Who wishes there was a simple switch to change the gears of our internal body clocks? So we could cross multiple time zones without missing a beat? Or change our sleeping patterns to take the graveyard shift? Researchers from the University of Notre Dame may be well on the way to finding the ‘pin’ of our bodies’ watches and influencing it to the advantage of many of those suffering from sleep-wake disorders and related illnesses.
A 24-hour circadian rhythm governs the fundamental physiological functions of almost all organisms (Corsi, 2008). The correct functioning of our internal human clock allows us to “anticipate daily environmental changes and temporally modify behavioral and physiological function appropriately” (Barnard, 2008). Molecular components oscillate daily in response to external stimuli; regulating almost every biological system, ranging from sleep cycles, levels of circulating hormones, body temperature and cardiac output. The master circadian clock is housed within the suprachiasmatic nucleus (SCN) of the hypothalamic brain which receives direct input from the retina; providing diurnal and seasonal information. Besides a central body clock, we also have autonomous, “peripheral circadian oscillators”, in tissues outside the SCN. Integrated signals are conveyed to the remote central neural circuits by the SCN where specific output rhythms are regulated; synchronizing rhythms of multiple cells.
When we experience jet lag, it is the mismatch between central and peripheral clocks and recovery persists while each organ shifts into sync at their own rate. Loss of synchrony between bodily tissues has been attributed to numerous health problems such as depression, cancer and metabolic disorders: causing obesity and diabetes. Research into our circadian rhythms could yield drugs and therapies to conceivably shift the clock to more readily adapt to schedule changes (Takahashi, 2000).
Through investigation into the DNA of mice, the researchers have identified a crucial gene dubbed the “Inhibitor of DNA-binding 2” (Id2), which is rhythmically expressed in various tissues, including the SCN. Experimentation involved scientists creating a “knockout” mouse which was null for the Id2 protein as it did not express the Id2 gene. Imposing a significant artificial time zone shift on the mice through changing their ‘light-dark cycle’ by an equivalent 10 hour delay, researchers were able to simulate the effect of jet lag on the mice. Comparing mice possessing the Id2 gene with the ‘knockout’, Id2 gene deficient mice, the researchers showed the unaltered mice took about twice as long to recover from the induced jet lag than the ‘knockout’ sample; four to five days for the average mouse in comparison to merely one to two days for the genetically modified mice.
The results have implicated that the gene regulates the magnitude of the response of our internal human clock to the signals sent by the SCN; signals stimulated by light. The absence of the Id2 gene appears to ease the re-synchronization of a person’s ‘peripheral circadian oscillators’ and effect of the SCN time-keeping signals , quickening the return to the same phase in the event of disruption of the circadian function. If only scientists could manipulate this target gene, it could be possible to reduce the effect of jet lag through rapid, internal clock shifts.
An interesting study considering the nocturnal habits many of us students develop to try to cope with immense workloads.
A 24-hour circadian rhythm governs the fundamental physiological functions of almost all organisms (Corsi, 2008). The correct functioning of our internal human clock allows us to “anticipate daily environmental changes and temporally modify behavioral and physiological function appropriately” (Barnard, 2008). Molecular components oscillate daily in response to external stimuli; regulating almost every biological system, ranging from sleep cycles, levels of circulating hormones, body temperature and cardiac output. The master circadian clock is housed within the suprachiasmatic nucleus (SCN) of the hypothalamic brain which receives direct input from the retina; providing diurnal and seasonal information. Besides a central body clock, we also have autonomous, “peripheral circadian oscillators”, in tissues outside the SCN. Integrated signals are conveyed to the remote central neural circuits by the SCN where specific output rhythms are regulated; synchronizing rhythms of multiple cells.
When we experience jet lag, it is the mismatch between central and peripheral clocks and recovery persists while each organ shifts into sync at their own rate. Loss of synchrony between bodily tissues has been attributed to numerous health problems such as depression, cancer and metabolic disorders: causing obesity and diabetes. Research into our circadian rhythms could yield drugs and therapies to conceivably shift the clock to more readily adapt to schedule changes (Takahashi, 2000).
Through investigation into the DNA of mice, the researchers have identified a crucial gene dubbed the “Inhibitor of DNA-binding 2” (Id2), which is rhythmically expressed in various tissues, including the SCN. Experimentation involved scientists creating a “knockout” mouse which was null for the Id2 protein as it did not express the Id2 gene. Imposing a significant artificial time zone shift on the mice through changing their ‘light-dark cycle’ by an equivalent 10 hour delay, researchers were able to simulate the effect of jet lag on the mice. Comparing mice possessing the Id2 gene with the ‘knockout’, Id2 gene deficient mice, the researchers showed the unaltered mice took about twice as long to recover from the induced jet lag than the ‘knockout’ sample; four to five days for the average mouse in comparison to merely one to two days for the genetically modified mice.
The results have implicated that the gene regulates the magnitude of the response of our internal human clock to the signals sent by the SCN; signals stimulated by light. The absence of the Id2 gene appears to ease the re-synchronization of a person’s ‘peripheral circadian oscillators’ and effect of the SCN time-keeping signals , quickening the return to the same phase in the event of disruption of the circadian function. If only scientists could manipulate this target gene, it could be possible to reduce the effect of jet lag through rapid, internal clock shifts.
An interesting study considering the nocturnal habits many of us students develop to try to cope with immense workloads.
Student Number: 42048002
Main Article:
Gilroy, W. (2009) Paper sheds new 'light' on fascinating rhythms of the circadian clock. (Internet) Provided by University of Notre Dame: PhysOrg.com. Available from: http://www.physorg.com/news154025101.html Accessed 13th March 2009
Related Articles:
Barnard AR, Nolan PM, (2008) When Clocks Go Bad: Neurobehavioural Consequences of Disrupted Circadian Timing. (Internet) PLoS Genetics. Available from: http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000040 Accessed 13th March 2009
Corsi, P. (2008) Circadian rhythm-metabolism link discovered. (Internet) Irvine: University of California. Available from: http://www.physorg.com/news136122147.html Accessed 13th March 2009
Phillips, L. (2009) Circadian rhythms: Of owls, larks and alarm clocks. (Internet) Nature Publishing Group. Available from: http://www.nature.com/news/2009/090311/full/458142a.html?s=news_rss Accessed 13th March 2009
Takahashi, J (2000) Gene Mutation Upsets Mammalian Biological Clock. (Internet) Howard Hughes Medical Institute. Available from: http://www.hhmi.org/news/takahashi2.html Accessed 13th March 2009
Picture:
http://www.physorg.com/news148053745.html
