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sleep
a recurring, homeostatic process of reduced physical, metabolic, and neurological activity (decreased wakefulness/ arousal and awareness)
Adaptive hypothesis
- based on differences in ecological niche, foraging habits, metabolism, body size, and safety considerations
- different animals sleep for different durations
Metabolic changes during sleep
- decreased body temperature
- decreased heart/ respiratory rate
- decreased cellular O2 consumption
- decreased response to stimuli
(sleep deprivation negatively impacts all organ system)
what is sleep drive affected by?
- affected by by circadian rhythms and sleep debt (sleep homeostasis)
relationship of caffeine to sleep debt and adenosine receptors?
caffeine blocks the effects of adenosine (which makes you sleepy) so you're up for longer
What type of technology helps distinguish distinct sleep phases?
Measurements via electroencephalography (EEG)
Awake
mix of alpha and beta waves
drowsy
alpha waves alone
Non-REM (NREM) sleep
- slow to no eye movement, other body movement possible
Stages of Non-REM sleep
- stage 1: theta waves
- stage 2: K complexes and sleep spindles
- stage 3: delta waves
REM sleep
- rapid horiziontal eye movement, atonia (paralysis)
- beta waves
- more vivid, bizarre dreaming
What is a full sleep cycle and what is a good amount for a good nights sleep?
- Full sleep cycle: N1 -> N2 -> N3 -> N2 -> REM
- each cycle is about 90 minutes
- 4-6 cycles over a good night's sleep
Relationship of sleep requirements and aging
- sleep requirements tend to diminish as we age
- in infancy, about half of sleep is REM
- by age 90, N3 tends to disappear
Reticular activating system (RAS)
set of functionally related nuclei in the rostral RETICULAR FORMATION, hypothalamus, BASAL FOREBRAIN , and thalamus that regulate wakefulness and sleep/ wake transitions (capitalized is bolded in Powerpoint)
ventrolateral preoptic area (VLPO)
- part of the hypothalamus
- initiates NREM sleep by inhibiting the monoaminergic, cholinergic, and orexinergic nuclei of the RAS
REM-on and REM-off neurons
- of the pons
- proposed to regulate NREM-REM and sleep-wake transitions
- certain REM-on cells indirectly inhibit lower motor neurons (atonia during REM sleep)
REM sleep behavior disorder
marked by dysregulation of this atonia pathway and often evolves into Parkinson's disease
parasomnias
pathological behaviors manifested while asleep of waking up
- NREM examples: sleepwalking, night terrors
- REM examples: REM sleep behavior disorder
sleep apnea
temporary cessation of breathing during sleep
narcolepsy and other hypersomnias
excessive daytime sleepiness despite normal nighttime sleep period
restless leg syndrome (RLS)
uncomfortable sensations leading to an urge to move the limbs during rest, inactivity, or while trying to fall asleep
insomnia
- the inability to sleep or obtain adequate-quality sleep
- can involve disregulation of falling asleep, staying asleep, or waking up earlier than desired
- etiologies vary but generally involve hyperarousal
- one neurological hallmark of this is reduced GABAergic activity
what are treatments for insomnia?
improved sleep hygience, cognitive behavioral therapy, pharmacology
narcolepsy
- an abnormal tendency to enter REM sleep directly from a wakeful state
- signs and symptoms: excessive daytime sleepiness, cataplexy (suddenly induction of REM-like atonia from awake state --> often triggered by laughter), dreamlike hallucinations, sleep paralysis while waking up
- linked to an orexin deficiency in the lateral hypothalamus
awareness vs vigilance
- vigilance: awake behavior, eyes open --> think of locked-in syndrome (being aware of what is going on, but not being able to speak or move, able to keep watch)
- awareness: level/ contents of consciousness
(look at diagram from slide 18 of the states of consciousness powerpoint)
bilateral lesions of what area may cause coma or other abnormal states of consciousness?
- cerebral cortex
- reticular activating system (RAS)
general anesthetics
- drugs that can render someone unconscious
- all these drugs are positive allosteric modulators of GABA receptors
coma
- disfunction of RAS and/ or extensive bilateral damage of cortex
- cerebral metabolism decreased by 50%, abnormal EEG
- etiologies: toxic derangement (#1) , stroke (#2), TBI, tumor, metabolic disorders, seizure
what is the diagnostic criteria for a stroke
- unconscious for > 6 hours
- eyes are closed
- no sleep-wake cycle
- unresponsive to strong verbal and painful stimuli
vegetative state
- after several weeks, coma may give way to a vegetative state
- technically unconscious
- no awareness/ purposeful responsiveness
- after four weeks in a vegetative state, the patient is said to be in a persistent vegetative state
emotion
a transient mental state that is usually accompanied by distinct feelings, behaviors, and physiological changes
james-lange theory
emotions are caused by the physiological changes accompanying them
cannon-bard theory
the brain simultaneously and independently generates emotion and accompanying physiological changes
cognitive attribution theory
emotion depends on cognitive context, with accompanying physiological changes modulating but not causing or determining specific emotions
emotions as an evolutionary adaptation
- some nonhuman animals apparently exhibit emotions based on homologous facial expressions and/or physiological responses
- possible adaptive roles of emotion: cooperation between conspecifics, sexual selection, developing parent-child dynamics, etc. (emotions apparently facilitate these processes rapidly)
Are human emotions universal?
- the facial expressions associated with specific emotions as generated by people across cultures seem to be fairly consistent
- sociocultural norms can influence how and when specific emotions are manifested
limbic system
- a set of anatomically heterogenous structures throughout the brain that serve functions including
1. homeostatic functions
2. olfactory
3. memory
4. emotions and drives
(HOME)
- modulates activity of the cortex, hypothalamus, and PAG
Major components of the limbic system
- hippocampal formation
- amygdala
- limbic association cortex
major integrative centers in the emotional brain
- amygdala
- orbitofrontal and other prefrontal cortical areas
- anterior cingulate cortex
- anterior insula
- ventral tegmental area/ nucleus accumbens
(emotional circuitry is distributed thrughout the brain)
amygdala
- provides emotional context for sensory stimuli
- greater emotional context --> better memory retention
- can differentially promote fear/ aggression or relaxation/ detachment
what is the context of fear in the amygdala? (2 routes)
- "high road": thalamus routs sensory information to amygdala via cerebral cortex
- "low row": thalamus routs sensory information directly to amygdala --> amygdala hijack
amygdala hijack
- with a sufficiently startling stimulus (negative), amygdala kicks in through the low road and an intense sense of dread will kick in before you can process what is going on
- you then soon after realize there is no threat (ex: if someone approaches you quickly but you know who they are)
Kluver-Bucy syndrome
- due to bilateral lesions of the anterior temporal lobe
- signs and symptoms: HIPHIP
1. Hypermetamorphosis (impulse to notice and react to everything)
2. Increased oral exploration
3. Placidity (lack of aggression)
4. Hypersexuality and hyperphagia
5. Impaired memory
6. Psychic blindness
psychopathy
- no consensus defintion
- sometimes likened to antisocial personality disorder
- psychopaths are typically intelligent people with superficial charm, poor self-control, a grandiose sense of self-worth, and little or no capacity for remorse or empathy
neural correlates of psychopathy
- reduced volume of prefrontal cortex
- reduced connectivity between the amygdala and orbitofrontal cortex
social cognition
- an individual's ability to understand the intentions and behavior of conspecifics
- in humans, involves integration of activity in both affective and cognitive brain networks
affective social network
- involves the anterior cingulate gyrus and anterior insula
- though to give rise to empathy (ability to intuit and share another's feelings)
cognitive social network
- underlies humans' theory of mind (TOM)
- TOM: decribes human ability to understand agency of human beings separate from our own --> tends to develop around 4-5 years of age, can be impacted in autism spectrum disorder, schizophrenia, and certain substance use disorders
mirror neurons
- cellular substrate of TOM
- these are neurons in a region of the ventral premotor cortex that are active 1) shortly before one initiates a movement and 2) when one watches another engage in the same movement
fusiform face area (FFA)
along with amygdala, integrate initial, implicit race-based evaluations
dorsolateral prefrontal cortex (diPFC)
along with acc, these both subsequently interpret and regulate initial racial perceptions
learning
the process of aquiring new information
memory
- the processes by which learned information is encoded, consolidated, maintained, and retrieved in the brain (neural substrates of learning)
- neurobiologically, learning and memory aren't distinct faculties
stages of memory (4 most general stages)
- iconic
- echoic
- haptic
- proprioceptive
short-term memory (STM)
15-18 seconds
long-term memory (LTM)
potentially indefinite
encoding
- the conversion of sensory information into stm
- stm used or manipulated to perform a cognitive-behavioral task is passed into working memory
consolidation
the conversion of stm to ltm
retrieval
the passing of ltm back into working memory for use
where does attention come into play in the stages of memory?
- you need to be attending to information consciously to remember it
- attention also plays a role of encoding sensory information into memory
working memory
- a temporary buffer for STM as it is being used and manipulated for cognitive-behavioral tasks
- can be consolidated into long-term memory
declarative memory
memory that can be conscious evoked and described
episodic memory
- event-related memory (time, location, emotional content, context)
- consolidation and retrieval via PFC and temporal lobe including HIPPOCAMPUS (all caps was bold on powerpoint)
whats the order of memory?
1. encoding
2. consolidation
3. retrieval
semantic memory
memory pertaining to information about oneself and the world
ex: BBH 203 meets @ Chambers building on Tu and Thurs from 12:05 to 1:20
non-declarative memory
unconscious memory that cannot be described and does not require attention
procedural memory
retrieval of motor and executive skills needed to perform tasks
priming
one stimulus unconsciously influencing a response to another stimulus
associative learning/ memory
- learning and remembering the relationship between stimuli or responses
- classical and operant varieties
non-associative learning/ memory
- learning and remembering based on repeated stimulation
- sensitization: increase of response magnitude
- habituation: decrease of response magnitude
hippocampus
- allocortical bilateral structure located in the medical temporal lobes
- forms the hippocampal formation with the dentate gyrus and subicular cortex
- plays roles in learning, consolidation and retrieval of declarative and spatial memory
- part of limbic system
anterograde amnesia
- inability to form new memories following brain injury to disease
- damage typically involves medial temporal lobes
retrograde amnesia
- inability to retrieve memories formed before a brain injury or disease
- amnesia may result from dementia, temporal lob epilepsy, herpes simplex encephalitis, wernicke-korsakoff syndrome, stroke, and schizophrenia
synaptic plasticity
- the capacity to change synaptic weighting
- may involve strengthening, weakening, forming, or remodeling synapses (astrocytes play a critical role)
homosynaptic plasticity
changes in the weighting of a synapse resulting from activity in a neuron intrinsic to that synapse (astrocytes play a critical role)
heterosynaptic plasticity
changes to the weighting of a synapse resulting from activity in a neuron extrinsic to that synapse (astrocytes play a critical role)
aplysia californica
- exactly 2 neurons this pathway (sensory neuron and motor neuron)
- motor neuron will innervate muscles of gill and it will retract
- if you target a certain area, it withdrawns as well as the gill by facilitating respiration
- HABITUATION: water jet stimulus (single stimulus to siphon)
- SENSITIZATION: ASK ON OFFICE HOURS
long-term potentiation
a stable and enduring increase in efficacy of synapses following repeated strong stimulation
steps of long-term potentiation
1. glutamate activated postsynaptic AMPA receptors (small EPSPs)
2. increased stimulation of presynaptic neuron, larger EPSPs and activation of NMDA receptors
3. postsynaptic NMDA activation triggers upregulation of postsynaptic AMPA receptors and increased AMPA sensitivity
4. LTP synapse is strenghthened
engrams
- the neural substrates of memory
what do engrams correspond to?
there isn't a distinct answer, but there is evidence that engrams correspond to discrete circuits in the brain
how does synaptic plasticity relate to an engram
- engrams are able to reconstruct themselves
- neurons within an engram are synaptively complex with one another and interact with each other
neurocognitive disorders
disorders characterized by a decline in cognitive function following a known insult to the nervous system
Varieties of cognitive disorders
1. dementia
- alzheimer's disease
- vascular dementia
- dementia with lewy bodies
- frontotemporal dementia
- creutzfeld- jakob disease
2. stroke
3. parkinson's disease
dementia
evidence of substantial cognitive decline from a previous level of performance in one or more cognitive domains (ex; attention, memory, language, sociality, perception)
- cognitive deficits are sufficient to interfere with independence
- dementia is ABNORMAL
- involves profound underlying neurodegeneration
- longevity is the single greatest risk factor
types of dementia
1. Alzheimer's disease (AD)
2. Vascular dementia
3. Frontotemporal dementia
4. Dementia with Lewy Bodies
- dementias are sometimes mixed (ex: alzheimers and vascular dementia)
mild cognitive impairment
- modest, noticeable cognitive decline, insufficient to interfere with independence
- may represent intermediate/ transitional stage between normal cognitive aging and dementia
alzheimer's disease
- an irreversible neurodegenerative disease characterized by progressive dementia and loss of neurocognitive function
- late-onset: > 65
- early-onset: <65
- ultimately incurable and fatal
- can only be definitively diagnosed postmortem
clinical presentation of alzheimers
1. pre-clinical
2. basic forgetfulness
3. noticeable memory problems
4. major memory loss
5. decreased independence
6. severe symptoms
7. compromised control of bodily functions
general risk factors of alzheimers
- little is known about what actually triggers alzheimers (likely multifactorial)
- longevity is #1 risk factor
- genetics
- mild cognitive impairment
- environment
- education level
- co-morbidities
genetic risk factors of alzheimers
- increased risk if one parent or sibling has alzheimers
- APOE4 allele increases risk
- a minority of early-onset AD patients possesses autosomal dominant mutations of PSEN1, PSEN2, and/or APP
what causes alzheimer's disease?
- AD is neurodegenerative
- marked by progressive neuronal and glial death
- any # of mechanisms can cause this neurodegeneration
(AMYLOID BURDEN AND TAU TOXICITY)
two cellular models of alzheimers
1. amyloid hypothesis: beta-amyloid plaques --> extracellular proteins
2. tau hypothesis: neurofibrillary tangles (hyperphosphorylated tau proteins --> normally help to maintain cytoskeleton)
significantly affected brain regions
1. medial temporal lobes
2. parietal lobes
3. prefrontal cortex
4. cingulate gyrus
5. nuclei producing acetylcholine
stroke
- also known as cerebrovascular accidents
- vascular insufficiency and INFARCTION (death of brain tissue due to hypoxia) in CNS tissue
- involve long-term, local, or global neurological deficits
- risk factors: age, sex, ethnicity, hypertension, diabetes, high LDLs, smoking, cardiac disease, family history
ischemic stroke
- occluded artery
- transient ischemic attack (TIA): transient episode of neurologic dysfunction without acute infarction
- embolic/ thrombotic
hemorrhagic stroke
ruptured artery
what type of stroke can be treated with tissue plasminogen activator (TPA)?
- ischemic stroke
- this medication is used to break up blood clots
vascular dementia (VaD)
- set of vascular-related causes of dementia, including multi-infarct dementia (MID) and subcortical vascular dementia
- memory and executive function not necessarily as impaired at VaD as in AD
- 2nd most prevalent dementia
- often comorbid with AD
multi-infarct dementia (MID)
presentation is similar to AD and other forms of dementia, but often involve a step-wise progression of both cognitive and sensory and/ or motor deficits