experimental results and conclusions are a clear indication that genes play a central role in influencing sleeping patterns of mammals to different degrees.