Homeostasis, biorhythms and sleep Flashcards

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1
Q

What is homeostasis?

A

Maintenance of equilibrium by active regulation of internal states - multiple mechanisms control the balance, emphasising its importance to survival
Set points not fixed - many homeostatic functions show daily rhythms which maintain levels appropriate for the level of activity - efficient in energy use e.g. heart rate dropping during sleep to conserve energy

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2
Q

What is meant by a circadian rhythm?

A

Bodily functions linked to day length - light/dark cycle important but not critical e.g. during winter dark hours are longer but we still sleep roughly the same amount so the light/dark time is not exclusively determining our body functions
24hr cycle

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3
Q

What are humans and most other primates like?

A

Diurnal i.e. active during light hours

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4
Q

What is a common way of studying circadian rhythms?

A

Place a rodent on a wheel and register each revolution –> an activity rhythm
Each revolution indicated as a dark mark - see activity begins shortly before dark period each day, remaining active during the dark
When PHASE SHIFT occurs i.e. light timing altered so lights go off later each day, there was also a phase shift in activity
When constant dim light, activity gets later each subsequent day - this is a FREE-RUNNING ACTIVITY RHYTHM and indicates that the endogenous clock has a periodicity slightly more than 24hrs

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5
Q

What is meant by periodicity?

A

Interval of time between two similar points of successive cycles e.g. sunset to sunset

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6
Q

How does the internal clock get set normally?

A

Using light cues - synchronise free running rhythm to, for example, the beginning of the dark period

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7
Q

What is the phase shift?

A

This shift of activity produced by a synchronising stimulus, and the process of shifting the biological rhythm to an environmental stimulus (entrainment)
We experience phase shifts when fly between time zones e.g. sunlight might wake us several hours earlier than we were expecting

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8
Q

What is a zeitgeber?

A

Any cue that an animal uses to synchronise its activity with the environment e.g. the light/dark cycle
Because light stimuli can entrain circadian rhythms, the endogenous clock must have inputs from the visual system
In normal light/dark cycles we say the rhythm is PHASE LOCKED

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9
Q

What is the main value of having circadian rhythms?

A

Allow us to synchronise our behaviour and body states to changes in the environment - day and night are significant for survival, and having an endogenous clock allows anticipation of an event such as darkness so we can begin physiological preparations in advance
So we say these rhythms provide the TEMPORAL ORGANISATION of animal behaviour

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10
Q

What is thought to be important in establishing circadian rhythms?

A

The suprachiasmatic nucleus
If we see a lesion of the optic tract, and light info no longer reaching visual cortex, rhythm is maintained i.e. light fluctuations aren’t essential. Periodicity does change, however - free-running rhythm rather than 24hr cycle
Lesions of the SCN fully abolish the circadian rhythm, no periodicity at all, no endogenous rhythm (some daily rhythms still able to be established using external cues, but without these behaviour becomes random) and arrhythmic
The SCN is the MASTER CLOCK

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11
Q

How does light actually reach the SCN?

A

Most vertebrates have photoreceptors outside the eyes e.g. the pineal gland in amphibians is light sensitive ad helps entrain rhythms; it is a secretory gland and main source of melatonin release, hormone responsible for regulating sleep-wake cycles
In mammals, it is photoreceptors in the eye that alert SCN to changing light levels - certain retinal ganglion cells send axons along the RETINOHYPOTHALMIC pathway and at the optic chiasm these split off to synapse directly with SCN

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12
Q

What are the retinal ganglion cells of the retinohypothalmic pathway like?

A

Don’t rely on traditional rods and cones but rather contain photopigment themselves - melanopsin
So even in the absence of rods/cones (essentially blindness), behaviour could still be entrained to light
(Melanopsin is most sensitive to light freq in blue range, which is why blue light has the largest effect on human circadian systems)

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13
Q

What is the sleep rhythm like?

A

Free-running rhythm is actually around 25 hrs but entrainment to light/dark cycle maintains 24hr periodicity (mediated by SCN)

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14
Q

What is jet lag the result of?

A

Rapid shifts in light/dark cycle - takes a few days for the endogenous rhythm to re-entrain

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15
Q

What was initially thought about the onset of sleep?

A

That it was a passive process - when midbrain surgically separated from forebrain –> state of permanent sleep
It was suggested that, in absence of sensory input, the cortex becomes quiescent i.e. sleep

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16
Q

What did Moruzzi and Magoun do?

A

Electrically stimulated the midbrain and woke sleeping animals
Lesions to this area –> persistent sleep
Suggested some kind of activating system in midbrain which acts on the cortex - where there is a lack of tonic activating influence of midbrain, cortical neurones cease their firing and sleep ensues

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17
Q

How has this passive view of sleep been challenged?

A

By electroencephalographic recordings which show abundant neuronal activity in a sleeping cortex

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18
Q

What are the characteristics of SLOW WAVE SLEEP?

A

Can be further divided into several stages, all marked by slow waves of electrical potential representing widespread synchronisation of cortical activity (contrasting with the different functions different regions all fulfil separately during waking)

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19
Q

What are the 4 stages of slow wave sleep?

A

1) Drowsy/relaxed - alpha waves, distinctive rhythm regularly oscillating around 8-12Hz
2) Stage N1 (Theta waves) - time spent at alpha rhythm starts to decrease, events of smaller amplitude and irregular frequency occur along with sharp waves, heart rate slows and muscles relax
3) Stage N2 (sleep spindles) - waves of around 12-14Hz occur in periodic bursts
4) Stage N3 (delta waves) - Larger amplitude and lower freq delta waves (transition from light to deep sleep)

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20
Q

What physiological changes occur during slow wave sleep?

A

Progressive decrease in spinal reflexes, heart rate, breathing rate, brain temp and cerebral blood flow. Hormone secretion increases

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21
Q

What are the characteristics of REM sleep?

A

Occurs about an hour after SWS; quite abruptly we see pattern of small amplitude and high freq which resembles activity of an awake person but skeletal muscles completely relaxed

22
Q

When do we see sleepwalking?

A

During the REM stage of sleep, where there is INCOMPLETE INHIBITION of motor outputs by the brainstem

23
Q

What physiological changes occur during REM sleep?

A

Rapid eye movement
Irregular breathing and pulse rate
Desynchronised cortical activity (much like during waking) and it is at this stage that we vividly dream with a sense of actually “being in the dream”
Absent spinal reflexes

24
Q

What is a typical night of adult human sleep like?

A

Shows repeating cycles of 90-110 mins, recurring 4-5 times a night; the cycles change In subtle but regular manner during the night - cycles earlier on have more stage 3 but this decreases as night goes on, REM sleep stages get progressively longer later on, and a brief arousal occurs immediately following an REM period

25
Q

How does the sleep cycle change with age?

A

16wks = 24hr rhythm generated
Infant = shorter cycles and greater amount of REM than in adults
Puberty = circadian rhythm shifts so natural waking is later in the day
Older age = total amount of sleep decreases and waking periods during nightly cycles increase, also greater decline in stage 3 sleep

26
Q

Which 4 interacting neural systems underlie sleep?

A

Forebrain system - generates SWS
Brainstem (reticular formation) - activates forebrain into wakefulness
Pontine (pons, near locus coeruleus) system that triggers REM sleep
Hypothalamic system affects the other 3 regions to determine whether the brain will be awake of asleep

SO the cortex is kept awake by ascending activation from the midbrain

27
Q

What is the neurochemical basis of REM sleep?

A

Inhibitory NTs, GABA and Glycine produce powerful IPSPs in spinal motor neurons that prevent formation of action potentials - muscles are not just relaxed, but completely flaccid

28
Q

What neurotransmitters are involved in sleep?

A

5HT - Inputs inhibit midbrain activating system areas and thus promotes sleep
NA - potentially responsible for inhibiting muscle tone during REM
Dopamine - involved in general arousal
ACh - Inducing REM sleep
“Sleep-promoting substances” e.g. factor S, DSIP and melatonin (it may be that these modulate circadian rhythmicity rather than sleep per se)

29
Q

What is thought about REM sleep?

A

No one single stimulation site can promote it (but lesions to specific brainstem areas can abolish it)
It is more to do with a series of circumstances converging, so while disrupting one can disrupt everything, stimulating one isnt enough to get everything going

30
Q

What are the characteristics of insomnia?

A

Disorder of initiating or maintaining sleep, can be transient or persistent and can also be drug-induced
More common in older and female people, or users of caffeine/alcohol
Shorter sleep cycles

31
Q

What can cause transient sleep-onset insomnia?

A

Situational factors e.g. shift work, time zone changes etc

32
Q

What is sleep-maintenance insomnia?

A

Caused by drugs, respiratory issues e.g. sleep apnoea, and psychiatric factors

33
Q

What is Hypersomnia?

A

Also known as narcolepsy, this is a condition of excessive drowsiness/falling asleep
Episodes can be 5-30 mins and can occur any time during normal waking hours, multiple times a day
Tend to enter REM in first few minutes of sleep
Overwhelming tiredness in day
Many individuals show CATAPLEXY i.e. sudden loss of muscle tone, leading to collapse despite being conscious

34
Q

What is meant by sleep-wake schedule disturbance?

A

Can be transient or persistent due to factors such as shift work

35
Q

What is meant by partial arousal?

A

Sleep walking/nightmares

Sleep walking generally during phase 3, so more common in first half of night

36
Q

What is REM behaviour disorder?

A

Characterised by organised behaviour despite being asleep (more common late in adulthood while normal sleepwalking is more common in children)

37
Q

What are nightmares?

A

Long and frightening dreams that can awaken a sleeper from REM sleep
Occasionally confused with NIGHT TERRORS - these are sudden arousal from stage 3 sleep marked by intense fear and autonomic activation (more a disorder of arousal in which feelings more likely to be remembered than imagery)

38
Q

What are all sleep disorders associated with?

A

Factors such as anxiety and psychological disturbance/drug taking

39
Q

What are 3 examples of somnogenic drugs i.e. hypnotics?

A

Morphine - widely used sedative
Barbiturates - and anaesthetics, produce slow waves resembling those in SWS (may utilise natural brain networks that promote sleep); some are glutamate antagonists so block excitation, while virtually all anaesthetics are GABA agonists boosting inhibitory effect in forebrain
Benzodiazepines - widely used as anxiolytics

40
Q

What do none of these drugs do?

A

Actually induce natural sleep patterns - there is a reduced amount of REM (which then also increases in drug withdrawal as a rebound effect –> vivid dreams)
Increased drowsiness and memory gaps during waking hours - “sleep drunkenness”

41
Q

What are 2 options to produce more natural sleep patterns?

A

Melatonin - weakly hypnotic and helps with jet lag
Tryptophan - Serotonin precursor, weakly hypnotic, produces more natural sleep

Neither of these act immediately so are thought to act on circadian rhythmicity rather than sleep directly

42
Q

What happens when we eat and digest our food?

A

Insulin released to make use of the newly available glucose (brain is only part of body not reliant on insulin to meet energy demands)

43
Q

What does insulin do?

A

Enables immediate utilisation of glucose and also prompts conversion of excess glucose to glycogen (stored in liver and muscles)

44
Q

What does the liver do?

A

Communicates with pancreas - info from glucodetectors in liver travels via vagus nerve to nucleus of solitary tract in brainstem –> relayed to hypothalamus, indicating circulating glucose levels and contributing to hunger
Lower levels of insulin indicate lower levels of circulating glucose, and thus greater motivation to eat more (however, very high insulin doesn’t automatically signal low hunger - could lead to hypoglycaemia due to over-conversion of glucose into glycogen)

45
Q

What is known for certain about food and energy regulation?

A

Hypothalamus is a key player - the arcuate nucleus contains a highly specialised appetite controller governed by circulating levels of a variety of hormones aside from insulin
Usually has an inhibitory effect on food intake

46
Q

What are 2 other hormones involved in food and energy regulation?

A

LEPTIN - peptide hormone produced by fat cells; brain monitors circulating levels to measure energy reserves in the form of fat (defects in leptin prod/sensitivity leads to false underestimation of body fat –> over-eating); indicates current body composition and affects appetite system over LONGER TERM
GHRELIN - Released by endocrine cells of stomach, affects growth hormone secretion, powerful appetite stimulant (circulating levels rise during fasting); a mechanism of obesity could be ghrelin system unresponsive to feeding, thus always slightly elevated and prompting continual hunger; provides rapid, hour-to-hour hunger signals

47
Q

What does the appetite system rely on?

A

Two sets of arcuate neurons with opposing effects:
NPY/AgRP neurons - stimulate appetite while reducing metabolism –> weight gain
POMC/CART neurons - inhibit appetite and increase metabolism

48
Q

What effects do leptin and ghrelin have on the arcuate neurons?

A

Leptin - activates POMC/CART (suppressing hunger), and inhibits NPY/AgRP
Ghrelin doesn’t really act on POMC/CART, but activates NPY/AgRP

49
Q

In addition to appetite signals from the hypothalamus converging on the nucleus of the solitary tract in the brainstem, what other info surrounding appetite signals and feeding behaviour can be integrated?

A

Stomach distension - signals transmitted via spinal and cranial nerves
Information about nutrient levels conveyed directly by vagus nerve e.g. Cholecystokinin released in gut after feeding, acting directly on receptors of the vagus nerve to inhibit appetite

50
Q

What is the Hunger Loop?

A

Arcuate nucleus inhibitory effect on food intake
Ghrelin released by empty stomach blocks this inhibitory effect
Food taken in
When stomach full, block on inhibition removed

51
Q

Describe the satiety loop

A

Food intake leads to stomach distention and assessment of food content e.g. whether correct calorific value
CCK and distension activate vagus nerve, which signals to solitary tract nucleus of brainstem
This activates the arcuate nucleus and inhibits further food intake