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2007PSY > Week 7 - topic 1 > Flashcards

Week 7 - topic 1 Flashcards

1
Q

Sleep research

A
  • EEG (brain waves)
  • EMG (muscles)
  • EOG (eyes)
  • Heart rate
  • Respiration
  • Skin conductance
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2
Q

Sleep EEG

A

(a) If the cells are active at about the same time, their electrical messages recorded by EEG are synchronized and appear as a large, clear wave in the EEG data.
(b) If neurons are active at different times, their electrical messages are desynchronized and appear as small, chaotic waveforms without a clear pattern in the EEG data

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3
Q

Stages of sleep

A

EEG records have particular patterns of waveform activity that correspond with different periods (stages) of sleep:

  1. Wakefulness stage (stage W)
  2. Non-REM sleep stage 1
  3. Non-REM sleep stage 2
  4. Non-REM sleep stage 3
  5. REM stage seep (Stage R)

REM sleep = rapid eye movement sleep

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4
Q

Waking stage

A

ALPHA – regular, medium frequency waves of 8–12 Hz
Associated with resting wakefulness

BETA - irregular, mostly low amplitude waves of 13–30 Hz. Desynchronised neural activity that is associated with increased alertness and attention.

*look up image

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5
Q

Stage 1 (NREM 1)

A
  • A transition between sleep and wakefulness
  • Presence of theta activity (3.5-7.5 Hz) = more synchronized neural activity
  • Experience hypnic jerks
  • Lasts about 10 minutes

*look up image

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6
Q

Stage 2 (NREM 2)

A

• Irregular neural activity but there are periods of Theta
activity - Sleep spindles and K complexes
• Might report that they had not been sleeping

*look up image

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7
Q

Stage 3 (NREM 3)

A
  • Slow-wave sleep
  • High amplitude delta activity (< 3.5Hz) – synchronized
  • Deepest stage of sleep
  • Lasts about 1 hour

*look up image

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8
Q

REM sleep (Stage R)

A
  • Abrupt change, EEG becoming desynchronized
  • Rapid eye movement
  • Paralyzed (loss of muscle tone)
  • Dreams
  • Easily awoken by meaningful stimuli
  • look up image
  • look up images: sleep cycles (1 and 2)
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9
Q

Brain activity in REM and dreaming

A
  • Cerebral blood flow = proxy for brain activity
  • Blood flow is high in the extrastriate cortex (visual)
  • Blood flow is low in the striate (primary) visual cortex and prefrontal cortex (PFC)

*look up image

  • Lucid dreaming = awareness that you are dreaming
  • Could be an active PFC that is normally inactive during REM
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10
Q

Brain activity in SWS

A
  • We can experience dream like imagery in SWS and brain activity accompanies it
  • Regional cerebral blood flow is generally decreased throughout the brain in SWS compared to waking
  • However, localized increases of cerebral blood flow in visual and auditory cortexes
  • Blood flow to thalamus and cerebellum is decreased
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11
Q

Effects of sleep deprivation

A
  • Several cognitive functions are disrupted - especially tasks that require attention or vigilance
  • Obesity
  • Diabetes
  • Hypertension
  • Stroke
  • Depression
  • Impaired immune function
  • Increased pain
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12
Q

Fatal familial insomnia

A
  • inherited neurological disorder is a progressive insomnia that results in damage to portions of
    the thalamus and eventually death.
    • Deficits in attention and memory and dreamlike confused state
    • Reductions in sleep spindles and K complexes
    • Eventually SWS disappears and only REM remains.
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13
Q

Physical activities and sleep

A

• It has been proposed that SWS might be needed to
recover from a day of physical activity/physiological
functioning.
• Therefore, sleep and exercise should be related
• Mixed evidence for the relationship between sleep and exercise
-> Some studies suggest there is a positive relationship
between sleep quality/quantity and physical exercise
-> Other studies suggest no changes. E.g. Sleep of
someone who suffered spinal paralysis has similar
sleep to control participants
• Thus, the primary function of sleep is unlikely to be physical restoration

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14
Q

Cognitive functioning and sleep

A
  • If the primary function of SWS is to permit the brain to rest and recover from cognitive activity, then we would expect someone to sleep more after an intense day of cognitive activity
  • Research shows SWS increases after a day or weeks of intense cerebral activity (e.g. working memory training)
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15
Q

How do our daily activities influences REM sleep?

A

• REM sleep is a time of intense physiological activity, so likely has different functions to SWS
• REM sleep is controlled by a regulatory mechanism
-> A Deficiency in REM sleep is made up later
-> Called the rebound phenomenon
• Highest proportion of REM sleep is during the most active phase of brain development, infancy and childhood
• REM sleep facilitates learning

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16
Q

Sleep and memory consolidation

A
  • there are two types of long term memory:
  • > Declarative memory (explicit memory) - facts and memory that can be explicitly recalled (for example, a birthday).
  • > Nondeclarative memory (implicit memory) - procedural skills that don’t require conscious thought (for example, driving or riding a bike)
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17
Q

REM sleep and consolidation

A

1) REM sleep helps to consolidate nondeclarative memory
- In a study by Mednick (2003) participants had to learn a visual discrimination task involved nondeclarative memory.
- They were then tested on the task 10 hours later.
- Some participants took a nap during the day. Some experienced SWS and some experienced both SWS and REM sleep. Some participants did not take a nap.
- The results in the test 10 hours later *look up image

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18
Q

SWS sleep and memory consolidation

A
  • In a study by Tucker et al. (2006), participants were trained on both a declarative task (learning a list of words), and a nondeclarative task (tracing a picture looking at a mirror image of it).
  • Some participants took a one hour nap that involved only SWS. Some participants did not take a nap.
  • Performance was tested 6 hours later *look up image
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19
Q

A potential regulator of sleep

A
  • Brain produces a sleep-promoting chemical that accumulates during wakefulness and is destroyed during sleep
  • Adenosine, a type of neuromodulator, promotes sleep (Benington et al., 1995)
  • Astrocytes maintain a small amount of nutrients in the form of glycogen
  • When there is increased brain activity, glycogen is converted into neuron fuel
  • When you are awake for a long time, there are decreased levels of glycogen in the brain
  • This causes an increase in extracellular adenosine
  • Increased adenosine promotes sleep
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20
Q

Glycogen and adenosine - prolonged wakefulness and sleep deprivation

A
  • If wakefulness is prolonged, adenosine accumulates, inhibiting neural activity and works as a sleep promoting substance
  • Inhibiting neural activity can also produce the cognitive and emotional effects seen during sleep deprivation
  • During SWS neurons in the brain rest, and the astrocytes renew their stock of glycogen.
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21
Q

Caffeine and adenosine receptors

A
  • caffeine can make you stay awake longer than what you normally would (i.e. lowers feelings of sleep deprivation) and it also blocks deep sleep (SWS)
  • when you have a cup of coffee, it blocks the adenosine receptors in your brain.
  • > Generally speaking, increased levels of adenosine signal that you should have a rest - it helps to initiate sleep. so, if you block adenosine, then you will stay awake longer
22
Q

Five neurotransmitters involved in arousal

A
  1. Acetylcholine
  2. Norepinephrine
  3. Serotonin
  4. Histamine
  5. Orexin

*look up image

23
Q

Acetylcholine (ACh)

A
  • Key neurotransmitter involved in arousal
  • Acetylcholine is released from the cortex and hippocampus
  • Ach high during waking and REM sleep and low during SWS
  • Acetylcholingeric agonists increase signs of cortical arousal and antagonists decrease signs of cortical arousal
24
Q

Norepinephrine (NE)

A

• Catecholamine (subtype of monoamine) agonists produce arousal and sleeplessness (e.g. amphetamine)
• These effects are mediated by noradrenergic system of the locus coeruleus (LC) of the dorsal pons which projects widely throughout the brain.
• Noradrenergic LC neurons increase vigilance
• High during wakefulness
- lowers during SWS and even moreso during REM

25
Q

Serotonin (5-HT)

A

• 5-HT plays a role in activating behaviour
• Almost all of brain’s serotonergic neurons are in the raphe nuclei of the reticular formation and project widely throughout the brain.
• Stimulation of the raphe nuclei causes locomotion and cortical arousal
• PCPA (which prevents 5-HT synthesis) reduces cortical arousal
- lowers from wakefulness to drowsy to SWS to REM
- instant increase after REM sleep

26
Q

Histamine

A
  • Histaminergic neurons are located in the tuberomammillary nucleus (TMN) of hypothalamus
  • Projections to the cortex directly increases cortical activation and arousal
  • Projections to ACh neurons in the basal forebrain and dorsal pons. Increases the release of acetylcholine in the cortex – thus indirectly increasing arousal
  • High during waking, low during SWS and REM
27
Q

Orexin

A
  • Orexin = hypocretin (peptide neurotransmitter)
  • Lateral hypothalamus contains cell bodies of neurons that secrete orexin
  • Projects to almost every part of the brain with an excitatory effect
  • High firing rate of orexin neurons during alert or active waking, especially exploratory activity. Low rate of firing during SWS and REM Sleep
28
Q

Preoptic area

A
  • The preoptic area (part of the hypothalamus) is involved in the initiation of sleep
  • As such, preoptic neurons = sleep neurons
  • Most sleep neurons are located in the ventrolateral preoptic area (vlPOA)
  • Sleep neurons are connected to the arousal neurons
  • When sleep neurons become active, they secrete GABA (inhibitory NT), and they suppress the activity of the five arousal neurons throughout the brain.
  • Remember, the activity of the five arousal neurons causes cortical activation and behavioural arousal. So these regions have to be inhibited for sleep
29
Q

Preoptic area - inhibition

A

• The sleep neurons in the preoptic area also receive
inhibitory inputs from some of the same regions they
inhibit (TMN, raphe nuclei and the locus coeruleus).
• So sleep neurons are inhibited by histamine, serotonin and norepinephrine.
= MUTUAL INHIBITION
• Mutual inhibition might play a role in establishing sleep-waking periods, similar to a type of electronic circuit called a flip-flop.
• Flip-flop: either sleep neurons are active and inhibit the arousal neurons, OR, the arousal neurons are active and inhibit the sleep neurons.

30
Q

Flip-flop circuits

A
  • Flip-flop circuits have a great advantage in that when it changes states, it happens really quickly.
  • You want to be either asleep or awake, not somewhere in between.
  • However, flip-flops can become unstable - people with Narcolepsy who have damage to orexinergic system exhibit this characteristic.
  • They find it difficult to stay awake when nothing interesting is happening, and have trouble remaining asleep for extended periods
31
Q

The role of orexin in homestasis

A
  • Orexin neurons receive a signal from the part of the brain that controls rhythms of sleep and waking (i.e. the circadian part)
  • Orexin neurons receive signals from the parts of the brain that monitor our nutritional state. Being hungry activates the orexin neurons, helping us to stay awake so that we can find food (i.e. homeostasis part).
  • Finally, orexin neurons receive inhibitory input from the vIPOA. This means that sleep signals that arise from the accumulation of adenosine can eventually overcome excitatory input to orexinergic neurons such that sleep can occur (allostatic factors)
32
Q

Neural control of transition to REM

A

We have two sides to the flip-flop. The REM-ON state and the REM-OFF state:

  • When we fall asleep, orexin releasing neurons stop being active. In turn, there is less excitatory input being sent to the REM-OFF region of the brain
  • Next, norepinephrine releasing and serotonin releasing neurons gradually decrease activity. Again, this means that there is less excitatory input being sent to the REM-OFF region.
  • Steps 1 and 2 cause the flip-flop to turn to the REM-ON state. This change in state causes REM sleep to begin
33
Q

REM-ON and REM-OFF regions of the brain

A

REM-ON = REM-ON neurons are found in the sublaterodorsal nucleus (SLD) and are active during REM sleep.

REM-OFF = REM-OFF neurons are found in the ventrolateral periaqueductal gray matter (vIPAG)

  • The REM-ON and REM-OFF regions are connected via inhibitory (GABA releasing) neurons
  • Stimulating REM-ON neurons produces REM sleep, and stimulating REM-OFF neurons suppresses REM sleep
34
Q

Insomnia

A

Primary Insomnia: Difficulty falling asleep after
going to bed or after awakening during the night

Secondary Insomnia: Inability to sleep due to a
mental or physical condition

Hard to diagnose due to self-report

35
Q

Treating insomnia

A

Non-Pharmacological: Cognitive behaviour therapy (CBT), progressive relaxation techniques, and changes in sleep hygiene (e.g. waking up and going to sleep at same time each day)

Pharmacological: Hypnotics (GABA agonists),
benzodiazepines, and over-the-counter antihistamines
• Chronic use can lead to tolerance and rebound insomnia (return and increase in insomnia)

36
Q

Narcolepsy

A 
Narcolepsy is a neurological disorder characterized by sleep (or some of its components) at inappropriate times
Symptoms
1. Sleep attacks
2. Cataplexy
3. Sleep paralysis
37
Q

Sleep attacks - narcolepsy

A
  • Primary symptom of narcolepsy
  • Overwhelming urge to sleep
  • Generally lasts for 2–5 minutes
38
Q

Cataplexy - narcolepsy

A
  • Muscle weakness, could lead to temporary paralysis
  • Muscle paralysis is a part of REM sleep. Here, it happens at the wrong time due to massive inhibition of motor neurons in the spinal cord
  • Precipitated by strong emotional reactions or sudden physical effort
39
Q

REM Sleep paralysis

A

• REM sleep paralysis intruding into waking such as
just before or just after normal sleep
• Inability to move just before the onset of sleep or on
waking
• Cognitive component of REM sleep intruding:
-> Possibility of dreaming while lying awake, paralyzed,
called hypnagogic hallucinations

40
Q

Physiological basis and treatment of narcolepsy

A
  • Caused by a hereditary autoimmune disorder
  • People born with orexin neurons, but the immune system attacks neurons in teenage years
  • Strongly influenced by unknown environmental factors
  • Symptoms of narcolepsy treated with medication
  • Usually stimulants to lower sleep attacks or antidepressant drugs that facilitate serotonergic and noradrenergic activity to help alleviate cataplexy and sleep paralysis
41
Q

REM sleep behaviour disorder

A
  • During REM sleep, neurons in our motor cortex and subcortical motor areas are extremely active.
  • However, as you know, during REM our muscles are also paralysed.
  • It therefore seems likely that people would actually act out their dreams if their muscles were not paralysed.
  • In REM Sleep behaviour disorder an individual does not become paralyzed during REM sleep and thus acts out their dreams.
  • REM Sleep behaviour disorder appears to be neurodegenerative disorder with a genetic component. - In fact, it has been linked to Parkinson’s Disease. It is normally treated with benzodiazepines which bind to GABAA receptors, and enhance inhibitory processes throughout the brain
42
Q

Slow wave sleep problems

A
  1. Bedwetting
  2. Sleepwalking
  3. Night Terrors
    All most frequently occur with children
43
Q

Sleep related eating disorder

A

A disorder in which the person leaves his or her bed and seeks out and eats food while sleepwalking, usually without a memory for the episode the next day
• Can be treated with dopaminergic agonists
• Provoked by the use of benzodiazepines

44
Q

Suprachiasmatic Nucleus (SCN)

A

The Suprachiasmatic Nucleus (SCN) contains a
biological clock that is responsible for organizing
many of the body’s circadian rhythms.

45
Q

Role of Superchiasmatic Nucleus in circadian rhythms

A
  • The SCN receives light information from the environment and uses it to entrain behaviours to a 24- hour light/dark cycle
  • Provides the primary control over the timing of sleep cycles
  • If SCN is damaged, circadian control of sleep impacted, but not homeostatic control of sleep
46
Q

Light and the SCN

A
  • Light is the main zeitgeber for our activity cycle – therefore, the SCN receives information about light from the visual system
  • The visual system projects from the retina to the SCN via the retinohypothalamic pathway
47
Q

Melanopsin

A
  • The photoreceptors in the retina that provide photic information to the SCN are neither rods nor cones
  • There appears to be a special photoreceptor that provides information about ambient light levels and helps to entrain circadian rhythms
  • Melanopsin is a photopigment present in ganglion cells that appears to be responsible for this.
  • Melanopsin containing ganglion cells have their axons terminate in the SCN
48
Q

SCN control of sleep and waking

A
  • Efferent axons of the SCN responsible for organising sleep cycles terminate in the subparaventricular zone (SPZ)
  • The ventral SPZ projects to the dorsomedial nucleus of the hypothalamus (DMH), which in turn, projects to several brain regions:
  • Inhibitory connections to the vlPOA which inhibit sleep
  • Excitatory connections to the orexinergic neurons of the hypothalamus that promote wakefulness
  • Activity of these neurons varies across the day/night cycle
49
Q

The nature of the clock

A
  • SCN contains a physiological mechanism that parses time into units
    • Circadian rhythms in the SCN are produced as protein, which rises to a certain level in the cell until the maximal level is reached, creating a feedback loop
    • Time parsing is regulated by how long it takes to produce and degrade a set of proteins.
50
Q

Pineal gland and circadian and yearly rhythms

A
  • In response to input from the SCN, the pineal gland secretes melatonin during the night.
  • The melatonin then acts back on various structures in the brain (including the SCN) and controls hormones, physiological processes and behaviours that show seasonal variations.
  • For instance, during very long nights (i.e. in the winter), lots of melatonin is secreted, and then it makes animals go into the winter phase of their annual cycle. During short nights, less melatonin is secreted.

2007PSY (24 decks)

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