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Physio Psych
Sleep
Term | Definition |
---|---|
polysomnograph | EEG-brain activity EOG-eye movements EMG-muscle tone |
Wake State | Beta Waves |
Sleepy | Activity Slows, indicated by alpha waves |
Stage 1 Sleep | Slower Theta Waves, easy to wake |
Stage 2 Sleep | Characterized by sleep spindles and K-complexes. Harder to wake. Most sleep is spent in this stage |
Slow Wave Sleep (SWS) Stages 3-4 | Characterized by slow delta waves. Very hard to wake in this stage |
REM Sleep | -Look similar to awake beta waves, easier to wake up than SWS. --Woken up from this stage often reports dreaming. -Plays a large role in consolidation of procedural memories -Intensity increases after learning a range of tasks -Fast spiking EEG waves |
Beta waves-desynchrony | individual is attentive to the environment, aroused alpha waves-eyes closed, quiet rest |
Theta waves-brain | becoming more synchronized-between sleep and wakefulness-eyelids open from time to time, eyes roll up and down |
Sleep Spindles | short bursts of activity 2-5 times a minute throughout sleep stages 1-4; important for memory consolidation-more spindles correlated with better scores on intelligence tests |
the number of cycles increases | periods of SWS are shorted (or eliminated altogether), while REM periods increase in length and frequency. |
adaptive theory of sleep | posits that animals developed distinct sleep patterns that were beneficial to survival. |
Adaptive inactivity | the idea that inactivity could be beneficial to survival. |
Strong arguments for adaptive inactivity | -Hibernation during the winter, when food is not available. -Some species, such as bats, only hunt during twilight, so sleeping the rest of the time possibly protects them from predators. |
homeostatic theory of sleep regulation | the primary purpose of sleep is to provide “rest and renewal.” the idea that the body builds up a pressure to sleep as time awake increases. This pressure, or sleep pressure, gets stronger the longer someone stays awake and decreases during sleep. |
Sleep deprivation | -negative impact on many functions, such as cognition, motor performance, emotional state and immune system function. -Brain metabolism slows, allowing for the removal of metabolic waste products and other toxic substances. |
Sleep rebound effect | sleep deprivation leads to increased sleep time during the next opportunity for sleep-but only about 30% of lost sleep is made up. |
Rebound Sleep | SWS and REM sleep are prioritized |
Randy Gardner | Stayed awake for 11 days |
Important Sleep | Sleep also plays an important role in learning and memory-especially memory consolidation, or the process of making new, unstable memories into more stable memories integrated into the brain’s neural networks. |
ARAS | -Contributes to arousal and wakefulness -Group of nuclei that are necessary for different aspects of arousal, wakefulness and consciousness |
The tegmental nuclei (PPTg and LDTg) and basal forebrain; acethycholine projections; arousal; release | is high during wakefulness and REM |
The locus coeruleus; norepinephrine projections; vigilance; | high levels of activity during wakefulness, low levels during sleep |
The raphe nuclei; serotonin projections; locomotion and arousal; | highest levels of activity during wakefulness |
The tuberomammillary nucleus; histamine projections; arousal and increased Ach release; | highest levels of activity during wakefulness |
The lateral hypothalamus; orexin projections; arousal and increased histamine release | highest levels of activity during active wakefulness |
How do we sleep? | -Astrocytes have stores of glycogen, and when this glycogen is broken down for energy, extracellular levels of adenosine rise. -Rising levels if adenosine bind to adenosine receptors, inhibiting neural activity. |
How do we sleep? pt2 | -Differences in adenosine metabolism have been found to underlie different sleep patterns. |
Sleep | (except for REM) in generated by ventrolateral preoptic area (VLPO) of the hypothalamus. While most of the brain is inhibited, VLPO neurons increase their activity during sleep. - 30% of our lives sleeping |
VLPO (ventrolateral preoptic area ) | -Most VLPO neurons use GABA or galanin (an inhibitory neuropeptide) for transmission. -They project to areas of the ARAS, inhibiting them. -The VLPO is also inhibited by the ARAS, creating a flip-flop circuit. |
Pontogeniculooccipital (PGO) spikes | electrical waves that start in the pons and travel through the lateral geniculate nucleus of the thalamus, to the occipital cortex (vision pathway). |
Circadian rhythms | -Govern our daily rhythms of sleep, wakefulness, arousal, hormone levels, body temperature, etc. -Generally, our circadian rhythms are generated via external and internal stimuli (known as time-givers, or zeitgebers). |
External Stimuli in the circadian rhythms | emphasis on the sun |
ultradian rhythms | shorter than 24 hours |
infradian rhythms | longer than 24 hours |
Internal Stimuli in the circadian rhythms | emphasis on molecular clock and melatonin |
photo-entrainment | The sun helps pattern circadian rhythms via changes in light and darkness |
Special light-sensitive ganglion cells | ipRGCs |
suprachiasmatic nucleus | -SCN -indirectly projects to the orexin neurons in the LH, as well as the VLPO. -is an internal clock that can run independent of external stimuli. |
Light cues | will govern circadian rhythms when present. |
absence of external zeitgebers | -humans show a circadian rhythm that is between 24 and 25 hours. -These examples show that external cues typically regulate our internal rhythms, but they can also run on their own. |
Phase Shift | Changing our external zeitgebers -Temporary sleep disruption, other health effects. -“Jet lag” -Shift workers |
pineal gland | -secretes melatonin, which is an important internal zeitgeber -Important for biological rhythms -Darkness causes the pineal gland to produce melatonin, which facilitates sleep. Melatonin secretion peaks around 3-4am |
Insomnia | individuals who have trouble falling asleep or staying asleep, which is usually associated with sleepiness during the waking hours. ~25% of the population occasionally affected -Both Biological and environmental |
Treatments of Insomnia | pharmacotherapy that increase GABA effects, and/or cognitive behavioral therapy and changes in sleep hygiene. |
Sleep apnea | -individuals stop breathing while they are asleep. -In the blood, levels of O2 drop and levels of CO2 rise, activating chemoreceptors. -Repeated waking can lead to loss of sleep. -Overactivity of sympathetic nervous system can lead to hypertension |
Chemoreceptor activation | triggers sympathetic nervous system activation, waking us up. |
Fatal familial insomnia (FFI) | -is a neurodegenerative disease caused by the buildup of misfolded (prion) proteins. -Main site of degeneration is the thalamus -Leads to a progressive loss of sleep, followed by death. |
narcolepsy | -uncontrollable bouts of sleepiness during times of wakefulness. -cataplexy (temporary paralysis) and hypnogogic (sleep) hallucinations. -loss of orexin/hypocretin expressing neurons in the lateral hypothalamus, part of the greater ARAS. |
Parasomnias during SWS | Somnambulism -Sleep Walking -Night Terrors -Bruxism (Grinding of teeth) |
sleep cycles as measured by | hypnogram |
hypnogram | form of polysomnography; it is a graph that represents the stages of sleep as a function of time. obtained by visually scoring the recordings from electroencephalogram (EEGs), electrooculography (EOGs) and electromyography (EMGs) |
How do we measure sleep? | Sleep is primarily measured using polysomnography (PSG), also known as a sleep study. PSG is an in-lab test that uses surface electrodes to record brain waves, heart rate and breathing, eye movements, muscle activity, and respiratory function. |
How do our sleep patterns change throughout the night? Part 1 | Sleep patterns change throughout the night as you cycle through two sleep phases: rapid eye movement (REM) and non-REM (NREM) sleep. The first NREM-REM cycle is usually 70–100 minutes long, while later cycles are longer, lasting about 90–120 minutes. |
Part 2 | As the night progresses, REM sleep increases, and it's longest in the last third of the sleep cycle. As you continue sleeping, these stages get shorter, and more time gets spent in REM sleep instead. |
Synaptic homeostasis hypothesis | sleep is needed to reestablish synaptic homeostasis, which is challenged by the brain's plasticity. The SHY proposes that during waking, connections throughout the brain are strengthened to learn statistical regularities about the environment. |
Hippocampal replay-encoding memories to long-term memory | The hippocampus is believed to act as a shipping center for information, taking it in, registering it, and temporarily storing it before sending it to the cortex to be stored as long-term memory |
Memory enhancement study during SWS | Go through a learning task with olfactory cue. Exposed to cue during awake, SWS or REM sleep, selectively. Tested for recall. |
orexin neurons of the lateral hypothalamus. prt 1 | -send their axons to arousal-promoting areas. -produced in neurons of the perifornical lateral hypothalamus that project to monoaminergic nuclei in the midbrain and brainstem and... |
prt 2 | to basal forebrain areas, including the MPOA. Orx/hcrt regulates feeding and wakefulness and also enhances male sexual behavior. |
Role of adenosine in sleep onset | neurotransmitter that promotes sleep drive and is thought to act as a homeostatic regulator of sleep. It builds up in the blood when you're awake, causing drowsiness, and then slowly dissipates while you sleep. |
PGO Spikes | a programming of the brain and organism during development in species-specific motor activities and behaviors |
Role of the retinohypothalamic tract from the retina to the SCN prt 1 | - Allows the sun/light levels to directly influence circadian rhythms, melatonin release, and sleep/wake cycles. essential for regulating circadian rhythms. |
prt 2 | The RHT is a branch of the optic nerve that originates from retinal ganglion cells that contain melanopsin, a photopigment. The RHT's axons project directly to the SCN via the optic nerve and optic chiasm. |
REM sleep behavior disorder prt 1 | -lack of muscle inhibition during REM -is a sleep disorder that causes people to act out their dreams during REM sleep. |
prt 2 | RBD is characterized by dream-enactment behaviors that can range from benign hand gestures to violent thrashing, punching, and kicking. |