NEUR200 Exam 4

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Last updated 11:32 PM on 5/5/26
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85 Terms

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circadian rhythm

- 24 hour biological cycle

- influences regulation of sleep

- hypothalamus = circadian clock

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suprachiasmatic nucleus (SCN)

- groups of neurons in hypothalamus that regulate sleep-wake cycle

- influenced by light

- controls melatonin release (pituitary gland)

- watched video on hamster getting a different hamster's SCN --> completely changes sleep-wake cycle

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reticular formation

arousal

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locus coeruleus (LC)

main synthesizer of norepinephrine (arousal)

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histamine

- hypothalamus

- must be low to sleep well

- antihistamines make you sleepy

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orexin

- hypothalamus

- necessary to stay awake

- people with narcolepsy lack

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NREM stage numbers

1, 2, 3, 4

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stage 1 sleep

- lasts 5-10 minutes

- theta waves

<p>- lasts 5-10 minutes</p><p>- theta waves</p>
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stage 2 sleep

- brief bursts of higher frequency brain waves

- k-complex: sharp waves, helps to keep you asleep through noise

- sleep spindles: generated in thalamus, more = better sleep

<p>- brief bursts of higher frequency brain waves</p><p>- k-complex: sharp waves, helps to keep you asleep through noise</p><p>- sleep spindles: generated in thalamus, more = better sleep</p>
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stage 3 and 4 sleep

- slow-wave sleep, high amplitude

- synchronized low frequency delta waves

- memory consolidation

- some dreams

<p>- slow-wave sleep, high amplitude</p><p>- synchronized low frequency delta waves</p><p>- memory consolidation</p><p>- some dreams</p>
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REM sleep (stage 5)

- rapid eye movement

- high frequency beta waves

- dreams

- amount of REM increases as night goes on

<p>- rapid eye movement</p><p>- high frequency beta waves</p><p>- dreams</p><p>- amount of REM increases as night goes on</p>
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insomnia

- chronic problems in getting adequate sleep

- causes: anxiety (adrenaline), tension, depression

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narcolepsy

- irresistible onsets of sleep during normal waking periods

- causes: lack of orexin, Huntington's

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sleep apnea

- frequent, reflexive gasping for air that awakens a person

- causes: obesity, genetics, hormones, old-age

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night terrors

- abrupt awakenings from NREM (stage 2) sleep

- accompanied by intense autonomic arousal and feeling of panic

- common in children

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nightmares

anxiety-arousing dreams that lead to awakening

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REM behavior disorder

- people who move vigorously during REM, acting out dreams

- causes: GABA deficiency

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sleepwalking

motor cortex is awake

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lucid dreaming

monitoring areas (frontal lobe) are awake

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sleep paralysis

waking up while you still can't move

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fatal familial insomnia

- inherited rare disease

- initially looks like insomnia

- causes: large amounts of PrPres --> degeneration of thalamus

- consequences: absence of sleep spindles and k-complexes, deep sleep is reduced, weight loss, hallucinations, seizures, coma, death

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differences in sleep among species

- fishes that don't sleep live in caves with no difference between day and night

- humans have changed sleep habits (used to wake up for period of time in night)

- hibernation is analogous to how we sleep to conserve energy

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EEG during sleep

- resembles those that occur during learning

- sleep spindles increase after new learning

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dorsal pathway

- parietal --> prefrontal = ACTION

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ventral pathway

temporal --> prefrontal = PERCEPTION

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encoding

- from sensory system --> STM

- using memory to learn something

- visual objects: right prefrontal and right parahippocampal cortex

- concepts/words: left prefrontal and left parahippocampal cortex

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consolidation

- STM --> LTM

- be able to talk about things in the future

- medial temporal lobe

- key area = hippocampus and "what" pathway (ventral)

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retrieval

- bringing memories to consciousness using working memory

- requires attention (frontal areas)

- retrieval from LTM make memories plastic again and can be updated

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explicit memory

- conscious

- episodic and semantic

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episodic memory

memory of personal experiences

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semantic memory

memory of facts and general knowledge

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implicit memory

- unconscious

- priming, procedural, perceptual learning, and classical conditioning

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priming

past experiences influences thoughts of responses

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procedural memory

memory for how to do skills and tasks thru repetition (hard to consciously change once learned)

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perceptual learning

improved perception thru experience

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classical conditioning

learning connections between stimuli

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neural substrates for memory

- temporal-frontal lobes

- ventral stream

- temporal lobe (hippocampus and rhinal cortex)

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neurotransmitters for memory

- acetylcholine

- serotonin

- noradrenaline

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spatial memory

- place cells: hippocampus, directions and navigation (rainbow video), neuron fires when in same spot

- grid cells: entorhinal cortex, learning unknown space or room (black dots in grid), mapping the environment

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contextual memory

- memory for context surrounding an event

- hippocampus: links everything together

- parahippocampal cortex: processes scenes and places

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fear conditioning

- depends on amygdala (fear/anxiety)

- damage to amygdala abolishes emotional memory

- gut feeling like something is wrong but you don't know what (haunted house)

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procedural learning

- depends on basal ganglia (habits/skills)

- people with Parkinson's have this impaired

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basal ganglia

- includes striatum, globus pallidus, and substantia nigra

- gradual learning of habits (procedural learning)

- reinforcement- based teaching

- early in learning we rely on prefrontal cortex, but with practice the control shifts to basal ganglia (driving a car)

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prefrontal cortex

- used when learning new things for the first time before habits are developed

- can be changed more easily than procedural

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long-term potentiation

- glutamate receptors: AMPA and NMDA

- AMPA regularly allows sodium ions thru (causes depolarization)

- NMDA can allow sodium and calcium but is blocked by magnesium

- glutamate released --> sodium enters thru AMPA --> large depolarization --> magnesium unblocks NMDA --> sodium and calcium enter thru NMDA --> strengthens synapse

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anterograde amnesia

inability to form new memories

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retrograde amnesia

loss of memories formed before onset of amnesia

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time-dependent amnesia

- type of retrograde amnesia

- lose most recent memories first, childhood memories last

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HM patient

- had severe epilepsy --> surgeons removed hippocampus and part of amygdala

- suffered anterograde and retrograde amnesia

- severe impairment of episodic memory (personal events) and LTM

- difficult imagining the future and making plans

- intact STM/working memory, but when distracted info is lost

- intact procedural memory (video games)

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attention

narrowing or focusing awareness on specific part of environment

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alertness

state of arousal and readiness to respond to stimuli (part of attention)

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consciousness

primary level of awareness (yourself and surroundings)

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top-down processing

start with expectations/memory --> interpret what you're seeing

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bottom-up processing

start with what you see/hear --> brain figures out what it is

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alerting network

- function: maintains alertness / readiness to respond

- region: reticular activating system (RAS)

- neurotransmitter: noradrenaline (from locus coeruleus)

- prepares prefrontal and posterior parietal to detect stimuli quickly

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orienting network

- function: helps with prioritizing stimuli

- region: parietal and frontal cortex

- neurotransmitter: acetylcholine

- more stimulus-driven (bottom-up)

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dorsal attention system

- function: helps you stay focused on a task (goal-directed attention)

- region: frontal eye fields and intraparietal sulcus

- more top-down visuospatial

- right-lateralized (damage = neglect syndrome)

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neural synchrony

- neurons fire at same time --> timing makes signals more impactful and easier to transmit

- attentional system increases synchrony which boosts important signals and filters out noise

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resting potential

- sodium outside, potassium inside (-70mV)

- inside of neuron is more negative

- sodium-potassium pump moves 3 Na out, 2 K in

- creates electrical gradient that stores energy for AP

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action potential

- depolarization: Na enters neuron

- threshold = -55 mV

- at peak: Na channels close, K channels open

- K exits cell --> repolarization restores negativity

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refractory period

- neuron cannot immediately fire again

- Na channels closed, K channels open

- AP moves forward, triggers adjacent channels

- no backfiring due to hyperpolarization

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all-or-none law

if threshold is reached, full AP fires

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myelin sheath

- fatty insulation around axons

- oligodendrocytes (CNS) and Schwann cells (PNS)

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EEG

- measures electrical activity in brain

- high temporal (time) resolution

- poor spatial (place) resolution

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neuroimaging

- measures brain activity indirectly

- high spatial (place) resolution

- poor temporal (time) resolution

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primary motor cortex (M1)

- located in frontal lobe

- responsible for executing voluntary movements

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premotor cortex

- located in front of M1

- responsible for planning and organizing movements

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somatic nervous system

- part of PNS

- controls voluntary/conscious movement

- acetylcholine

- ex. walking, writing, waving

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autonomic nervous system

- part of PNS

- works automatically/unconsciously

- acetylcholine and norepinephrine

- ex. heart rate, digestion, pupil dilation

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visual field disorders

- hemianopsia: loss of half of visual field (opposite sides)

- blindsight/cortical blindness: no conscious visual perception but can respond to stimuli unconsciously

- cortical color blindness: cannot perceive color (V4)

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object agnosias

- apperceptive: cannot form perception

- associative: can perceive but not identify

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other agnosias

- prosopagnosia: face blindness (right FFA)

- alexia: word blindness (left FFA)

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simultanagnosia

- cannot perceive more than one object at a time

- damage to dorsal stream or Balint's syndrome

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amusia

- impairment in pitch discrimination

- Heschl's gyrus (musicians have larger)

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auditory hallucinations

- perception of sound without external stimuli

- caused by spontaneous activity in A1

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Wernicke's aphasia

- word deafness

- affects language comprehension

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Geschwind syndrome

- temporal-lobe personality

- egocentric, aggressive, pedantic speech

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central executive network

- present moment attention

- when central executive more active --> default mode is less active

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default mode network

- thinking about past, future, or mind-wandering

- when default mode more active --> central executive is less active

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salience network

- most active when behavioral change is needed

- snaps you out of mind-wandering

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nonfluent aphasias

  • Brocas

  • Transcortical motor (TMA) - good repetition


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fluent aphasias

  • Wernicke

  • Transcortical sensory (TSA) - good repitition

  • Conduction

    • disconnection between Broca and Wernicke areas

    • can understand and produce language but can’t relay info between


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pure aphasias

  • agraphia: writing

  • alexia: reading

  • anarthria: speech production problem


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meditation

reduces activity in default mode and increases salience and central executive

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dual executive networks

  • frontoparietal: active when you first get instructions, adjust strategies

  • congulo-opercular: active throughout entire rask, sustained attention