13) Rhythmic Behaviors and Sleep Flashcards
What are the 4 measurements for neural timing systems that affect biological processes or behaviors?
What cues influence our biorhythms? (2)
- Ultradian -Feeding cycles
- Circadian - daily, day-night rhythms
- sleeping cycles
- blood pressure, body temp., metabolic rate, cortisol levels
- Infradian - >day rhythms
- female menstrual cycles
- Circannual - yearly rhythms
- Migratory cycles
- hibernation
Our biorhythms are influenced by both internal cues - biological clocks on free-running rhythms and external cues - Zeitgebers (such as light)
Internal cues:
Define free-running rhythms
External cues:
Define Zeitgeber
What are zeitgebers disturbed by and what can this lead to?
Free-running rhythms - body’s own rhythm in the absence of all external cues
Zeitgeber - environmental cue to entrain a biological rhythm
- Ex: Light
Our zeitgebers can be disturbed by:
- Light pollution
- Long distance travel
- graveyard shift workers
These can lead to fatigue, jet lag, obesity, diabetes, stress, emotional distress
What is our master biological clock? What structure in our brain is regulating our biological cycles?
How did we find out this was the structure?
Superchiasmatic Nucleus (SCN) - located in the Hypothalamus
- Lesioning the SCN = animals still eat, drink, exercise and sleep BUT at random times.
- Neurons here are more active during the light cycle
- Rhythmic pattern is an intrinsic property
- SCN Rhythm is genetic
SCN rhythm is entrained usually by…?
Specialized …. hyperpolarize or depolarize to light?
What photopigment do these specialized cells have?
Also entrained by…?
SCN rhythm is usually entrained by light
- Specialized photosensitive RGCs (pRGCs) depolarize to light
- Contain the photopigment melanopsin
- Make up 1-3% of all RGCs spread across retina
Also entrained by exercise, feeding, arousal, etc. from other inputs into the SCN
How do SCN pacemakers drive slave oscillators? (Directly and Indirectly but how)
Example?
- Directly - axonal connections to other brain regions
- Indirectly - hormonal release from SCN themselves or by controlling hormonal release from other areas (pituitary or pineal gland)
EXAMPLE: Pineal gland release of melatonin during dark phase
- Promotes sleep and rest
- Supports parasympathetic system “rest and digest”
- inhibits hamster’s gonads and they shrink (circannual)
Why do we sleep?
How do we measure sleep?
We sleep to:
- Conserve energy - reduce metabolism and temp.
- Helps with memory consolidation
Sleep is a distributed process throughout brain
An EEG electroencephalogram is used
- Electrodes pasted onto standard locations of the skull record brain-wave activity
What are the stages of sleep?
What is the sleep-wake cycle largely controlled by?
- Awake
- Non-REM sleep
- 4 stages with decreasing frequency and increasing amplitude
- Stage 1 = shallow; Stage 4 = deep sleep (slow wave sleep)
- REM sleep - EEG looks like you are awake
The sleep wake cycle is largely controlled by the brainstem sending signals to the rest of the brain
Cycle through stages of sleep every … min?
Characteristics of Non-REM and REM sleep?
Cycle through stages of sleep every 90 min.
Non-REM
- Body temp. and blood flow decreases
- Heart Rate and respiration decreases
- Some muscle tone
- Tossing/turning, talking, sleepwalking
- little dreaming
REM
- Body temp. regulation stops = start to drift towards room temp.
- Heart rate and respiration increases
-
Atonia - No large muscle tone
- Descending brainstem projections inhibit motor neurons
- Dreaming
Does racking up sleep debt have effects? Short term, long term? What are they?
No long term effects of occasional sleep deprivation
Chronic sleep deprivation
- Impaired regulation of homeostatic processes
- Impairment in immune function
What are the 4 systems that promote wakefulness and their corresponding neurochemicals?
What nuclei modulate these systems and how? Where are they located?
- Cholinergic nuclei
- ACh
- Raphe nuclei
- 5-HT or Serotonin
- Tuberomamillary nucleus of hypothalamus
- Histamine
- Locus coerculeus
- NE
Nuclei that modulate all these above systems: Lateral hypothalamic area (orexin neurons) and Ventrolateral preoptic nucleus (VLPO)
These nuclei regulate sleep-wake by modulating thalamocortical projections
- VLPO is inhibitory
- Orexin (hypocretin) neurons are excitatory
Located above SCN
What is narcolepsy? How much of the population does it affect?
What structure is altered in narcoleptic type 1 people?
Differences between narcolepsy type 1 and type 2
Narcolepsy is the onset of irresistible attacks of sleep at any time. Fragmented sleep with increased REM (pink in image).
90% of Orexin neurons are lost in people with narcolepsy I
Narcolepsy type 1
- Cataplexy = sudden limb paralysis often triggered by strong emotions
- Brainstem nuclei inhibit motor neurons during REM
- But Amygdala can drive this inhibition without orexin
- Brainstem nuclei inhibit motor neurons during REM
- CSF orexin concentration low
- 0.014% of population
Narcolepsy type 2
- No cataplexy
- CSF orexin concentration is normal
- 0.064% of population