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Memory & Learning
Terms in this set (27)
What are the two routes to amygdala? Pros? Cons?
1. Direct from thalamus: Pros - quickest path, fast response Cons - less processed information, possibility of FALSE ALARMS
2. From thalamus to cortex/hippocampus: Pros - complex processing of info before alerting amygdala Cons - Slower path, slower reaction
Memory circuit (Papel circuit)
1. Cortex -->
2. Hippocampus --> (pass through fornix)
3. Mammillary body (hypothalamus) --> (mammillothalamic tract)
4. Anterior nucleus (thalamus) -->
1. Cortex -->
2. Amygdala -->
through stria terminalis --> hypothalamus (motor output) --> brainstem/spinal cord
through ventral amygdalofugal pathway --> Medial Dorsal nucleus of Thalamus (emotional output) --> Cortex
What parts of the brain are associated with 1.) Visceral response to emotion and 2.) Emotional response to emotion
2. medial dorsal nucleus of thalamus
Kluver-Bucy syndrome: symptoms? cause?
Symptoms: urge to put objects in mouth, memory loss, extreme sexual behavior, visual distractibility.
Cause: Damage to the temporal lobe AND amygdala just below it. Ultimately the "WHAT PATHWAY" is destroyed - cannot link an object to its significance.
Dorsolateral/Orbital Prefrontal Cortex: Role?
Nucleus accumbens: Role?
Dorsolateral/Orbital Prefrontal Cortex: working memory (problem solving/planning/organization)
Nucleus accumbens: reward/motivation/drive
Amygdala: emotion-associated learning
Neural mechanisms of memory: pruning? plasticity?
Pruning - cutting weak synaptic contact, strengthening important synaptic contacts
Plasticity - ability of neurons to remodel based on experience and environment
Retrograde vs. anterograde amnesia
Retrograde: problems recalling information prior to trauma
Anterograde: problems recalling information after trauma
Hippocampal damage causes?
Korsakoff's Syndrome: causes? symptoms?
Cause: thiamine deficiency in brain (alcoholism/diet)
Symptoms: patients confabulate - fill in gap in memory with falsification
Declarative vs. Nondeclarative memory
Declarative: deals with WHAT - facts/info, shown by telling others verbally
Non-declarative: deals with HOW - shown by performance before others, not recollection
Two types of declarative memory?
1. Semantic - generalized (stored in cortex, temporal lobes)
2. Episodic - detailed autobiographic information (stored in cortex, temporal regions)
Two types of non-declarative memory?
1. Skills - bike riding (uses regions: basal ganglia / motor cortex / cerebellum)
2. Conditioning - salivating when you see a steak (simple = cerebellar, complex = hippocampus + cortex)
What hemisphere of the prefrontal cortex is used... recalling pictures? recalling words?
Pictures: right prefrontal cortex + both parahippocampal hemispheres
Words: left prefrontal cortex + left parahippocampal hemisphere
What structure is involved in consolidation? Where does the actual consolidated information get stored?
Hippocampus - helps consolidate information
Cortex: long term memory storage site
PTSD: cause? treatments?
Cause: strong emotions can enhance memory formation and retrieval - many NTs participate. In PTSD memories produce a stress hormone.
Treatments: block chemicals acting on amygdala
How can changes in plasticity be made?
1. increased neurotransmitter release from existing synapses
2. formation of new synapses / rearrangement of existing
What life conditions are best for plasticity?
An enriched environment (socially, activity, environment)
What is long-term potentiation? What is tetanus?
A stable increase in the effectivness of synapases
tetanus is brief, fleeting increase of electrical stimulation
Nuerogenesis: where does it happen in adults? how can it be increased?
Where: mainly in the dentate gyrus
How: enhanced by exercise, environmental enrichment, memory tasks
Deterioration of what areas are associated with Alzheimers?
(Cholingeric pathways) septal complex and nucleus basalis of Meynert
Changes of the brain with aging:
1. Brain weight declines --> marked loss of hippocampus
2. Desposits/plaques on vessels and nerve cells
3. Cerebral blood flow declines
4. NT systems decrease
Transient Global Amnesia
Temporary loss of memory/cognition - usually caused by stroke of the MCA
What are two specific micro-level causes of Alzheimers?
1. Neurofibrillary tangles - INTRAcellular, accumulation of filamentous aggregates of protein tau
2. Plaques - EXTRAcellular, spherical accumulations of aggregates of amyloid-beta-peptide
Progression of Alzheimer's:
1. Mild Cognitive Impairment
2. Mild Dementia - short term memory loss, trouble reasoning, repetitive questions
3. Moderate - daily function impaired
4. Severe - Behavioral disturbances, total dependence
Beta-amyloid levels in those with Alzheimer's:
Raised in parietal and frontal lobes
Atrophy of frontal and temporal lobe, sparing of superior temporal gyrus
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