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Hypothetical means by which memory is stored, memory trace, parahippocampal areas |
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look at mice brains to figure out where memory is located- memory loss is correlated with size of lesion, but not location of lesion (on cortex) |
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why engram was not found o Cortical lesions all burned away- effects not easy to predict. Made unintended subcortical lesion (probably effected hippocampus too) which accounted for memory loss. Out of 37 rats, 21 had damage to HC. Lashley didn’t know HC lesions cause amnesia, so he ignored the damage to HC, thalamus, and striatum as less-evolved structures of brain. o HC is encoding of memory. |
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(bicycle injury and seizures- took out medial temporal structure, amygdala, perirhinal and entorhinal cortex, anterior HC; kept parahippocampal cortex, temporal neocortex) •Amnesia for new information •Could retrieve old information •Could get better at practiced skills/tasks, but could not remember having done task or explain how to do it (procedural memory, implicit memory) doesn’t rely on HC HM couldn’t develop some stuff from tower tests even though didn’t have damage to basal ganglia •HM could do mirror maze tasks |
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took out medial temporal structure, amygdala, perirhinal and entorhinal cortex, anterior HC; kept parahippocampal cortex, temporal neocortex) |
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oPredict dementia using memory tasks, ID for prevention Mild cognitive impairment- distinction between retrieval of info vs familiarity. Picture superiority effect- pictures not effected while verbal are effected More you rely on familiarity, not retrieval= dementia |
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•Different pathways of excitatory information in HC •Spatial information o Verbal vs nonverbal information in humans • HC integrates information, esp to help navigation |
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•Place cells fire when rat is in specific locations in water maze (based on landmark objects) o Damage to HC results in failure to encode memories of motor procedure/ directions |
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larger posterior HC volume from three years of training oTemporal relationship- ppl with larger HC are more likely to become taxi drivers o Innate navigation expertise tested o Tested non-taxi drivers to find relationship b/t larger HC and direction strengths |
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hyperactive HC behavioral effect(possibly from seizures, also mentioned in interictal behavioral symptoms from Liorah's presentation) |
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•In clinical, suddenly/ abrupt find meaning/purpose, something that is not typical for them- suddenly becomes very religious or very interested in an activity/concept |
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immediate/ eideic memory (sensory) |
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o Ie tested with box with bunch of numbers inside, short exposure o Maybe remember 4 out of 12 numbers, but can always remember number with arrow pointing to it after box disappears. Take in whole object, but can only retrieve certain amount (why?)- create average prototypes, only attend to important things, Sperling test o What happens to information we can’t retrieve- implicit learning, changes based on priming, not conscious |
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brain automatically combines images from two eyes, why we can't recall whole image, but evidence that you did encode the whole object |
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o Lasts for 20-30 seconds unless ongoing rehearsal o Information is pulled into stm from im and long-term-memory o ECT/ trauma- can disrupt short term memory, and therefore not put into LTM |
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= remembering several things at once, integrate, hold information in one setting, attentional buffer that temporarily holds and manipulates info, Forward span and backward span- more backward span •N-back tasks- when encounter same stimulus as what came right before it, respond (n=1, n=2) remember preceeding •Associated with g-factor, general factor of fluid intelligence •Problem solving |
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terms used for different sensory working memory |
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•Phonological loop, visiospatial sketch pad, episodic buffer |
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unlimited capacity Long lasting, some forgetting over time |
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Semantic (facts and events) •(don’t need to remember when/how you learned it, not context specific) |
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location of declarative memory |
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implicit; Procedural skills and habits; priming effects |
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location of nondeclarative memory |
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Procedural skills and habits(striatum in basal ganglia) Priming (neocortex) Classical conditioning •Emotional responses (amygdala) •Skeletal musculature (cerebellum) Non-associative learning (reflex pathways) |
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turning episodic into semantic memory Turn instance of learning information to fact |
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consolidation of STM to LTM |
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starts with HC, then limbic system (circuit of Papez), limbic structure loops, then hypothalamus/fornix- anterior thalamus |
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inability to encode or remember (usually episodic, but could be acquired/ procedural) |
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structures associated with working memory |
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dosolateral prefrontal cortex and hippocampus. activated simultaneously |
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type of nondeclarative memory that can be used as a test of malingering |
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priming- everyone should experience effects of priming. |
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damage in Korsokoff's syndrome |
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form new memories but cannot retrieve them in context due to damage to mamilliary bodies and dorsomedial nucleus of thalamus make links to various objects in the room, cannot take context into effect |
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frontal lobe lesion effects |
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can recognize but cannot recall information |
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inability to recall previously encoded memories |
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inability to create new memories |
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Right dorsolateral prefrontal cortext |
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left dorsolateral prefrontal cortex and memory |
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bilateral and right prefrontal cortext info |
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Nonverbal and episodic memories |
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left prefronal cortext: info |
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recall of verbal and nonverbal semantic info |
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•Familiarity- rapid automatic no context •Recollection- active retrieval, slow controlled, context |
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donald hebb/ "hebb's rule" |
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proposed synaptic change is due to repeated, persistent firing from cell A to cell B, metabolic change/growth= efficiency, increased firing= long term potentiation |
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Bliss and Lomo bunny study |
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few seconds of high frequency signals, 100Hz, tetanic/ half frequency. Larger EPSPs in the post stynaptic cell of fiber pathway in HC persist for weeks. *learning* |
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mechanism of long term potentiation |
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glutatmate binds to receptors in post-synaptic cell. Ampar and mmda receptors. Glutamate is excitatory/ lets in positive ions. Mmda typically blocked by a magnesium ion. Once post-synaptic cell becomes depolarized, able to pump magnesium cell out and Glutamte can bind, allowing Calcium to come in. Influx of calcium (DNA/action potential) with the help of serotonin among other proteins, triggers alterations in gene expression. |
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importance of calcium for long term potentiation |
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makes structural changes= causes production of new AMPAR receptors, synthesis of nitric oxide (NO gas retrograde messenger to the pre-synaptic cell ) that produces and releases more glutamate, faster process of depolarization, strengthening the synapse |
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2 methods of long term potentiation |
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a.Development of more receptors on post-synaptic neuron b.retrograde influence on the pre-synaptic neuron causing more NT release *could do both |
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2 properties of long term potentiation |
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a.Specificity: at active synpases, but not inactive synapses b.Associativity: pathway 1 strengthened with strong stimulus AND close pathway 2 strengthened with weak stimulus |
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ltm occurs at active synpases, but not inactive synapses |
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pathway 1 strengthened with strong stimulus AND close pathway 2 strengthened with weak stimulus |
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long term depression mechanism |
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Low frequency stimulation- not rapid, intermittent stimulation causes inhibition at that synapse. Decrease number of AMPA receptors. Activation of second messenger system that results in fewer AMPA receptors, less efficient. |
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Tsien studies- mice and LTP |
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When added genes from older mice to younger mice in NR2B subunit of protein machine, allow extra calcium into units Genetically engineered do better on milky maze and novel objects. Normal learning of older was restored and younger mice enhanced |
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properties of neurons that explain why relearning is quicker than starting from scratch |
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single sensory neuron has 1300 presynatpic neurons with 25 target cells. Only 40% of synapses are active. Others are dormat. i.Number of active synapses and terminals increases from 40-60% ii.As memory fades, presynaptic terminals decrease but still more than baseline iii.Once a task is learned, there are savings in relearning |
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explicit vs implicit memory: difference |
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consious vs nonconscious memory/ retrieval |
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episodic vs semantic memory |
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autobiographical (events) vs facts, information |
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declarative memory: location of encoding |
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prefrontal left hemisphere/ cortex |
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declarative memory: location of retrieval |
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prefrontal right hemisphere/cortex |
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declarative memory: location of consolidation |
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medial temporal lobes, HC, basal forebrain |
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in working memory, attention controlling portion |
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speech based information in working memory |
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visual based information in working memory |
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temporary, limited capacity storage, integrate different modalities |
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