Chapter 13 Flashcards
Biorhythms
cyclical changes in behaviour or bodily functions
Period of a cycle
Time required to complete one cycle
Circannual rhythms
Period of about a year
Migratory and mating cycles
Infraradian rhythms
Periods greater than a day but less than a year
Monthly or seasonal
Menstrual cycle
Circadian rhythms
Daily period
Sleep-wake
Ultraradian rhythms
Periods of less than a day
Eating
Endogenous origin of circadian rhythms
Produced by a biological clock that synchronizes behaviour to the passage of a day
Allows us to anticipate and prepare for events
Measuring circadian rhythms
Running wheels for animals
Sensors in smart watches and phones
Free-running rhythms
Rhythm of the body’s own devising in the absence of all external cues
About 24.1-24.2 hours in humans
Zeitgebers
Environmental events that entrains biological rhythms
eg light
Entraining a circadian rhythm
When a Zeitgeber resets the biorhythm
Examples of nonphotic zeitgebers
Temperature, activity, mealtimes, work, social events
Light pollution
Extent to which artificial lighting floods our environments and disrupts circadian rhythms
Jet lag
Fatigue and disorientation resulting from rapid travel through time zones
Exposure to a changed light-dark cycle
Suprachiasmatic biological clock
Region of the hypothalamus that acts as the master biological clock
Keeps time
Other areas involved in the biological clock (other than the SCN)
Intergeniculate leaflet
Pineal gland
Keeping time in the SCN
Timing of the rhythm depends on groups of cells that synchronize their activity
SCN receives info about light through the ________
Retinohypothalamic tract
Melanopsin detects the blue ligh
Why is there still an entrained biorhythm in blind people?
The information comes from the retinohypothalamic tract not rods or cones
Two parts of the SCN
the core: activated by the retinohypothalamic tract, not rhythmic
the shell: entrained by the core cells. rhythmic
Pathway of nonphotic events influencing the SCN
projections of the intergeniculate nucleus of the thalamus and the raphe nucleus of the serotenergic activating system
Immortal time
the rhythm of the SCN cells is not learned it is genetically programmed
Feedback loop of the biological clock
2 proteins combine to form a dimer, the dimer then inhibits the genes that made the original proteins
Then the dimer degrades and the process begins again
Increases and decreases in protein synthesis each day produce the cellular rhythm
light, the SCN, and slave oscillators
Light entrains the SCN, the SCN then drives a number of slave oscillators that are responsible for the rhythmic occurrence of 1 activity
SCN is not directly responsible for producing behaviour but exerts control over the whole body
SCN control over melatonin
Sends indirect messages to autonomic neurons in the spinal cord to inhibit pineal gland from making melatonin
Melatonin
Promotes rest during the dark portion of circadian cycle
Glucocorticoids
Controlled by SCN
Promotes arousal during the light portions of circadian rhythms
Hamsters breeding activity and melatonin
During shorter days there is more melatonin release and the gonads shrink, less sexual behaviour
During longer days there is less melatonin release and the gonads grow, stimulates sexual behaviour
Chronotypes
Individual variation in circadian activity
Likely produced by differences in SCN neurons and the genes that influence them
Circadian period influence on emotional behaviour
Time-of-day effect may account for emotional responses to daily events independent of the events themselves
Eg: night time fear independent of lighting
3 parts of measuring sleep
Brain activity: EEG
Muscle activity: EMG
Eye movement: EOG
REM sleep (R sleep)
faster brain wave pattern, rapid eye movement
Atonia: other than twitches muscles are inactive
Non-REM sleep (N sleep)
Slower waves with large amplitude
Beta rhythm
When a person is awake
Small amplitude and high frequency
Alpha rhythm
Larger brain waves when people relax and close their eyes
Theta waves
Low amplitude with a mixed frequency
N1 sleep
Sleep onset
Theta waves
Muscles somewhat active
N2 sleep
Asleep, theta waves
Periodic sleep spindles: brief periods of high frequency waves
K-complexes: well-defined sharp waves followed by slow waves
N3 sleep
Deep sleep delta rhythms
Some muscle activity
Eyes don’t move
Delta rhythms
Large amplitude slow waves during deep sleep
A typical sleep
depth of sleep changes throughout the night
Non-REM- REM sequence lasts about 90 minutes
First half dominated by N sleep, second by R sleep
Vivid dreaming
Occurs during R sleep
Take place in real time
Freud’s theory of dreaming
Dreams are the symbolic fulfillment of unconscious wishes especially sexual ones
Manifest content: the dream
Latent content: the true meaning of the dream
Carl Jung’s theory of dreaming
Dream symbolism signifies distant human memories lost to conscious awareness
the collective unconscious
Activation synthesis theory of dreaming
During a dream the cortex is bombarded by signals from the brainstem
Cortex then generates images, actions, emotions from personal memory
No intrinsic meaning
Bottom-up approach
Dreams as a coping strategy
Top-down approach
Dreams are biologically adaptive and lead to advances coping strategies for threatening events
Problem solving during sleep
Sleep as a biological adaptation
Conserving energy when food is scarce, metabolism decreases
Prey sleep less than predators
Basic-rest activity cycle
90 minute temporal packets of activity
Basic-rest activity cycle
90 minute temporal packets of activity
Cannot be turned off
Sleep deprivation
Individual differences in consequences
Multiple functions altered
Go into micro sleeps
Sleep after R-sleep deprivation
Increased tendency to enter R sleep in subsequent sleep sessions
R-sleep rebound: more than usual amount of R sleep in first available sleep session
Labile phase of memory
As memory is encoded
Fragile and must compete with existing memories
Storage phase of memory
Relatively permanent representation, structural changes in the nervous system
May be better formed in sleep
Recall phase of memory
Puts memory to work and integrates in into existing memory stores
We replay during sleep
Multiple-process theories of sleep and memory
Propose that different kinds of memories are stored during different sleep states
Explicit memory stored during N sleep
Motor memory during R sleep
Sequential process theories of sleeping and memory
Propose that different kinds of memory are stored during different ways during different sleep states
Memory is refined during N sleep and storied during R sleep
Storage process theories of sleeping and memory
Propose that brain regions that handle different kinds of memory during waking continue to do so during sleep
Synaptic homeostasis theory of sleeping and memory
Slow waves during sleep allow synaptic activity to shift to a resting state where they are more plastic and available to be engaged in the next waking period
During N-sleep they are in optimal condition to undergo structural changes without interference
Synapses involved in new learning experiences are more metabolically active
N sleep and explicit memory
Memory of food searching experiences in rats are replayed and stored during N sleep
Memory for place stored in N sleep
R sleep and implicit memory
Participants dream about motor skill leaning experience
Suggests replay during R sleep strengthens task memory
Study of sleep in chickens
Chickens alternate sleep in each hemisphere
Spatial memory formation is stored mainly in the right hemisphere
After a learning experience the right hemisphere showed more sleep than the left
Reticular activating system
Large reticulum that runs through the centre of the brainstem
Associated with sleep-wake behaviour and behavioural arousal
Normal waking up occurs when the RAS becomes active
Basal forebrain
Contains cholinergic cells that secrete acetylcholine onto cortical neutrons to stimulate a waking beta rhythm
Associated with alert but immobile attention
Median raphe
Midbrain structure that contains serotonin neutrons
Axons project to the cortex to stimulate a beta rhythm
Waking EEG associated with movement
Peribrachial area
Group of cholinergic neurons that contribute to R sleep in the dorsal brainstem
When destroyed R-sleep is reduced
Initiates R sleep by activating the medial pontine reticular formation
Medial pontine reticular formation (MPRF)
Activated by the peribrachial area to produce R sleep
Excites the basal forebrain cholinergic neurons
Excites the brainstem motor nuclei to produce eye movements and twitches
Produces atonia through the subcoerulear nucleus
Subcoerulear nucleus
Receives input from the medial pontine reticular formation
Excited the magnocellular cells of the medulla which sends projections to the spinal cord motor neurons to inhibit them and cause atonia
Insomnia
Inability to fall or stay asleep
Hypersomnia
Difficulty waking up or staying awake
Inability to sleep
Symptom of a number of conditions
Lifestyle choices, shift work, jet lag
Stress
Anxiety and depression
Sleeping pills
Promote N sleep but deprive R sleep
Drug dependence insomnia if they stop taking them
Fatal familial insomnia
Almost complete inability to sleep caused by a gene mutation
Death after a number of months
Sleep apnea
Inability to breath during sleep, have to wake up to breath
Causes daytime sleepiness
Sleeping beauty syndrome/Kleine-Levin syndrome
Recurring bouts of excessive sleeping
Sleep episodes of 15-20+ hours
Narcolepsy
Symptoms include sleep paralysis, hypnagogic hallucinations
Immediately fall into R sleep
Can have a genetic basis
Sleep paralysis
Atonia and dreaming that occur when a person is falling asleep or waking up
Cataplexy
Atonia of R-sleep that occurs when a person is awake and active
Loss of muscle tone and then fall to the ground
Hypnagogic hallucinations
Dream like events during cataplexy
Seeing imaginary creatures or voices
