Sleep Flashcards
what’s circadian rhythms?
Circadian rhythms are biological processes that follow a roughly 24-hour cycle in living organisms.
• These rhythms regulate behavioral, physiological, and biochemical functions.
Key Features（关键特征）
• Diurnal（日行性的）: Active during the day (e.g., humans).
• Nocturnal（夜行性的）: Active at night (e.g., owls).
• Free-running（自由运行）: Maintains an endogenous（内源性的，自身调节的） rhythm without external cues.
• Entrainment（同步）: The process of synchronizing to environmental cues (shifting the rhythm).
• Zeitgeber（时间给予者）: External cues (e.g., light（光照）) that adjust the rhythm.
Neural Mechanism（神经机制）
• Controlled by the suprachiasmatic nucleus (SCN, 视交叉上核) in the hypothalamus（下丘脑，调节生物钟的关键区域）.
• SCN lesions（SCN损伤） disrupt circadian rhythms.
• Retinohypothalamic pathway（视网膜-下丘脑通路） transmits light information to SCN via melanopsin-containing retinal ganglion cells（含黑视蛋白的视网膜神经节细胞，负责感知光照）.
Key Experiment（关键实验）
• SCN Transplant Study（SCN移植实验）:
• Hamsters with SCN lesions（损伤SCN的仓鼠） lost their circadian rhythms.
• Transplanting SCN tissue from short-period mutant hamsters (20-hour cycle) restored circadian rhythms but matched the donor’s cycle.
Key Takeaway
Circadian rhythms help organisms anticipate daily changes and synchronize sleep, metabolism, and behavior to the environment.
What is the role of the suprachiasmatic Nucleus (SCN) in circadian rhythms?
The suprachiasmatic nucleus (SCN, 视交叉上核) is a small region in the hypothalamus（下丘脑） responsible for regulating circadian rhythms.
Neural Mechanism（神经机制）
• SCN lesions（SCN损伤） disrupt circadian rhythms.
• Isolated SCN neurons can maintain synchronized electrical activity based on previous light cycles.
• Retinohypothalamic pathway（视网膜-下丘脑通路） transmits light information from the eye to SCN via melanopsin-containing retinal ganglion cells（含黑视蛋白的视网膜神经节细胞）.
Key Takeaway
The SCN acts as the body’s master clock, regulating circadian rhythms and synchronizing biological functions with environmental cues like light.
What did the SCN transplant experiment demonstrate about circadian rhythms?
Experiment Setup
• Objective: To determine whether circadian rhythms are generated by the SCN.
• Method:
• Hamsters with SCN lesions (which abolished circadian rhythms) received an SCN transplant from hamsters with a 20-hour circadian cycle (a genetic mutation called tau).
• Results:
• The transplanted SCN restored circadian rhythms in the hamsters, but the period matched the donor’s 20-hour cycle instead of the normal 24-hour cycle.
Conclusion
• The SCN is the primary generator of circadian rhythms.
• Circadian rhythm timing is intrinsically encoded within the SCN rather than being learned from external cues.
Key Takeaway
The SCN transplant study provided direct evidence that circadian rhythms are driven by an endogenous (internal) biological clock, rather than being solely controlled by environmental factors.
What inputs regulate the SCN and how do they influence circadian rhythms?
The suprachiasmatic nucleus (SCN) receives light-based input to regulate circadian rhythms.
• The primary pathway is the retinohypothalamic pathway (视网膜-下丘脑通路).
Neural Mechanism（神经机制）
• Retinohypothalamic pathway:
• Specialized retinal ganglion cells（视网膜神经节细胞） contain melanopsin（黑视蛋白）, a light-sensitive photopigment.
• These cells directly project to the SCN.
• This input does not rely on rods and cones, meaning it detects ambient light levels rather than forming images.
• Other inputs:
• Pineal gland（松果体） in amphibians and birds can directly sense light and contribute to circadian regulation.
Experiment Setup
• Researchers identified that retinal ganglion cells with melanopsin still respond to light even in animals lacking functional rods and cones.
Conclusion
• The SCN entrains to light via the retinohypothalamic pathway, making it the key environmental cue (zeitgeber) for circadian rhythm regulation.
What is the retinohypothalamic pathway, and how does it regulate circadian rhythms?
The retinohypothalamic pathway (RHT, 视网膜-下丘脑通路) is a direct neural pathway that transmits light information from the retina to the suprachiasmatic nucleus (SCN, 视交叉上核) of the hypothalamus.
• It plays a critical role in entraining circadian rhythms to the external light-dark cycle.
Neural Mechanism（神经机制）
• Specialized retinal ganglion cells（视网膜神经节细胞）:
• Contain melanopsin（黑视蛋白）, a light-sensitive photopigment.
• Respond mainly to blue light (~480 nm wavelength).
• Do not rely on rods and cones for light detection.
• Pathway function:
• These retinal ganglion cells project directly to the SCN.
• Light signals influence SCN activity, leading to changes in melatonin release from the pineal gland（松果体）, regulating sleep-wake cycles.
Experiment Setup
• Studies found that blind individuals with non-functional rods and cones but intact retinal ganglion cells still show circadian entrainment to light, confirming the role of the RHT.
Conclusion
• The retinohypothalamic pathway is the primary route by which light resets the SCN, allowing circadian rhythms to synchronize with environmental light cycles.
How does the mammalian circadian system regulate biological rhythms?
The mammalian circadian system consists of multiple interacting components that regulate biological rhythms, primarily through the suprachiasmatic nucleus (SCN, 视交叉上核) in the hypothalamus.
• It integrates light-based environmental cues to maintain circadian rhythms.
Neural Mechanism（神经机制）
1. Light input via the retinohypothalamic pathway
• Specialized retinal ganglion cells（视网膜神经节细胞） contain melanopsin（黑视蛋白）, which detects ambient light.
• These cells directly project to the SCN, adjusting its activity based on external light levels.
2. SCN as the central pacemaker
• Located in the hypothalamus（下丘脑）, the SCN acts as the master clock.
• SCN neurons generate endogenous circadian rhythms and orchestrate physiological and behavioral cycles.
3. SCN regulates peripheral clocks
• The SCN sends signals to other brain regions and organs, ensuring synchronization of circadian rhythms across the body.
• These peripheral clocks exist in tissues like the liver, heart, and kidneys, maintaining local rhythmic functions.
4. Hormonal regulation via the pineal gland
• SCN activity influences melatonin（褪黑素） secretion from the pineal gland（松果体）.
• Melatonin is secreted at night, promoting sleep and reinforcing circadian timing.
Experiment Setup
• SCN lesion studies in mammals demonstrated disrupted circadian rhythms, confirming its role as the master pacemaker.
• SCN transplant experiments restored rhythms but followed the donor’s cycle, further proving the SCN’s intrinsic rhythmic control.
Conclusion
• The mammalian circadian system relies on the SCN to integrate light cues, regulate peripheral clocks, and control hormonal rhythms to maintain synchronization with the environment.
How does light influence human circadian rhythms?
Light is the primary zeitgeber (时间给予者) that entrains the human circadian system.
• The SCN (suprachiasmatic nucleus) adjusts circadian rhythms based on natural light exposure, influencing sleep-wake cycles.
Key Findings
• People on the western side of a time zone experience sunset later than those on the eastern side.
• Because they are exposed to daylight for a longer period in the evening, their circadian clock shifts later, delaying sleep onset.
• Even though the clock time is the same across the time zone, their biological night starts later, leading to a later bedtime.
Conclusion
• Later natural light exposure pushes back the circadian rhythm, causing people on the western side of a time zone to stay up later than those on the eastern side, even when the clock time is the same.
What are EEG, EOG, and EMG, and what do they record?
• Electroencephalography (EEG, 脑电图): Measures electrical activity in the brain. (Awake human’s EEG is desynchronized.)
• Electro-oculography (EOG, 眼动电图): Measures eye movements.
• Electromyography (EMG, 肌电图): Measures muscle activity and tone.
Key Findings
• EEG placement: Electrodes are placed on the scalp to detect brain waves.
• EOG placement: Electrodes are placed near the eyes to track eye movements.
• EMG placement: Electrodes are placed on muscles (e.g., chin, limbs) to measure muscle tone and movement.
Conclusion
• EEG, EOG, and EMG are essential tools for monitoring sleep stages, distinguishing between NREM and REM sleep, and identifying sleep disorders.
What is Non-REM sleep, and what are its different stages?
Non-REM (NREM) sleep is a phase of sleep that lacks rapid eye movements and is characterized by progressively deeper sleep stages.
• It is divided into three stages (NREM 1, NREM 2, and NREM 3), each with distinct EEG patterns and physiological characteristics.
Key Findings
• NREM 1 (Stage 1):
• Lightest sleep; transition between wakefulness and sleep.
• EEG shows low-amplitude, mixed-frequency waves.
• EOG detects slow rolling eye movements.
• EMG shows a decrease in muscle activity.
• NREM 2 (Stage 2):
• Deeper sleep than Stage 1, but still light sleep.
• EEG shows sleep spindles (sudden bursts of rhythmic activity) and K-complexes (large waves associated with sensory processing).
• Eye movements stop, and muscle activity decreases further.
• NREM 3 (Stage 3, Slow-Wave Sleep, SWS):
• Deepest stage of NREM sleep; also called slow-wave sleep (SWS).
• EEG is dominated by high-amplitude, low-frequency delta waves.
• Difficult to wake up from; waking up during this stage causes grogginess.
• Plays a role in memory consolidation, growth hormone release, and physical restoration.
Conclusion
• Non-REM sleep progresses from light sleep (Stage 1) to deep sleep (Stage 3), with gradual reductions in muscle activity and brain activity slowing down.
• Stage 3 (SWS) is the most restorative stage, essential for physical recovery and memory processing.
What are the characteristic EEG patterns and rhythms in each stage of Non-REM sleep
Key Findings
• NREM 1 (Stage 1) – Light Sleep
• EEG Pattern: Low-amplitude, mixed-frequency waves.
• Rhythm: Theta waves (4–7 Hz).
• Alpha Rhythms (8–12 Hz): Present in wakefulness and early Stage 1, associated with relaxed drowsiness.
• Vertex Spikes: Sharp, sudden waveforms signaling the transition into sleep.
• NREM 2 (Stage 2) – Intermediate Sleep
• EEG Pattern: Sleep spindles and K-complexes.
• Rhythm: Theta waves with sleep spindles and K-complexes.
• Sleep Spindles (12–16 Hz bursts): Short bursts of high-frequency activity, generated by thalamocortical circuits, playing a role in memory consolidation and sleep stability.
• K-complexes: Large, slow waves associated with sensory processing and arousal suppression.
• NREM 3 (Stage 3) – Slow-Wave Sleep (SWS)
• EEG Pattern: High-amplitude, low-frequency delta waves.
• Rhythm: Delta waves (<4 Hz) dominate, representing deepest sleep and brain recovery processes.
Conclusion
• Alpha rhythms appear in wakefulness and early sleep onset.
• Vertex spikes mark the transition into sleep.
• Sleep spindles and K-complexes define Stage 2, aiding in memory consolidation and sensory regulation.
• Slow-wave delta activity dominates Stage 3, signifying deep, restorative sleep.
What is REM sleep, and how is it different from Non-REM sleep?
Rapid Eye Movement (REM) sleep is a unique sleep stage characterized by desynchronized brain activity, rapid eye movements, and muscle atonia (loss of muscle tone).
• It is also known as paradoxical sleep because the EEG resembles an awake state, but the body remains immobile.
Key Findings
• EEG Pattern:
• Low-amplitude, high-frequency waves, similar to wakefulness.
• Increased activity in the pons, limbic system, and visual areas.
• Eye Movements (EOG):
• Rapid, jerky movements under closed eyelids.
• Muscle Activity (EMG):
• Complete muscle atonia, preventing movement (except for minor twitches).
• Dreaming:
• Most vivid, narrative-like dreams occur during REM sleep.
• Brain activity in the posterior cortex predicts dream intensity.
• Autonomic Changes:
• Irregular breathing and heart rate compared to Non-REM sleep.
Conclusion
• REM sleep is a highly active brain state combined with muscle paralysis, crucial for memory consolidation, emotional processing, and dreaming.
How do sleep stages progress throughout a typical night?
Key Findings
• A typical night consists of 4–5 sleep cycles, each lasting 90～110 minutes.
• Sleep cycles sequentially transition through NREM and REM sleep.
• Stage 3 (Slow-Wave Sleep, SWS) is prominent early in the night but disappears halfway through.
• As Stage 3 decreases, it is replaced by longer Stage 2 and REM periods.
• Stage 2 acts as a transition into REM sleep.
• Stage 1 is the shortest stage, mainly appearing after REM or brief awakenings.
• Wakefulness totals around 3 hours, including short, natural awakenings between cycles.
Conclusion
• Early sleep cycles prioritize deep sleep (Stage 3), while later cycles shift toward REM sleep.
• The decrease in Stage 3 is compensated by an increase in Stage 2 and REM, shaping the characteristic sleep architecture of the night.
How does sleep change during adolescence, and what are the effects of later school start times?
Key Findings
• Circadian Shift in Adolescents:
• During puberty, the circadian rhythm naturally shifts later, making teenagers want to sleep and wake up later.
• School schedules conflict with this shift, causing chronic sleep deprivation.
• Effects of Sleep Deprivation in Teenagers:
• Increased risk of depression
• Lower cognitive performance and attention deficits
• More in-class sleepiness
• Benefits of Later School Start Times:
• Improved attendance and enrollment
• Better mental health and emotional well-being
• Reduced daytime sleepiness and better academic performance
Key Takeaway
• Teenagers’ biological sleep needs are misaligned with early school schedules, leading to negative effects on mental health, cognition, and academic success.
• Delaying school start times can significantly improve adolescent well-being and performance.
What brain regions are active during dreaming, and in which sleep stages does dreaming occur?
Key Findings
• Dreaming occurs in both REM and NREM sleep, but REM sleep is most associated with vivid, narrative-like dreams.
• Brain regions activated during dreaming:
• Limbic system (emotion processing) – Especially the amygdala, involved in emotional intensity.
• Visual association areas – Particularly in the posterior cortex, which generates visual imagery.
• Hippocampus – Plays a role in memory-related dream content.
• Motor-related areas (but movements are inhibited) – The motor cortex can be active, but the pons suppresses movement through muscle atonia in REM sleep.
Key Takeaway
• REM sleep is the primary stage for dreaming, with brain activation resembling wakefulness but without voluntary movement.
• Dreams involve emotional and sensory processing, engaging the limbic system, visual cortex, and hippocampus.
How does sleep differ in infants compared to adults?
Key Findings
• Infants sleep more than adults
• Newborns spend a majority of their time asleep.
• Sleep cycles are shorter than in adults.
• Higher percentage of REM sleep
• 50% of infant sleep is REM sleep, compared to ~20–25% in adults.
• REM sleep in infants is believed to provide essential stimulation for brain development (They also have more movements in REM sleep, while adults generally have no movements in REM sleep).
• Development of Circadian Rhythms
• A 24-hour sleep rhythm starts forming around 16 weeks of age.
• Newborn sleep patterns are initially irregular and gradually become more structured.
Key Takeaway
• Infants have shorter sleep cycles and spend a greater proportion of time in REM sleep, which is essential for early brain development. Their circadian rhythms take several months to mature.
Adult sleep patterns:
Total sleep time decreases with age.
• The number of awakenings increases, leading to more fragmented sleep.
• Aging and Stage 3 (Slow-Wave Sleep, SWS) Decline
• By age 60, Stage 3 sleep is reduced by half compared to young adults.
• By age 90, Stage 3 disappears completely.
• Loss of Stage 3 sleep is linked to cognitive decline and is a characteristic of senile dementia.
Key Takeaway
• Sleep structure changes significantly across the lifespan—infants spend more time in REM sleep, while older adults experience shorter sleep, more awakenings, and a decline in Stage 3 sleep, which may contribute to cognitive aging and neurodegenerative diseases.
What are the effects of short-term and total sleep deprivation?
Key Findings
• Short-Term Sleep Deprivation (Partial Sleep Loss)
• Cognitive and Emotional Effects:
• Increased irritability
• Difficulty concentrating
• Episodes of disorientation
• Effects vary with age and individual factors, such as sleep debt and resilience.
• Total Sleep Deprivation (Complete Lack of Sleep)
• Severe physiological consequences:
• Compromised immune system
• Higher risk of infections
• Animal studies:
• Mice die within ~19 days due to bacterial infections, highlighting immune system failure.
• Fatal Familial Insomnia (FFI):
• Genetic disorder where individuals lose the ability to sleep in midlife.
• Leads to progressive neurodegeneration in the cortex and thalamus.
• Death occurs within 7–24 months after symptom onset.
Key Takeaway
• Short-term sleep deprivation affects cognition and mood, while total sleep deprivation leads to immune failure and can be fatal, demonstrating the essential role of sleep in survival and overall health.
What is sleep recovery, and how does the body compensate for lost sleep?
Key Findings
• Sleep recovery refers to the process of compensating for lost sleep by altering sleep architecture after a period of deprivation.
• Key compensatory mechanisms:
• Increased Stage 3 (SWS) and REM intensity:
• After sleep deprivation, the body prioritizes Stage 3 sleep (deep sleep) to recover lost restorative functions.
• REM sleep becomes more intense, with longer and more frequent episodes.
• No full “make-up” for lost sleep:
• While the body recovers some functions, total sleep hours lost are not fully regained.
• Stage 3 is prioritized, while Stage 2 sleep is reduced to compensate.
Key Takeaway
• Sleep recovery helps restore essential functions, but lost sleep cannot be fully regained—the brain compensates by prioritizing deep sleep (SWS) and more intense REM sleep.
Why and how did sleep evolve?
Key Findings
1. Energy Conservation Hypothesis
• Sleep reduces metabolic demands, allowing organisms to conserve energy.
• Small mammals with high metabolic rates tend to sleep more than larger ones (especially for plant eater, while predator’s size is not related with the length of sleep).
2. Niche Adaptation Hypothesis
• Sleep patterns evolved to align with an animal’s ecological niche.
• Nocturnal and diurnal sleep behaviors help organisms avoid predators and optimize survival.
3. Restorative Hypothesis
• Sleep restores brain and body function, allowing for protein synthesis, tissue repair, and immune system strengthening.
• SWS (Stage 3 sleep) is linked to growth hormone release and glial clearance of brain waste. (Night shift working are more likely to develop cancer)
4. Memory Consolidation Hypothesis
• Sleep plays a critical role in processing and consolidating memories.
• SWS is associated with declarative memory consolidation, while REM sleep is linked to procedural and emotional memory processing.
5. Sleep Variability Across Species
• Mammals and birds show REM and NREM sleep, supporting its evolutionary significance.
• Dolphins and some birds exhibit unihemispheric sleep, where only one brain hemisphere sleeps at a time, allowing continued movement.
Key Takeaway
• Sleep likely evolved for multiple adaptive reasons, including energy conservation, ecological survival, brain restoration, and memory consolidation, making it essential for both physiological and cognitive functions.
What does the key press sequence study tell us about sleep and motor learning?
Key Findings
• Study Setup:
• Participants practiced a motor skill task involving a specific sequence of key presses.
• Performance was measured before and after a period of either sleep or wakefulness.
• Key Results:
• 20% improvement in speed and accuracy after a night of sleep, but only minimum improvement after 12 hours of wakefulness.
• Sleep-dependent enhancement was linked to the amount of Stage 2 NREM sleep during the last quarter of the night (Stage 2 nREM sleep is the highest correlates to the performance).
• Implications:
• Motor skill learning is consolidated during sleep, especially during Stage 2 NREM sleep.
• Sleep facilitates neural plasticity, allowing the brain to refine motor skills.
Key Takeaway
• Motor skill performance improves after sleep, not just time alone, indicating that sleep, particularly Stage 2 NREM sleep, plays a crucial role in motor memory consolidation.
Another study: Is nap enough to improve performance?
Nap vs no nap groups
Results: people with a 90 minutes nap outperformed the people who have no nap. And we find enhance spindle activity only in the learning hemisphere (So maybe is spindle activity driving information needed for learning).
What does fMRI data reveal about sleep-dependent motor memory consolidation?
Key Findings
• Study Setup:
• Participants performed a motor learning task (key press sequence).
• Brain activity was measured using fMRI before and after sleep to assess changes in neural activation.
• Key Results:
• Enhanced activity in brain regions involved in motor learning after sleep, including:
• Cerebellum – crucial for motor coordination.
• Medial prefrontal cortex – involved in planning and decision-making.
• Primary motor cortex – responsible for movement execution.
• Increased hippocampal activity, suggesting a role in motor memory reorganization.
• Reduced activity in regions related to conscious control, such as: • Parietal lobe – linked to spatial processing. • Left insular cortex, temporal pole, and fronto-polar region – areas involved in effortful task performance (Skills becomes for efficient and automotive). • Implications: • Sleep facilitates neural reorganization, shifting motor skill execution from conscious, effortful control to more automatic processing.
Key Takeaway
• fMRI data confirms that sleep enhances motor memory consolidation by strengthening activity in motor-related brain regions while reducing reliance on conscious control areas, making movements more automatic and efficient.
How does sleep contribute to memory consolidation, and what do Born et al. (2005) and EEG studies reveal?
Key Findings
• Born et al. (2005) Study:
• Tested declarative memory (paired-word association task) after either early-night sleep (rich in SWS) or late-night sleep (rich in REM).
• Memory improved significantly after early-night sleep, showing that SWS is crucial for consolidating declarative memory.
• If SWS was missing, memory performance was impaired.
• Proposed hippocampal-neocortical transfer model:
• During SWS, hippocampal sharp-wave activity reactivates memories and transfers them to the neocortex for long-term storage.
• EEG Data Corroboration:
• EEG recordings showed increased sleep spindle density in Stage 2 sleep after learning.
• Higher spindle activity correlated with better memory recall, suggesting spindles play a key role in strengthening memory traces.
• Spindles facilitate communication between the hippocampus and neocortex, reinforcing long-term memory consolidation.
Key Takeaway
• SWS plays a critical role in declarative memory consolidation by transferring information from the hippocampus to the neocortex, and EEG studies confirm that sleep spindles in Stage 2 contribute to strengthening memory traces.
What is emotional memory, and how does sleep deprivation affect it?
Key Findings
• Emotional Memory Definition:
• Emotional memory refers to the ability to encode, store, and recall emotionally significant events.
• Sleep, particularly REM sleep, plays a key role in processing and consolidating emotional experiences.
• Effects of Sleep Deprivation on Emotional Memory:
• Study Setup:
• Participants were either sleep-deprived (one night of no sleep) or allowed to sleep before an emotional memory task.
• The task involved encoding positive, negative, and neutral words, followed by a recognition test two days later after recovery sleep.
• Key Results:
• Better retention of emotional (positive & negative) stimuli compared to neutral words in both groups.
• Sleep-deprived individuals still retained negative stimuli, but overall memory performance was lower than the control group.
• Implications:
• Suggests that emotionally charged experiences are prioritized for retention, even in sleep-deprived individuals.
• Sleep loss disrupts overall memory formation but preserves emotional content, possibly contributing to heightened emotional reactivity in sleep-deprived states.
Key Takeaway
• Sleep, especially REM sleep, plays a vital role in consolidating emotional memories. Sleep deprivation impairs general memory processing but preserves emotional memories, which may explain increased emotional sensitivity after sleep loss.
How does NREM sleep contribute to memory consolidation, and what role does reactivation play?
Key Findings
• Neuronal Activity Replay:
• Patterns of brain activity observed while learning a task during wakefulness are replayed during NREM sleep.
• This suggests that the brain “rehearses” learned information, reinforcing memory traces.
• Reactivation Studies Using External Cues:
• Some studies introduced specific cues (e.g., odors) during learning and later re-exposed participants to the same cue during NREM sleep.
• Results showed enhanced memory performance, suggesting that reactivating memories during sleep strengthens consolidation.
Key Takeaway
• NREM sleep plays a critical role in memory consolidation by “replaying” neural activity from prior learning, and targeted reactivation (e.g., odor cues) can further enhance memory retention.
What does the Yoo et al. (2007) study reveal about the effects of sleep deprivation on emotional processing?
Key Findings
• Study Setup:
• Researchers deprived participants of sleep for 35 hours and compared their brain activity to a control group that had normal sleep.
• Participants viewed increasingly negative emotional images while undergoing fMRI scans.
• Key Results:
• In sleep-deprived individuals:
• The amygdala (emotion-processing center) showed a +60% increase in reactivity compared to the control group.
• The prefrontal cortex, which normally regulates amygdala activity, showed reduced functional connectivity.
• Emotional responses were exaggerated and less regulated.
• Control group (well-rested participants):
• Showed more balanced amygdala activity with stronger prefrontal cortex regulation.
• Implications:
• Sleep deprivation weakens top-down control from the prefrontal cortex, leading to heightened emotional reactivity.
• Explains why sleep-deprived individuals experience stronger negative emotions and mood instability.
• Could be relevant for understanding mental health disorders, as sleep disturbances are linked to anxiety, depression, and PTSD.
Key Takeaway
• Sleep deprivation disrupts the brain’s emotional regulation system, leading to exaggerated amygdala responses and impaired prefrontal control, which may contribute to mood instability and increased emotional sensitivity.
How does REM sleep influence emotional processing, and what happens when it is disrupted?
Key Findings
• REM sleep plays a crucial role in processing emotional experiences and integrating them into long-term memory.
• Disruptions in REM sleep impair emotional regulation, making it harder to process and integrate traumatic memories.
• Findings from PTSD and Sleep Studies:
• Spoormaker & Montgomery (2008):
• REM sleep disruptions are linked to heightened re-experiencing symptoms (e.g., intrusive memories, flashbacks).
• Germain (2013) Neuroimaging Studies:
• PTSD-related sleep disturbances are associated with:
• Hyperactivity in the amygdala (excessive emotional responses).
• Reduced prefrontal cortex regulation (weakened emotional control during sleep).
• Sleep problems before trauma predict PTSD severity:
• Individuals with poor sleep before a traumatic event are more likely to develop severe PTSD symptoms.
• Interrupting REM sleep after trauma is linked to later PTSD development.
Key Takeaway
• REM sleep is essential for emotional processing and trauma integration. Disruptions in REM sleep can exacerbate PTSD symptoms by increasing emotional reactivity and impairing memory regulation, making sleep a critical factor in trauma recovery.
What is the cellular explanation for the function of sleep, and what does the Sleepy mutation tell us?
Key Findings
• Cellular Explanation for Sleep Function:
• Sleep is essential for synaptic homeostasis—the balance between synaptic strengthening and weakening.
• Studies suggest that synapses are strengthened during wakefulness (due to learning and experience) and then scaled back during sleep, preserving only the most relevant connections.
• Sleep allows for protein synthesis, synaptic remodeling, and removal of metabolic waste, preventing neuronal overload.
• The Sleepy Mutation (Sik3 Mutation in Mice):
• Researchers screened over 8,000 mice and identified one with excessive sleep duration (~15 hours/day) due to a mutation in the Sik3 gene.
• The mutation led to hyperphosphorylation of synaptic proteins, increasing the need for sleep.
• Similar hyperphosphorylation occurs in sleep-deprived wild-type mice, suggesting that waking experiences increase synaptic phosphorylation, and sleep helps reverse this process.
• Supports the idea that sleep regulates synaptic strength and prevents excessive accumulation of synaptic proteins.
Key Takeaway
• Sleep is crucial for synaptic homeostasis, allowing the brain to prune unnecessary connections and consolidate important ones. The Sleepy mutation (Sik3) supports this by showing that excess synaptic phosphorylation increases sleep need, linking sleep to cellular regulation and neural efficiency.
What are the major neural systems that regulate sleep, and which brain areas are involved?
Key Findings
Sleep is controlled by four major interacting neural systems:
1. Forebrain System (Basal Forebrain) – Induces Slow-Wave Sleep (SWS)
• The basal forebrain (BF, 基底前脑) promotes SWS (Stage 3 deep sleep) by releasing GABA, which inhibits wake-promoting regions.
• Lesions in the basal forebrain reduce SWS, leading to sleep disturbances.
2. Brainstem System (Reticular Formation) – Maintains Wakefulness
• The reticular formation (网状结构) in the brainstem helps maintain arousal and wakefulness.
• Lesions in this area cause persistent sleep-like states, showing its role in wakefulness.
3. Pontine System (Pons, Subcoeruleus) – Controls REM Sleep
• The subcoeruleus (下蓝斑核) in the pons triggers REM sleep and associated phenomena like rapid eye movements and muscle atonia.
• Lesions in the subcoeruleus cause REM sleep without atonia, allowing animals to act out dreams.
4. Hypothalamic System (Hypothalamus) – Coordinates Sleep-Wake Regulation
• The hypothalamus (下丘脑), particularly the tuberomammillary nucleus (TMN) and lateral hypothalamus, releases hypocretin (orexin) to stabilize sleep-wake states.
• Hypocretin deficiency is linked to narcolepsy, a disorder causing sudden sleep attacks.
Key Takeaway
• Sleep regulation relies on four key neural systems:
• Basal forebrain (induces SWS)
• Reticular formation (maintains wakefulness)
• Subcoeruleus in the pons (triggers REM sleep)
• Hypothalamus (stabilizes and regulates transitions between states)
• These systems interact dynamically to control the sleep-wake cycle.
What do transection studies tell us about sleep regulation, and which brain areas contribute to sleep?
Key Findings
• Transection studies involve cutting specific brain regions to study their role in sleep and wakefulness.
• Bremer’s Classic Experiments (1930s):
• Cerveau isolé (Isolated Forebrain) Transection:
• Cut at the midbrain level, separating the forebrain from the brainstem.
• Result: The animal remained in continuous SWS (slow-wave sleep), showing that the forebrain can generate deep sleep but wakefulness requires brainstem input.
• Encéphale isolé (Isolated Brain) Transection:
• Cut at the medulla level, separating the brainstem from the spinal cord.
• Result: Normal sleep-wake cycles persisted, proving that the essential sleep-wake control structures are above the medulla (in the midbrain and pons).
• Key Contribution of Brain Regions to Sleep:
• Everything above the medulla contributes to sleep regulation.
• The forebrain generates SWS (Stage 3 deep sleep).
• The reticular formation in the brainstem is necessary for wakefulness.
• The pons (subcoeruleus region) controls REM sleep and muscle atonia.
Key Takeaway
• Transection studies confirmed that sleep regulation depends on brain regions above the medulla, with the forebrain generating SWS, the brainstem maintaining wakefulness, and the pons controlling REM sleep.
What are common sleep disorders, and what specific sleep disorders affect children?
General Sleep Disorders:
1. Insomnia (失眠症) – Difficulty falling asleep, staying asleep, or waking too early.
2. Sleep Apnea (睡眠呼吸暂停症) – Breathing interruptions during sleep, leading to poor sleep quality and excessive daytime sleepiness.
• Obstructive Sleep Apnea (OSA) – Caused by airway collapse.
• Central Sleep Apnea – Due to the brain failing to send proper signals to breathing muscles.
3. Narcolepsy (嗜睡症) – Sudden, uncontrollable sleep episodes during the day, often linked to hypocretin (orexin) deficiency.
4. REM Behavior Disorder (RBD, REM行为障碍) – Lack of muscle atonia during REM sleep, leading to acting out dreams.
5. Parasomnias (睡眠异常行为) – Unusual behaviors during sleep, including nightmares, sleepwalking, and night terrors.
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Sleep Disorders in Children:
1. Night Terrors (夜惊) –
• Occur during NREM Stage 3 (deep sleep, not REM nightmares).
• The child screams, appears terrified, but remains unresponsive and does not recall the event.
2. Sleepwalking (梦游症) –
• Also occurs during NREM Stage 3, when the child is in deep sleep.
• The child may walk or perform activities without conscious awareness.
3. Bedwetting (夜遗尿, Nocturnal Enuresis) –
• Often linked to delayed bladder control development.
• Usually resolves with age as the nervous system matures.
4. Obstructive Sleep Apnea (OSA) in Children –
• Caused by enlarged tonsils or adenoids, leading to breathing interruptions.
• Can result in daytime attention problems (mimicking ADHD).
Key Takeaway
• Sleep disorders range from insomnia and breathing-related issues (apnea) to movement disorders (narcolepsy, RBD) and parasomnias (sleepwalking, night terrors).
• Children are more prone to parasomnias like sleepwalking, night terrors, and bedwetting, which often resolve with age but can impact sleep quality.
How do sleeping pills work, and what are their effects on sleep?
Key Findings
Mechanism (原理)
• GABA Agonists: Enhance GABA_A receptor activity, increasing inhibition in the brain.
• Benzodiazepines (如Valium, Ativan): Induce sleep but reduce SWS and REM, causing next-day drowsiness.
• Z-drugs (如Ambien, Sonata): More selective, promoting sleep with fewer residual effects.
• Orexin Receptor Antagonists (如Suvorexant): Block wake-promoting orexin, preventing insomnia without GABAergic side effects.
Effects
✔ Short-term benefits: Faster sleep onset, increased sleep time.
❌ Negative effects:
• Reduced SWS & REM → Weaker memory consolidation.
• Next-day grogginess & cognitive impairment.
• Risk of tolerance, dependence, and withdrawal with long-term use.
Key Takeaway
• Sleeping pills suppress wakefulness or enhance GABAergic inhibition, but long-term use disrupts sleep architecture and increases dependence risk. Best used short-term.
Review session: What are the stages of sleep, and what are their characteristic EEG patterns
Key Findings
1. Wakefulness
• EEG: Beta waves (15–30 Hz) → low-amplitude, high-frequency, desynchronized activity.
• Features: Brain is active, ready for processing external stimuli.
2. NREM Stage 1 (Light Sleep, Drowsy State)
• EEG: Theta waves (4–7 Hz).
• Features: Transition from wakefulness to sleep; somewhat awake, drowsy.
3. NREM Stage 2 (Intermediate Sleep)
• EEG: Theta waves, with distinctive:
• K-complexes → Large-amplitude, single high-voltage spikes.
• Sleep spindles → High-frequency (12–16 Hz), small-amplitude bursts, linked to memory consolidation.
• Features: Sleep becomes more stable, reduced responsiveness to external stimuli.
4. NREM Stage 3 (Slow-Wave Sleep, SWS, Deep Sleep)
• EEG: Delta waves (<4 Hz, low frequency, high amplitude, synchronized activity).
• Features:
• Deepest sleep, hardest to wake up from.
• Essential for restoration and memory processing.
5. REM Sleep (Paradoxical Sleep)
• EEG: Beta waves, similar to wakefulness.
• Features:
• Brain looks awake, but the body is paralyzed (muscle atonia).
• Rapid eye movements (EOG detects eye ball movement under closed eyelids).
• Often followed by brief wakefulness before the next sleep cycle.
Key Takeaway
• Sleep progresses through cycles (~90 min each), transitioning from NREM (Stages 1–3) to REM.
• Stage 2 is marked by K-complexes and spindles (linked to memory), Stage 3 is deep sleep (SWS, delta waves, big amplitude, low frequency), and REM mimics wakefulness (beta waves, rapid eye movement, muscle atonia).
Review session: When do dreams occur, what brain regions are active during sleep, and when are night terrors most likely to happen?
Key Findings
• Dreaming can occur in all sleep stages, but most vivid and frequent dreams happen during REM sleep.
• Brain activity during sleep:
• Occipital lobe (visual processing area) is highly active, contributing to vivid and immersive dream content.
• Frontal lobe (responsible for logical thinking and reasoning) is less active, which may explain why dreams often lack logical structure.
• Night Terrors:
• Occur during Stage 3 (Slow-Wave Sleep, SWS), not during REM sleep.
• Involves sudden fear, screaming, or panic, but the individual is unresponsive and does not recall the episode upon waking.
• More common in children and tend to disappear with age.
Key Takeaway
• REM sleep produces vivid dreams due to high occipital lobe activation and reduced frontal lobe involvement, making dreams visual but often illogical.
• Night terrors are different from nightmares—they occur during deep sleep (Stage 3, SWS), are not dream-related, and often involve intense fear reactions without memory of the event.
Review session: What are the key functions of sleep, and what evidence supports them?
Key Findings
1. Memory Consolidation
• Sleep strengthens learning and memory retention, especially for motor skills and spatial navigation.
• Supporting evidence:
• Motor learning studies → People who sleep after practicing a task (e.g., key press sequence) perform better the next day.
• Mouse Maze Study → Mice that slept after learning a maze showed improved navigation, suggesting sleep consolidates spatial memory.
2. Restoration and Waste Clearance
• Sleep is essential for physical and neural restoration.
• Supporting evidence:
• Sleep deprivation studies → Mice and humans die if completely sleep-deprived, showing sleep is necessary for survival.
• Glial Flushing Hypothesis → During sleep, the glymphatic system (glial cells and cerebrospinal fluid) flushes out toxic waste, including beta-amyloid, which is associated with Alzheimer’s disease.
• Sleep statistics → People who sleep 6 hours or less per night have a higher mortality risk compared to those who get 7+ hours.
3. Niche Adaptation (Ecological Perspective)
• Sleep helps animals adapt to their ecological niche by keeping them inactive during times of high risk.
• Supporting evidence:
• Nocturnal and diurnal species evolved sleep patterns to avoid predators.
• Animals that are vulnerable during sleep tend to sleep less or in protected environments.
4. Energy Conservation Hypothesis
• Sleep reduces metabolic demands, allowing energy savings during periods of inactivity.
• Supporting evidence:
• Small animals (e.g., bats, rodents) sleep longer because they have higher metabolic rates and need more recovery.
• Sleep helps lower body temperature and metabolic activity, reducing energy consumption when food is scarce.
Key Takeaway
• Sleep is essential for memory consolidation (learning and spatial tasks), restoration (glial flushing and repair), niche adaptation (predator avoidance), and energy conservation (metabolic efficiency), with strong support from sleep deprivation, neurophysiological, and ecological studies.
