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PSYC 322 Midterm 1 Study Guide

by: Alexandra Brown

PSYC 322 Midterm 1 Study Guide 322

Marketplace > Emory University > Psychology (PSYC) > 322 > PSYC 322 Midterm 1 Study Guide
Alexandra Brown
Emory University

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Lectures covered for midterm 1
Biological Basis of Learning and Memory
Dr. Joseph Manns
Study Guide
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This 17 page Study Guide was uploaded by Alexandra Brown on Saturday April 9, 2016. The Study Guide belongs to 322 at Emory University taught by Dr. Joseph Manns in Fall 2016. Since its upload, it has received 20 views. For similar materials see Biological Basis of Learning and Memory in Psychology (PSYC) at Emory University.


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Date Created: 04/09/16
Lecture 1 1. Early Philosopher’s speculations on memory Aristotle (ca 350 BC)  One of the earliest thinkers to contemplate workings of memory  Considered psychological distinction between recollection and familiarity o Recollection  EX: see someone on campus named Sally from chemistry lab o Familiarity  EX: Sally is walking up to you, but you can’t remember her name…unable to recollect  Was a philosopher; NOT a scientist o Does not know how brain supports memory  Thought was that the heart was the source of intellect o Thought this was where cognition was located Maine de Biran (1804)  Envisioned three types of memory: o Representative memory  Everyday “memory”  What we will call declarative memory o Mechanical memory  Unconscious memory for actions  We now know involves several types of memory o Sensitive memory  Unconscious emotional memory  We now know to be supported in part by amygdala  Acquisition of dispositions  Whether I like it or I don’t  Was a philosopher; not a scientist  Did not consider biology of memory o NO EXPERIMENTATION! Franz Gall (1825)  Originator of phrenology o Phrenology- idea that parts of the brain that you use the most are going to be the biggest; also idea that the external shape of your skull has nothing to do with brain size  Thought different parts of the brain supported different functions o Important for different aspects of cognition  Thought that one could discern another’s strong traits by feeling bumps on the skull  Imagined that some brain areas were important specifically for memory 2. Darwin and his impact on scientific thought Charles Darwin (1859)  Developed idea of natural selection as mechanism of evolution  Idea had an enormous impact on study of biology  Idea that randomness and natural selection are at the core of life led scientific thought away from creationism  Indirectly led to scientific investigation of memory  Suggested natural selection and sexual selection as mechanisms of evolution  Idea of natural selection led to ability for natural world to be explained William James (1890)  Philosopher who often thought of as one of first American psychologists o Began doing experiments on memory o Used data to create falsifiable hypotheses  Used others’ investigations of reflex pathways as a starting point for thinking about memory  Distinguished habits from true memory  Distinguished working memory from long-term memory (he called them primary memory and secondary memory)  Representative of transition from introspection to experimentation 3. The question of memory localization How does your brain store new information? Localized or diffused Karl Lashley (1929)  Asked whether memory for maze was stored in a particular brain region  Trained rats to run maze  Carefully removed different parts of the brain in different rats  Retested brain damaged rats to see if they could still remember the maze  RESULTS: o Found that particular location of damage did NOT seem to matter o Instead, HOW MUCH of the brain was damaged was what mattered  Concluded that all areas of cortex contribute to memory equally, that is, that memories were distributed Wilder Penfield (1938)  Neurosurgeon who stimulated brains of awake patients during surgery to treat epilepsy  Wanted to know what parts of the brain did what  Looked at severe epileptic patients o KNOWN cure for severe epilepsy is to take out the dysfunctional part of the brain  Delivered electricity to parts of the brain and asked “what did that do”  Stimulation in some areas elicited specific memories  Medial temporal lobe o Elicited specific memories  Finding that stimulation specific areas led to specific memories suggested that memories were localized Donald Hebb (1949)  Suggested a reconciliation between Lashley’s and Penfield’s findings o Suggested that memories are supported by networks of interconnected neurons o He called this type of network a cell assembly o Idea of cell assembly:  Data that memories are distributed and data that memories are localized BOTH make sense  Brain is an interconnected web of neurons Hebb’s “Cell Assembly” (1949)  Memories depend on the connections between different points, or nodes in the network  Memories are both localized and distributed  To the extent that a memory depends on each individual connection, it is localized  To the extent that recalling a full memory depends on reactivating the entire network, it is distributed o Think of connections o Full memory- ability to remember the memory and be able to speak it  One new experience can change direction  New fact strengthens one synapse 4. Behavioral Psychology B.F. Skinner (1938)  One of the most prominent figures in behavioral psychology or behaviorism o Behaviorism- focus on behaviors and the stimuli that correlarte with them  Argues that all behaviors could be explained by a series of stimuli and responses  Unobservable mental events were best ignored  Purposeful avoidance of brain and cognition set tone of psychology during middle of 1900s  Thus, the influence of Hebb’s ideas was not as great as ne might have otherwise suspected 5. Patient HM Brenda Milner (1957)  Neuropsychologist who studied patient H.M.  H.M. had medial temporal lobes removed bilaterally as last effort to curb epilepsy  Surgery led to memory impairment that is called anterograde amnesia  However, surgery left intact language, IQ, personality, perception, and working memory  H.M.’s case indicated that medial temporal lobes were important for memory  H.M.’s case was beginning of modern study of memory systems  H.M.’s surgery” o Surgery reduced epilepsy o Acquired NO MORE NEW declarative memories o Surgery was selective to memory specifically declarative  Speech, language, problem-solving was all intact o Medial temporal lobes NOT important for vision, speech, problem solving o H.M. could maintain things in working memory, but ONLY is he held onto it 6. Early study of cellular aspects of memory Terje Lomo and Timothy Bliss (1973)  Discovered long-term potentiation (LTP)  LTP refers to the strengthening of the connection between two neurons  Thought to reflect a cellular basis of memory  Found a way to measure strength between two memories MAIN POINTS  Some early philosophers had good ideas about memory but did not ground their thinking in empirical data  Darwin’s ideas about evolution led to more empirical research in many areas, including psychology and neuroscience  One of the earliest questions about memory and the brain was whether memory was localized or distributed. Answer is both  Hebb’s idea of “Cell Assembly” is how we will conceptualize memory  Behavioral psychology probably delayed the modern era of memory research  Patient H.M. marks the start of the modern era of memory research  Lomo and Bliss were the first to study a neural mechanism of memory—how a connection between two neurons could be strengthened Lecture 3: Amnesia 1. Recap: Working memory, declarative memory, and H.M.  H.M. lost a large chunk of his hippocampus and amygdala  Medial temporal lobes removed bilaterally  Surgery led to memory impairment that is called anterograde amnesia o Anterograde amnesia- inability to form new memories going forward (after damage)  H.M. exhibited a problem with encoding and retrieving memories 2. E.P.: another patient like H.M. How bad was E.P.’s memory?  Presented a figure  Asked to copy the figure  E.P. was able to copy the figure with no problem  After a 15-minute delay and asked to draw the figure again E.P. responded by saying “what picture?” o Doesn’t remember drawing a figure o No memory of that event occurring 15 minutes ago  E.P.’s damage was specific to declarative memory E.P. Video  Logical reasoning intact  Intact working memory o EX: word recall  Repeats himself o Unaware that he tells the same stories over and over  Could not remember the name of the scientist who was testing him, even though they’ve met over 100 times  Damage to hippocampus and surrounding tissue results in E.P. constantly living in the present  new memories CANNOT be recorded  Hippocampus is crucial for recording new memories E.P. was asked about his childhood neighborhood  E.P. can easily remember his childhood neighborhood o Intact declarative memory from his past  Does NOT know the street names of the neighborhood he is currently living in E.P. remembers his old neighborhood quite well  E.P. performed well on all 3 navigation tasks o Familiar navigation: how to get to grocery store and back o Novel navigation: how to get to grocery store and back using a different road o Alternative navigation: how to go from grocery store to home if street A is closed  However, E.P. CANNOT remember anything about his current neighborhood because he moved there after he became amnesic; after the brain damage 3. Damage restricted to the hippocampus  E.P.’s damage included the hippocampus and cortical areas surrounding the hippocampus  Patient R.B.’s damage was restricted to the hippocampus Patient R.B.: a case of moderately severe amnesia  R.B. was presented with a figure  Asked to copy the figure  15 minutes later, he was asked to draw the figure again, but this time from memory  Had a slight memory of the figure (knew it included boxes and triangles)  Damage to the hippocampus only produces BAD amnesia, but not severe  Damage to the entire medial temporal lobe produces SEVERE amnesia 4. Amnesia: anterograde and retrograde  Tested amnesic patients with damage to the hippocampus and normal patients  Asked them a series a questions about things that happened in the world  Amnesic patients have “normal” memory of events 15-30 years prior to brain damage  Amnesic patients have an impaired memory of event that occurred 5-10 years prior to brain damage o Temporal gradient  Anterograde amnesia: memory impairment of events that occurred AFTER brain damage  Retrograde amnesia: memory impairment of events that occurred BEFORE brain damage  Retrograde amnesia may extend back many decades in patients with large medial temporal lobe damage o In E.P.’s case, his retrograde amnesia is extended back approximately 30-35 years prior to his brain damage  When you’re told new information you hold it in your working memory or 0-5 seconds  Getting information from your working memory to your long term memory (5 secs to 1 year) depends on making a record in your brain o Hippocampus is NOT connected to working memory  To keep that information in your long term memory (1 to 5 years), you need brain reactivation while you are sleeping o Stable structural changes in the brain o After memory is formed, neocortical connections need to be made involving the hippocampus  After 15 to 40 years, the connections throughout the brain are either overly redundant or not needed at all o Damage to the hippocampus would leave the connections unaffected Consolidation and retrograde amnesia  Damage to the medial temporal lobe results in temporally- graded retrograde amnesia  The process by which memories that were once dependent on the hippocampus (and rest of MTL) become independent of the hippocampus (and rest of MTL) is called memory consolidation o Information that was once dependent on your hippocampus becomes independent over time o Redundant connections with neocortex become stronger until memory no longer needs the hippocampus  Memory consolidation provides an explanation for the observation of temporally-graded retrograde amnesia  Full memory consolidation takes 10-15 years to be independent from the hippocampus 5. Working memory in absence of declarative memory  Short delay tasks  Flash image on the screen and ask participants to pick out the image a few seconds later  All patients begin to perform poorly at 6-10 seconds  Persistent neural activity because you can’t do sub-vocal rehearsal for an image  Long term memory can be useful in ~10 seconds 6. Nondeclarative memory and the concept of memory systems  Mirror drawing task  As you repeat the task, you get fewer errors  H.M.’s performance improved with repetition  H.M. does not remember this task, but acquired good performance at a normal rate  H.M. learns new memories, just not declarative ones  Mirror-reversed text reading  Get better at reading mirror-reversed text over time  Amnesic patients improved with repetition o Same level of performance between both controls and amnesic patients  Medial temporal lobe is responsible for conscious memory o Memories you can bring to mind as conscious recollection  Somewhere other than the medial temporal lobe is responsible for nonconscious memory o Memories that aren’t available to conscious recollection MAIN POINTS  Damage to medial temporal lobe results in profoundly severe anterograde amnesia  Damage restricted to hippocampus results in moderately severe anterograde amnesia  Damage to medial temporal lobe (or just hippocampus) leads to temporally-graded retrograde amnesia  Damage to medial temporal lobe leaves intact working memory  Damage to medial temporal lobe leaves intact non-memory abilities  Damage to medial temporal lobe leaves intact examples of nondeclarative memory  One distinction between declarative and nondeclarative memory is the distinction between conscious and unconscious memory Lecture 4: Hippocampus, part 1 1. Review 2. Why does the brain work this way? 3. Definitions of episodic and semantic memory  Episodic memory and semantic memory are 2 types of declarative memory o Episodic memory= memory for events  single episode  personally-experienced  includes contextual details (EX: time, place, temperature)  e.g. “I ate Philly rolls for lunch.” o Semantic memory= memory for facts  Knowledge about the world  Not necessarily tied to original learning incident  e.g. “Philly rolls are raw salmon and cream cheese.”  Distributed cognitive network of semantic memory o Knowledge about the world is semi-categorical o Interrelated webs of knowledge  Distributed neural network of semantic memory o Represent different parts/modalities of information in different parts of the brain  EX: action, sound, motion, words, shape, color, etc.  Patients with focal lesions of neocortex can exhibit sematic dementia o Semantic dementia= lose memories of category specific information about the world o Shown a vegetable and asked what color vegetables normally are  Response: green (CORRECT) o Shown a pumpkin (which is also a vegetable) and asked what color it normally is  Response: green (WRONG) 4. Three ideas about episodic memory, semantic memory, and the brain  IDEA #1: Episodic memory depends on the medial temporal lobe. Semantic memory does not depend on the medial temporal lobe. o Supporting evidence:  Patient K.C. had widespread brain damage including some to the medial temporal lobe  Patient K.C. could learn new “facts” (3-word facts)  i.e. he had intact semantic memory  Dentist cured _______ (answer=hiccup)  But he could not remember the testing sessions  i.e. he had impaired episodic memory o Opposing evidence:  Patient E.P. had extreme difficulty learning 3-word “facts”  E.P. only had damage to the medial temporal lobe  E.P. could not use flexibly the “facts” that he learned  When given a synonym for “cured” E.P. did not know how to respond, but control patients did  E.P.’s responses were habitual responses  IDEA #2: Episodic memory depends specifically on the hippocampus. Semantic memory does not depend on the hippocampus. o Supporting evidence:  3 people with damage to the hippocampus sustained before age 4 (developmental amnesics)  Asked to copy a figure  Minutes later asked to draw the figure from their memory  BAD RESULTS  Bad episodic memory o Opposing evidence:  Developmental amnesics show that the brain can compensate  Episodic memory was bad, but semantic memory was normal  IDEA #3: Episodic memory and semantic memory both depend on the hippocampus and on the rest of the medial temporal lobe. o Patients with confirmed damage restricted to hippocampus are impaired in acquiring both episodic memory AND semantic memory o Declarative memory depends on the hippocampus o All declarative memories are acquired as part of an event o Initially, those memories are distinct and rich in detail for the contextual details. You could call them episodic details. o Over time, those memories are consolidated into our existing fund of knowledge. o The aspects of the memories that made them distinct – the episodic details – are sacrificed so as to emphasize the aspects of the memories that are shared with other memories –the relationships between semantic features o The process of consolidation is also a process of semanticization  Semanticization- turning episodic memories into semantic ones  Not all episodic memories semanticize  For a few minutes, you can’t separate a new fact from when and where you learned it o Although the hippocampus seems ideally situated for acquiring episodic memory, a closer look suggests that the process of acquiring semantic memory also depends on the hippocampus 5. Why the hippocampal memory system is better than a hard drive  Better than a hard drive because it is flexible, dynamic, and can make connections between other memories in order to enhance them. Hard drives store things one by one; file by file. Unlike the hippocampal memory system which overlaps memories and makes connections. Lecture 6: Amygdala, part 1  Really matters WHERE synaptic plasticity occurs  Amygdala can have plasticity in and of itself BUT ALSO modulate plasticity in other parts of the brain Amygdala plays many roles in emotion  Emotion regulation  Emotion and social behavior  Emotion and perception  Emotion and memory o Nondeclarative acquisition of positive and negative dispositions to stimuli o Modulation of declarative memory for emotion-inducing material  Undergrads studied and learned words  Watched a video (immediately, 10min delay, 30min delay, 45min delay, no video) o Oral surgery video o Funny video  STUDY QUESTION: Can you boost the consolidation of the declarative event by pairing it with an emotional experience?  RESULTS: Undergrads who watched the video immediately, 10 min after, and 30 min after learning the words performed BETTER than control participants who didn’t watch the video o Those who watched the oral surgery video (negative stimulus) performed BETTER than those who watched the funny video (positive stimulus)  Remember emotional experiences better than neutral ones because you are better attune to that threat 1. Amygdala and the physiological response to an emotional incident  The amygdala is located right in front of the hippocampus  Amygdala shows high level of anatomical hemology o Seen in front of hippocampus in most/all mammals  Sight of bear  visual cortex  cortex  reaches amygdala and hippocampus  amygdala reacts (fight or flight) o Triggers an emotional reaction  Hormonal response o Through indirect activity, amygdala activates adrenal glands o Adrenal glands secrete 2 things:  Adrenalin (epinephrine)  Glucocorticoids (cortisol) o Adrenalin/epinephrine CANNOT pass the blood-brain barrier and therefore must stimulate the peripheral nerves via the vagus nerve and release norepinephrine into the amygdala o Amygdala then projects to brain structures, including the hippocampus, telling the hippocampus to remember this event o Glucocorticoids/cortisol directly influences amygdala and hippocampus o Cycle feeds back on itself o Boosts synaptic plasticity in brain structures including the hippocampus  epinephrine- acts in seconds  Cortisol- lingers for hours after the event  Amplify and extend the event 2. Selective damage to the amygdala eliminated the improvement in memory for emotional material  Study participants (normal, brain damaged, and amygdala damage) were told a story via pictures with either an emotional or nonemotional twist o 1. A mother and son leave home one morning o 2. Make-up artists simulated an injury OR surgeons reattached the boy’s severed feet o 3. The mother heads home from the hospital  Participants were later asked about details from the story and percent correct was measured  RESULTS o Normal and participants with brain damage NOT to their amygdala remembered more details about the slide with the gruesome version of the story  Due to memory enhancement from emotions o S.M. did NOT have any emotional enhancement on her declarative memory 3. Activity in the human amygdala correlated with declarative memory performance for emotional material but not neutral material  Amount of activation in amygdala correlates with how much emotional material you will remember, but NOT neutral material  Hippocampal activity correlates with memory for neutral material and emotional material  Amygdala (and hippocampus) activity correlates with memory for material that arouses positive emotion too 4. Studies in rats show the importance of amygdala activation for emotional memory  Inhibitory Avoidance Task  Rat placed in box with bright light  Door opens to darker part of the box  When rats run to dark part they get a small jolt  Scientists, put rat back into the original box with bright light, opened the door to the dark part and recorded how long the rat waited before going into the dark part of the box again o Short wait = no/little memory of dark and jolt pairing o Long wait = good memory of dark and jolt pairing  Measured norepinephrine levels in amygdala at shock o Indicated how much amygdala is telling the hippocampus to remember this event (level of communication)  How much norepinephrine released in amygdala should determine how long ray waited before entering dark part o Predicted memory of declarative event  Emotion is not always beneficial to memory  Upside down ‘U’ shaped graph  EXAMPLE: PTSD PATIENTS  Overactive amygdala in PTSD patients  PTSD patients and combat controls both showed an increase in amygdala activity when played combat sounds, but PTSD patients had an overactive amygdala response almost as if they were reliving the event 5. Emotion is not always beneficial to memory  More cortisol in plasma (Cushing’s Syndrome)  smaller hippocampus  worse memory  Emotions could distort your accuracy  Asked college students how they heard the news of OJ Simpson (on that day) (flashbulb memory)  Asked same students 32 months later how they heard the news and they showed extreme levels of memory distortion MAIN POINTS  Amygdala is involved generally in emotional processing  We are considering its role in emotional memory  Amygdala plays two roles in emotional memory o Enhancing memory for emotion-inducing material o Attaching positive and negative dispositions to items  The cascade of physiological responses includes release of norepinephrine in amygdala, which triggers amygdala’s modulation of hippocampus (and other memory areas)  Too much emotion or arousal can be bad  Although emotion DOES enhance memory under some circumstances, “flashbulb” memories are probably not entirely accurate Lecture 7: Amygdala, part 2 1. Recap  How does the amygdala know that the visual stimulus of the bear is scary? o There are SOME innate fears o Lots of things that trigger your amygdala, the amygdala learned to be triggered by 2. Fear conditioning to a tone in rats  Put rat in a box and play a tone and at the end of the tone rat gets a small shock o Tone and shock co-terminate in the brain o Rat jumps from shock during training stage  Bring rat back later, play tone, and see how long the rat freezes or how long it takes the rat to freeze o Freezing = hunched back, rigid tail, stiff, “hiding” o Freezing indicated remembrance of tone and shock pairing  Did the rat show a negative disposition to the tone?  RESULTS: o Non-lesioned rats froze when tone was played. However, when they weren’t shocked for repeated sessions they displayed acquisition extinction  Acquisition extinction- when you continuously give the tone alone (not paired with shock) the rat UNLEARNS the pairing of tone and shock o Rats with amygdala damage showed NO freezing (they did not remember the tone and shock pairing) o Rats with hippocampus damage showed acquisition extinction over time  Tone and shock conditioning does not depend on the hippocampus  Pathways from auditory areas to the amygdala  Simple stimuli triggers thalamus and does not require extensive processing in/from the cortex  Stimuli that need more processing need the cortex 3. Fear conditioning to a context in rats  Same situation (rat in box and tone is played with a shock)  Bring rat back later and put in box again but DO NOT play tone or shock  How much freezing do you see when you put rats back in the same box?  We are looking for remembrance of the box (context)  RESULTS: o Rats with damage to hippocampus showed little to no freezing to context  Need the hippocampus to make the box-shock connection  Amygdala needs help from the hippocampus  Association between box and shock is more complicated o Need hippocampus to remember box in order to respond to tone  Hippocampus uses more of a conscious, declarative memory  Amygdala uses subconscious  Spatial recognition of the hippocampus helps amygdala form negative disposition  WHERE IS THE ESSENTIAL/INITIAL PLASTICITY?!??!  Amygdala is ESSENTIAL site of plasticity for emotional and nondeclarative memories 4. Fear conditioning in humans  Triangle = shock conditioning  S.M. (amygdala damage) shows NO fear conditioning, but can tell you everything about the event itself (where the experimented was standing, wearing, etc.)  Hippocampal damaged patient shows normal fear conditioning, but could not tell you what the experimented was wearing (NO CONTEXT) 5. Extinction of fear in phobias  Phobias can interfere with day to day life  Gradual exposure and prevention  How to reduce fear of heights o Virtual elevator o Drug to increase synaptic plasticity in the brain  Virtual training PLUS drug accelerated learning that elevator isn’t so bad/scary  Increasing synaptic plasticity is good MAIN POINTS  Amygdala required for fear conditioning to either a single stimulus (e.g., tone) or a context  Hippocampus required for fear conditioning to a context but not to a tone  Plasticity in the amygdala itself may directly support acquisition of positive or negative dispositions to individual stimuli  Fear conditioning may be related to phobias  Extinction of fear responses (including phobias) represents new learning


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