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Summary Case 5 shift problems
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Case 5 from the course sleep and sleeping disorders from the bachelor psychology and advanced minor in psychology. I got a 9.5 for the exam myself.
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Case 5 shift problemsBollinger: Circadian rhythms – from genes to physiology and disease
- A central pacemaker in the suprachiasmatic nucleus (SCN), located in the ventral
hypothalamus, coordinates all overt rhythms in our body through neuronal and
humoral outputs. The SCN consists of two tiny clusters of ~100,000 neurones in
humans, each harbouring a self-sustained, cell-autonomous molecular oscillator.
Research conducted during the past years has shown, however, that virtually all of our
thirty-five trillion body cells possess their own clocks and that these are
indistinguishable from those operative in SCN neurones
- for the SCN to stay in synchrony with the outside world, its circadian clocks must be
readjusted every day by a few minutes. This is accomplished mainly by the
photoperiod. Light signals, perceived by photoreceptors and intrinsically
photosensitive ganglion cells in the retina, are transmitted to SCN neurones via the
retinohypothalamic tract. The SCN neurones convert the electrical into chemical
signals that reset their molecular oscillators by influencing the phase of clock gene
expression.
- circadian cellular oscillators have been described in virtually all cell types, suggesting
that we have nearly as many circadian oscillators as we have cells
- these rhythms persist under constant conditions under which the organisms do not
receive time cues from the environment, and they are
therefore most likely driven by the endogenous
circadian timing system
- CLOCK and BMAL1 form heterodimers and activate
the genes encoding the Period proteins PER1 and
PER2 and the Cryprochrome proteins CRY1 and
CRY2. and once these multi-subunit complexes have
reached a critical concentration/activity they bind to
the CLOCK-BMAL1 heterodimer and thereby
attenuate its capacity to stimulate transcription
(messenger RNA [mRNA] synthesis). Therefore,
CRY and PER mRNAs and proteins are no longer
synthesised, and owing to their relatively short half-
lives, decrease in cellular concentration until the PER-
CRY complexes can no longer interfere with the
activity of CLOCK-BMAL1 heterodimers. As a
consequence, a new PER/CRY accumulation cycle
can ensue. In a second feedback loop CLOCK and BMAL1 regulate their own
circadian transcription, by activating the transcription of the genes specifying the two
nuclear receptors REV-ERBα and REV-ERBβ. REV-ERBα and REV-ERBβ recruit
the corepressor NCoR1 and the histone deacetylase HDAC3, which silence the
transcription of nearby genes
- SCN: the coordination of rest-activity cycles and the synchronisation of clocks in
peripheral cells. During the day the endogenous clock must be resilient to photic cues,
since otherwise its phase would constantly change during the light phase. Light signals
capable of phase-entrainment are not only perceived by classical rod and cone
photoreceptor cells expressing rhodopsin and conopsin, respectively, but also by
intrinsically photosensitive ganglion cells in the inner retina layer. all rods and cones
projecting to the SCN via the retinohypothalamic tract use intrinsically photosensitive
inner ganglion cells as relay stations. Hence, in the absence of these cells no photic
cues perceived by melanopsin or classical photo pigments can reach the SCN. Photic
1
, signals transmitted from the retina to SCN neurones lead to an influx of Ca2+ in
postsynaptic neurones, which activates a series of protein kinases and stimulates the
activity of cAMP response element binding protein (CREB). CREB is a transcription
factor that boosts the transcription of the Per1 and Per2 genes. The sudden increase of
PER1 and PER2 attenuates their own expression and that of the other two core clock
repressors CRY1 and CRY2. As a consequence the phase of the transcriptional rhythm
of period and cryptochrome genes is reset. Thus, Per1 and Per2 are not only integral
parts of the clockwork circuitry but also immediate early genes sensing input signals.
Immediate early genes are genes which are rapidly transcribed after an adequate
stimulus.
- Many circadian overt output cycles of the circadian timing system involve circadian
clocks in peripheral cell types. These peripheral timekeepers are thought to be
synchronised by the central pacemaker in the SCN. feeding cycles are dominant
Zeitgebers (timing cues) for the oscillators operative in most peripheral organs,
including liver, pancreas, kidney, heart, lung and skeletal muscles. Body temperature
rhythms are perhaps unexpected Zeitgebers for peripheral clocks. Glucocorticoid
hormones also participate in the synchronisation of peripheral timekeepers. They
activate the glucocorticoid receptor, which binds to glucocorticoid-responsive
elements within promoter and enhancer sequences of the Per1 and Per2 genes.
glucocorticoid hormones are used by the SCN as synchronisation signals that
antagonise nutrient-dependent signals when the phase of feeding rhythms is in conflict
with the phase of the SCN. Another blood-borne signal of proteinaceous nature has
recently been shown to govern the diurnal activity of serum response factor (SRF),
another immediate early transcription factor activating Per2 gene expression.
- The consolidation of circadian sleep-wake cycles and physiological parameters like
body temperature and heart rate may take several months to over a year. Surprisingly,
circadian sleep-wake cycles and heartbeat rhythms are clearly detectable in human
foetuses during the last weeks of pregnancy. During the human lifetime two
parameters of overt circadian rhythmicity change: the amplitude and the phase. The
amplitudes of sleep-wake cycles, hormone secretion, body temperature, and other
physiological parameters decrease with progressing age, and in extreme cases, old
human subjects can become arrhythmic. A common way of assessing the phase of
human subjects is to determine mid-sleep time on free days, that is, when there is no
pressure to get out of bed early in the morning. Based on this parameter, human
subjects can be divided into different chronotypes ranging from very early active
“larks” to very late active individuals “owls”. extreme larks and owls hardly overlap
with regard to their sleep-wake cycles. Second, the chronotype changes significantly
during the lifetime of an individual. At least in part, genetic variability may account
for the dramatic differences in human chronotypes. The genetics of such complex
behaviours is likely to be complex, in that the interaction of many different genes
influences the time of sleep-wake cycles.
- Seasonal affective disorder (SAD) is a mood disorder frequently affecting people
living in countries with low light exposures during winter time. SAD causes profound
depression with severe comorbidities. It is believed that SAD is caused by the inability
to synchronise the clock at the low light intensity of morning light in the winter
season. As the average period length of the human circadian clock is somewhat longer
than 24 hours, this leads to progressive phase delays and an associated social
discomfort. In many cases SAD can be effectively treated with light therapy.
- Shift work: cardiovascular diseases, metabolic syndrome and malignancies such as
breast and colon cancer, Breast cancer
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