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PSY - P 304 : FINAL EXAM

Circadian Rhythm
a daily cyclical change in behavioral and physiological processes (circadian= "about a day")
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Suprachiasmatic Nucleus (SCN)
Act as a brands internal clock -Generates circadian rhythyms in a genetically controlled manner -Single cell extracted from the SCN produces action potential in rhythmic pattern -Damage to SCN disrupts circadian rhythyms
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Zeitgeber
a stimulus (like the morning sun) that acts to reset the biological clock
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Zeitgeber Stimlulus
light sensitive retinal ganglion cells send axons to the suprachiasmatic nucleus to provide an input that rests the biological clock every morning
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Without Zeitgeber
(e.g. animal living in complete darkness) circadian rhythyms have a cycle slightly longer than 24 hrs (~25 hrs)
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Lesions of the Suprachiasmatic Nucleus
-After lesions animal more active in the darks, but sleep cycle loses its rhythm -Withs lights off, sleep cycle becomes completely random
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Awake
-Alpha (8-12 Hz) relaxed state -Beta (13-30 Hz) aroused state
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Stage 1 Sleep
Theta (3.5-7.5 Hz) transitions between sleep and wakefulness
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Stage 2 Sleep
Theta (3.5-7.5 Hz) sleep spindles K complexes
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Stage 3 (slow wave) Sleep
Delta (<3.5 Hz) deepest sleep
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REM Sleep
Beta (13-30 Hz) Rapid Eye Movements No muscle tones most associated with dreams
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Restorative Theory of Sleep
sleep provides a chance for the body/brain to repair what & tear -prolonged mental activity is increased sleep that night -high levels of growth hormones released during sleep that facilitates repair of damaged tissues -sleep strengthens immune system -provides a time for metabolites to be rinsed from the brain tissue
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Sleep alters cleaning efficiency of CSF
-Interstitial space (space between neurons, glia, blood vessels, etc) expands during sleep, allowing greater flow of CSF -Greater CSF flow cleans out metabolites from the brain (including some associated with Alzheimers Disease)
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Energy Conservation Theory
sleep conserves energy during a time (nighttime) in which it would be difficult to replace the calories spent forging/hunting for food (hibernation is an extreme example of this)
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Niche Adaption
quiet period makes it easier to remain undetected by predators
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Facilitation of Learning
sleep allows for a period of memory consolidation & clean-up
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Preliminary findings
-Memories of learned facts (names, vocabulary, etc) reinforced in deep sleep -PAttern recognition (grammas, logic, etc) reinforced by REM sleep -Motor skills (musicians, athletes) reinforced by Stage 2 sleep
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Dreams
often occur during REM sleep
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REM Sleep Dreams
-Associated with narrative storyline ~Often bizarre/illogical, but accepted unquestioningly -Perceptions and actions within the dreams are associate with activation in associated brain areas ~Motorneurons are inhibited so that the dream is not acted out (REM-related paralysis, except for eye movements)
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non-REM dreams
-Less of a narrative component ~Often a simple feeling or emotion -Sometimes associated with: ~somnambolism: sleep-walking ~night terrors: dreams associated with abstract feelings of intense dread/fear (not nightmares)
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Theories of dream meaning
Freudian theory, Action-Synthesis Theory, Evolved Threat-Rehearsal Theory
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Freudian Theory
dreams reflect unconsious conflicts within the mind of the dreamer, in a symbolic for disguised to avoid direct confrontation with conflict ~No evidence supports this
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Action-Synthesis Theory
dreams reflect the brain's (left hemisphere interpreter's?) attempt to create a narrative to explain the random firing of neurons that occurs during the dream, with the deactivation seen in the frontal lob contributing to the illogical nature of dream
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Evolved Threat-Rehearsal Theory
dreams provide a virtual simulation of threatening or unusual circumstances so the strategies for coping can be tested and rehearsed
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Reticular Formation
located in brainstem from the midbrain to medulla, sends axons throughout the brain
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Functions of Reticular Formation
-recieves visual, auditory and somatosensory input (hence their alerting effects) -stimulation of reticular formation awakens a sleeping animal; lesions make an animal drowsy/sleepy
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Ventrolateral preoptic areas (VLPA)
located in the basal forebrain rostral to hypothalamus -elctrical stimulation of VLPA evokes slow-wave sleep
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Control of REM Sleep
peribrachial area of the pons: controls the onset of REM sleep
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Peribrachial area of Pons
stimulation of it induces REM sleep; lesions decrease the occurrence of REM sleep
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REM-related Muscle Atonia
Produced by inhibitory neurons in nucleus magnocelluraris
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REM Behavior Disorder (REM without atone)
-results for lesions of the nucleus magnocelluraris -defect in the neural system that causes REM-related paralysis results in the animal acting out its dreams
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Narcolepsy
neurological disorder characterized by the urge to fall asleep at inappropriate times
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Cataplexy
complete loss of muscle tone during the awake stat, related to a hyper excitability of the neurons of the nucleus magnocellularis 
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Recent findins in Narcolepsy
found to be related to a deficiency in the neuromodultor orexin (hypocretin) -possible autoimmune disease eliminates hypocretin neurons in humans, genetic defect of hypocretin receptors in dogs
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What an emotion includes
1. A subjective feeling 2. A behavioral response 3. A physiological reaction
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Racial Expression Suggests Basic Emotions
-strong cross-cultural similarities -suggests a biological basis for expressive emotions
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Neural Circuits for Facial Expressions
Genuine Smile and Volitional Smile
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Genuine Smile
Circuit passes through orbitofrontal cortex & hypothalamus - A genuine smile (Duchenne Smile) also includes a tightening of muscle around the eyes (Duchenne muscles), causing a slight squint
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Volitional Smile
Circuit passes through Primary Motor Cortex
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Volitional Facia Paralysis
right hemisphere is lesioned and left side is paralyzed -only right side of face response to making volitional smile -genuine smile works fine
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Emotional facial paralysis
left hemisphere lesioned and right side paralyzed -hase muscle strength to move muscles on both sides of mouth -genuine smile only engages left side of face
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Dominance of Production of Facial Expression
Right Hemisphere show dominance for production of facial expressions
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Theories of Subjective Feeling of Emotions
Common Sense View, Cannon-Bard Theory, James-Lange Theory, Schachter's Cognitive Theory
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Common Sense View
is that the subjective feeling is experiences first, then this drives the autonomic response ~good evidence that this is incorrect
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Cannon-Bard Theory
an emotional event simultaneously evokes the feeling of the emotion and the physical changes that accompany it
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The James-Lange Theory
How we feel depends on the interpretation of the physical changes (autonomic, behavioral) that occur in body as response to an emotional event
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James-Lange Theory
-Environmental event triggers behavioral, autonomic, and endocrine response -Feedback from responses produces feelings of emotions
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Schacters Cognitive Theory
The physical changes evoked by an emotional event are attributed to the prevailing environmental conditions, leading to an emotional feeling that corresponds
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Testing of Schacters Theory
Misattribution of arousal is shows evidence of this theory
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Misattribution of Arousal
Misattribution of Arousal participants who were misinformed or uniformed about the cause of their arousal felt either angry or euphoric, depending on whether a confederate was angry or euphoric
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Limbic System
traditionally associated with emotion -Limbic=border between forebrain and brainstem
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Amygdala
-almond shaped structure buried in the temporal lobe -processes emotional significant of stimuli -key structure in fear and anxiety -single unit recordings and fMRI show cells that are responsive to emotional situations/stimuli -Stimulation evokes behavioral effects of strong emotional states (e.g fear or rage)
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Kluver-Bucy Syndrome
Unusual social behavior and emotional responses: -emotional bluntness/tameness -tendencey to approach objects that should elicit a fear reponses -hyperorality -hypersexuality
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Amygdala Damage in Humans (Patient S.M)
-Rare genetic disease causing bilateral amygdala damage -General fearlessness -Little autonomic nervous system activation to fearful stimuli -Impaired at recognizing and drawing fearful expression
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Amygdala & Fear Conditioning
can condition a fear response in stimuli that would not usually invoke a fear response
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Damage to Amygdala
impairs fear conditioning
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 Orbital & Medial Prefrontal Cortex
-regulates emotions according to circumstances -can override initial appraisal of emotional stimuli -control impulses to approach/withdraw
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Phineas Gage
demonstrated that damage to orbital and medial prefrontal cortex caused erratic emotions: frequent outbursts of anger, rage, couldn't inhibit inappropriate behavior
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Frontal Lobotomies
-surgical procedures that isolates the prefrontal cortex from rest of brain -Developed by Antonio Moniz as treatment for various psychiatric disease (e.g. schizophrenia) won the Nobel Prize Walter Freeman perform thousands in 1940s-60s -Typically cause loss of emotions, passivity, difficulty planning, reduced initiative, impulsivity
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Medial Forebrain Bundle & Nucleus Accumbens
Pleasure/Reward Center in the brain
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Hypothalamic Attack Area
-Region in hypothalamus associated with aggression -Single unit recordings show increase in activity before/during aggressive behaviors, decrease mating -Artificial stimulation prompts aggressive behaviors
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Neuropharmacological Basis of Aggression
-Testosterone increases in many species -Relationship in humans less clear -Experience & dominance can affect testosterone levels; winners show higher levels than losers
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Birth position and aggression in female rats
Number of male "neighbors" in the womb affects levels of aggression in female rats -Increases in aggression in 2M females relative to 0M and 1M -Thought to be due to increases in prenatal androgens that spread between neighbors
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Serotonin and Aggressive Behavior
-Serotonin (5-HT) decreases aggression -Low serotonin levels in primates associated with risk taking and aggression -Monkeys with low serotonin end up dying earlier, either from injuries resulting from aggressive behavior or accidents due to risky behavior
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Learning
changes that occur within the brain to allow the acquisition of new information for long-term storage
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Memory
the storage and retrieval of information previously acquired through learning
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Information Processing Model of Memory
Sensory Memory, Working Memory (short-term memory), and Long-term Memory
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Sensory Memory
A trace of the sensory inout for a brief period -High capacity & very short duration (up to few seconds) -Easy accessible, but vulnerable
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Working Memory (short-term memory)
Attentive/conscious processing occurs here. Information can enter from both sensory memory and LTM -Small capacity and short duration (seconds, or minutes w active rehearsal) -Easy accessible, but vulnerable
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Long-Term Memory (LTM)
The stored representation of knowledge gained from previous experience -Large capacity and indefinite duration (up to decades/lifetime) -Difficult to access, but durable
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Types of Memory
Declarative Learning, Implicit Learning
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Declarative Learning
learning facts and info of which we can be aware (what we normally think of as memory) -Episodic memory and semantic memory
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Episodic Memory
autobiographical memories
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Smenatic Memory
generalized memory of facts
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Nondeclarative learning
memory about perceptual and motor procedures of which we are typically unaware -Priming, Motor (skill) learning, and Associative learning (Conditioning)
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Priming
exposure to one stimulus alters response to another
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Motor (skill) learning
learning how to control the body in order to respond appropriately
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Associative learning (conditioning)
learning the relationship between stimuli (classical conditioning), or between behaviors and outcomes (operant or instrumental conditioning)
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Unconditioned stimulus (US)
A stimulus that reflexivily elicits a response, without prior learning
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Unconditioned response (UR)
the response reflexively elicited by unconditioned stimulus, without prior learning
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Neutral stimulus
a stimulus that elicits no reflexive response
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Conditioned stimulus (CS)
a stimulus that elicits a particular response only after learning
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Conditions response (CR)
the response to a conditioned stimulus, after learning has occurred
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Synaptic plasticity
the basis of learning involving a change in the synaptic structure or biochemistry that alters the efficiency of the synapse in a positive or negative way (Plasticity=the capacity for being molded of altered)
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Hebbian Rule
a synapse is strengthened if it is repeatedly active when the postsynaptic neuron fires "Neurons that fire together, wire together"
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Long-Term Potentiation (LTP)
a mechanism by which synaptic connections are strengthened, allowing for a larger excitatory postsynaptic potential (EPSP) in the postsynaptic neuron (Potentiation=to strengthen or make more potent)
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NMDA receptors
-ion channel opens when bout w/ glutamate neurotransmitter -but channel blocked by Mg2+ ion -unless neuron is depolarized already (pushing Mg2+ away) when glutamate is bound -Na+ and Ca2+ can enter ~depolarizes neuron ~Ca2+ acts as a 2nd messenger
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Effects of LTP
-causes the insertion of additional glutamate receptors into postsynaptic membrane -causes structural changes of the synapse that lead to the creation of new synapse -causes creation of the neuromodulator Nitric Oxide, which diffuses to presynaptic neuron and enhances glutamate release
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Evidence for Role of LTP in Learning
-LTP prominent in brain areas involved in learning -Drugs that block LTP also impair learning abilities -Drugs that facilitate LTP also enhance learning abilities -Mice genetically-enhanced to have more NMDA receptors have better learning abilities (Doogie mice)
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Instrumental (Operant) Conditioning
is in which the likelihood that an act will be performed depends on the consequences of the reinforcing stimuli that follows
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Biological Basis of Reinforcement
positive reinforcement is associate with the release of the neurotransmitter dopamine in the "Reward Centers" of the brain (e.g. nucleus accumbent, ventral segmental area) -Food, sex, $$$. addictive drugs -Amount of dopamine released sets a reinforcers reward value ~more dopamine= more effective reward
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Long-Term Declarative Memory
relies on the hippocampus and medial temporal lobe
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Morris Water Maze
Environmental cues in room provide info that permits animal to orient themselves in space and learn the location of hidden platform
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Hippocampus and Spatial Navigation
PET scan showing activation of right hippocampal formation from subjects navigating through town
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Medial Temporal Lobectomy (Patient H.M: Henry Molaison)
-underwentd surgery for severe epileptic seizures -bilateral removal of medial temporal lobe, including hippocampus -almsot total loss of the ability to encode new long term memories -but preserved short term memory..can hold normal conversations, intact reading ability, and other skills that require only temporary maintenance of info
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Medial Temporal Lobe Lesion of Clive Wearing
-In 1985 damage to the medial temporal lobe due to an encephalitis infection -Profound anterograde and retrograde amnesia -Can still play the piano, although he has no recollection of ever having been trained
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Amnesia
a profound impairment of memory as the result of brain injury; the extent of both retrograde and anterograde amnesia depends on severity of injury
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Retrograde Amnesia
can't remember events prior to brain damage
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Anterograde Amnesia
can't later remember events that occur after brain damage
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Anterograde Amnesia as Evidence for a Consolidation Process
H.M. had: -normal long-term memory of distant past -normal short-term memory (could carry on conversation, could remember numbers w/ rehearsal, et.) -but could not for new long-term memories ~Thus hippocampus involved in consolidation
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Consolidation
process by which immediate memories become lasting (long-term) memories
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Memory Storage
-hippocampus needed for consolidation, but not where memories are stored -memories are though to be stored in cortex
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Consolidation view of memory
is when memories are consilidated from short-term to long-term and retrieved for use
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Reconsolidating view of memory
memories are retrieved from long-term memory for use and then reconsolidated back to long-term memory
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Reconsolidation
allows for memory disruption in memory
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Anisomycin
prevents reconsolidation only after recollection of the information so that the info is forgotten
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Reconsolidation allows
for memory distortions
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Motor Learning
relies primarily on the cerebellum and the basal ganglia
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Alzheimers Disease
a degenerative disorder (cause unknown) that results in a progressive dementia, loss of memory, confusion, hallucinations, motor deficits and eventual death - Wide sulci indicate thinning cortex due to cell death -associated with neuronal degeneration, neuritic plaques, and neurofibrillary tangles
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