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| 3 principles of sensorimotor |
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1)motor outputs are guided by sensory inputs 2)learning changes the nature and locus of sensorimotor control 3)neural basis of movement is hierarchical |
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| sudden, quick, fast, all or nothing movement |
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| type of ballistic movement where your eye moves from one point of fixation to another |
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| different units have different functions |
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1) Skeletal (striated) 2) Smooth 3) Cardiac |
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-relax/contracts quickly -rapid bursts making strength of speed -fatigues quickly (sprinting) |
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-relax/contract slowly -generate extended contractions -resistant to fatigue (marathon) |
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-opposite movements at a joint Flexor: muscles that flex or raise Extensor: muscles that extend or straighten |
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| where one neuron synapses with muscle cells |
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| ACH is the neurotransmitter in motor neurons that depolarizes and opens Ca2+ channels which initiates contraction |
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| one motor neuron and all fibers it innervates (ranges from a few to many) |
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-nicotinic ACH receptors -located on motor end plate -activation causes contraction |
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-most potent protein known to man -prevents synaptic vessicles w/ ACH from fusing with pre synaptic membrane -leads to paralysis -also known as BOTOX |
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1-Dorsolateral Tract 2-Ventromedial Tract |
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| 2 parts of Dorsolateral Tract |
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1-Rubrospinal 2-Corticospinal |
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| 3 Parts of Ventromedial Tract |
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1-Vestibulospinal 2-Tectospinal 3-Reticulospinal |
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-not important in primates -motor cortex to red nucleus |
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-aka pyramidal -axons going from cortex to spinal cord -crosses at medulla forming "pyramids" |
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-starts in vestibular nuc. in inner ear -maintains head position while moving |
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-starts in tectum -eye orientation while moving |
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-starts in reticular formation -maintains posture |
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| Motor Cortex consists of how many primary and how many secondary areas? |
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-1 primary and 2 secondary -the 2 secondary areas are known as supplementary (homonculus) and premotor |
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| neural systems are integrated, not sequential |
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-axons extend to brainstem and spinal cord, not directly to muscles -brief stimulation causes twitches, while extended stim. causes complex movement |
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-no fixed movement -specific muscle movements differ depending on starting point |
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-integrates sensort info w/ info about body (from posterior parietal) -helps select appropriate movement -eg) you see a step and prepare to go down it |
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-neurons in the premotor cortex that fire when animal performs action and when same action is performed by another animal -integrating same behavior from YOU to ME -may play part in autism |
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| Why are Mirror Neurons important? |
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-play role in imitation/social learning -turns sensory info from others and turns it into personal muscle info |
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-you see others and understand their behavior b/c they have minds too. -a lot of theory, no data |
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| Supplementary Motor Cortex |
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-involved in planning, organizing sequence of events -includes complex movements from memory -learned sequences |
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| Posterior Parietal Cortex |
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-receives visual, somatosensory, & motor info -helps you move relative to environment -connects to premotor & supplementary motor |
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-involved in coordination -order of muscle contraction & timing -damage causes awkward movements that appear drunk |
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-includes caudate, plutamen, globus -uses info from primary and secondary motor areas and somatosensory cortex -inhibits some behaviors to let others work effectively -role in Parkinson's Disease -involved in REWARD BEHAVIOR |
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1-Myasthemia Gravis 2-Tourette's Syndrome 3-Huntington's Disease 4-Parkinson's Disease 5-Multiple Sclerosis |
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-Autoimmune disease CAUSE: reduced sensitivity of ACH receptors SYMPTOMS: varying degrees of weakness of skeletal muscles, breathing problems. TREATMENT: agonists that reduce acetylcholinerase for temp. relief
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SYMPTOMS: involuntary movements and speech TREATMENT: Haloperidal (a dopamine agonist) -predominantly heritable, but manifestation of symptoms gets worse with environment. |
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CAUSE: autosomal dominant inheritance. mutation of Huntington gene SYMPTOMS: before diagnosis, jerky movements from impaired error correction. later, involuntary movements that get a lot worse. motor system degenerates & cell loss due to Huntington gene
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CAUSE: nigrostriatal dopamine neurons die. alters ability of basal ganglia to start movement
SYMPTOMS: rigidity, tremors, hard to start moving
TREATMENT: L-Dopa-high side effects that increase with dosage |
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| Effect of Genetics vs. Environment on Parkinson's Disease |
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Genetics: -early onset (<50) has strong genetic tie -late onset (>50) has weak genetic tie
Environment: -toxins like pesticides -head trauma -drug use (coffee and cigs reduce risk, marijuana increases risk) -CORRELATION only, not CAUSAL |
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autoimmune disorder SYMPTOMS: deterioration of myelin -->neuron death. scar tissue forms. speed and strength reduced. NOT FATAL OR PARALYZING
TREATMENT: drugs that modify immune activty. slow MS but never fix it |
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| Types of Waves during Sleep Stages |
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Awake: Alpha and Beta Stage 1: Theta Stage 2: Sleep Spindles, K Complexes Stage 3: Slow Delta Stage 4: Slow Delta |
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Electroencephalogram -lets us see difference in wave patterns in differing stages of sleep |
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| large spike in stage 2 waves |
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| short burts of 12-14 Hz. occurs 3-5 times a minute. during stage 2 sleep. |
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electromyogram -muscular activity -REM sleep = muscles lose their tone (atonic) -can't act out dreams b/c dreams are in REM |
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electro oculogram -traces ocular movement of eyes -REM is rapid eye movement, other stages no eye movement |
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1,2,3,4,3,2,REM,2,3,4,3,2,REM,2,3,2,REM
Lose stage 4 near the end of sleep -second half is mostly REM sleep
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| Dolphins and porpoises sleeping patterns |
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-dolphins sleep for 4-60 seconds all day to accumulate about 7 hrs of sleep -porpoises let one side of brain sleep at a time |
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| What kind of sleep do you make up for when deprived of sleep? |
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| you make up slow wave and REM sleep and lose stages 1 and 2 |
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| Why we need slow wave sleep... |
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-not because we need rest from exercise -more related to head temperature -most active areas when we are awake are least active during sleep |
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-only seen in warm blooded vertebrates -changes w/ age: older you get, the less time you spend in REM. 70% to 15% -MAO inhibitors, SSRIs, antidepressants all reduce REM but show no side effects on learning/memory
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-small animals = more metabolism = more sleep - related to safety and eating |
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| Does sleep help us learn/remember? |
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-people get better at visual discrimination tasks over time -the NIGHT BEFORE YOU ARE TRAINED IS MOST IMPORTANT -lack of sleep night after causes loss of remembering too |
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| Does REM sleep help us remember? |
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REM sleep increases as animals are actively learning REM deprivation impairs maze learning -REM aids in learning new tasks |
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-serve in learning and memory -Slow wave early in night. neurons replay activation that occurred while awake, representing recall and amplification -REM later in night: upregulation of genes in synaptic plasticity, implementing transfer of memory from hipp. to cortex. |
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| How does REM promote neurodevelopment? |
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relationship of REM with age related to regulation of genes linked to plasticity and myelination |
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No one is completely sure, but there are a few theories: -Activation Synthesis -Default Theory |
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| Activation Synthesis Theory of Dreams |
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-forebrain integrates info. in your memory with activation from brainstem. -our brains link the unknown with stories and synthesize stories to explain brain activation |
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| Default Theory of Dreaming |
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Definition
REM represents a state like stage 1 which occurs simply because we cant stay in nREM to long and we dont need to get up and do anything. -no drowsiness for missing REM -allows us to be awaken |
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| Areas that promote being awake/alert |
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Definition
-Basal Forebrain -Reticular Formation -Hypothalamus |
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| Basal Forebrain and Sleep |
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-major cholinergic output (ACH neurons) -promotes arousal (think nicotine) -adenosine receptors on cholinergic receptors are inhibitory and make us tired. caffeine is an antagonist |
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| Ventrolateral Preoptic Area (VLPA) and sleep |
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Definition
-monitors and regulates body temp -warm = tired -destruction causes no sleep -Adenosine acts here -sends out inhibitory GABA |
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| Reticular Formation in sleep |
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-high activity = awake -low activity = sleep -similarity b/w REM and wakefulness suggest that some areas may be involved in REM -each part of REM is associated with a nuclues in RF.
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Pons-->Geniculate Nucleus-->Occipital Lobe -precedes, predicts start of REM -pons serves as control center for REM
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| Peribrachial Area and sleep |
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Definition
-connects all nucleui -part of pons -made of PPT nucleus and LDT nuclues -ACH neurons here project to areas that cause: paralysis eye movement cortical activation |
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-tuberomamillary nucleus and histamine -neurons using histamine as NT project to cortex. stim leads to arousal and less REM sleep.antihistamines make you tired
-also has lateral hypothalamus and hypocretin (neurotransmitter) -high during wake -narcolepsy may destroy hypocretin |
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-organized cycle -includes hormones, arousal, learning ability, sleep cycle |
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| stimuli that control timing of circadian rhythms. control timing and external cues |
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| usually about 25 hours in humans, means there must be an internal clock! |
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| Suprachiasmatic Nucleus (SCN) |
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Definition
-in hypothalamus -location of major circ. clocks -tell us when to sleep -transplant SCN = transplant sleep cycle -light/dark cycle goes from optic nerve to SCN, so even blind people know when to sleep. -SCN controls release of MELATONIN from pineal gland |
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1-Physician created 2-Sleep Apnea 3-Nocturnal Myoclonus 4-Restless Leg Syndrome |
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| Physician Created Insomnia |
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-sleeping pills, hypnotics, etc. -work at first, but cause dependency and withdrawal |
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-stop breathing during the night -caused by muscle spasms or atonia types: 1)Central: dont trigger resp. 2)Obstructive: physical block of air 3)Complex: both 1 & 2
-most common in males and obese |
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| excessive twitching of legs. unaware of why you feel unrested |
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| uneasiness in legs that prevents sleep |
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SYMPTOMS: severe daytime sleepiness, or cataplexy- loss of muscle tone while awake (like REM). -sleep paralysis while falling asleep or waking up -dreaming while awake |
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| Hypnagogic Hallucinations |
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Definition
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-abnormality in mech. that causes REM, causes narcolepsy -Narcs enter straight into REM -caused by loss of hypocretin |
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| REM sleep-related disorders |
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REM without Atonia: able to act out dreams, no paralysis. caused by damage to reticular formation. associated with neurodegenerative disorders.
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