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92 Cards in this Set
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What are perceptual-motor skills?
What are cognitive skills? |
Learned movement patterns guided by sensory inputs (ex. driving a car/dancing) Problem solving/application of strategies (playing cards/budgeting money/test taking) |
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Memories for events and facts have 3 parts: 1 - Can be communicated flexibly in different formats 2 - Have content consciously accessible 3 - Can be acquired in a single exposure How do skill memories compare? |
1 - Are difficult to convey except by direct demonstration 2 - Can be acquired without awareness 3 - Need several repetitions |
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Because skill memories are not easily put into words, they are considered ________________ memories. Because skill memories can be acquired/retrieved without feelings of remembering associated with recalling episodic memories, they are ___________ memories |
Nondeclarative memories Implicit memories |
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Skills can be learned in many ways, the most common is practicing/instruction/observation of others performing the skills. What is one way?
An ability is not a skill because of how it is acquired/how difficult it is to learn, but because? |
Operant conditioning It improves with practice |
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Skills can require perceptual-motor and cognitive skills, as well as open skills and closed skills. What are open skills? What are closed skills? |
Skill where moves are made on the basis of predictions about changing demands of the environment (ex. basketball) Skill that involves performing predefined movements that never vary (ex. gymnastics) |
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Which precedes the other, perceptual motor skills or cognitive skills? Give two pieces of evidence that other animals can acquire cognitive skills |
Perceptual-motor skills [ex producing speech/drawing lines/many animals can have these skills] precede cognitive skills Tool use [recognition that a tool/strategy can be useful in solving problems] Dolphins can 'repeat' a trick by recalling what they did [recall/reenactment of past episodes = cognitive skill] |
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What i necessary for practice of skills to be effective? What is the power law of practice? |
Knowledge of results - feedback about performance of a skill The degree to which a practice trial improves performance diminishes after a certain point, so additional trials are needed to further improve the skill [learning occurs quickly at first, then slows] |
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How can the power law of practice be overcome? |
Observational learning to improve practice/additional source of feedback about how successful one's skill is relative to what is possible |
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Frequent feedback in simple perceptual-motor tasks leads to good performance in _____-term but mediocre performance in _____-term. Whereas infrequent feedback gives the opposite |
Short-term, long-term |
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What is massed practice? Is it better for performance in short or long term? What is spaced practice? Is it better for performance in short or long term? How does one identify the best schedule for learning a skill? |
Concentrated practice of a skill; better in short-term Practice of a skill over several sessions; better in long-term Nobody knowwwws |
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What is constant practice? Ex? What is variable practice? Ex? What type of variable practice has been shown to be very effective? Which is usually better? However, it can be worse.. but? |
Practice with a constrained set of materials/skills - repeatedly practicing same skill - mastering a single trick shot in pool Practice skill in variety of contexts - practicing several trick shots in pool Gradually increasing difficulty of trials during training Variable, but performance becomes superior later |
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What is explicit learning? What is implicit learning? Which is used more often? |
Learning w/ability to verbalize about actions/events being learned Learning w/out awareness of improvements in performance or awareness of practice having occurred [if have amnesia] Implicit |
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What does serial reaction time task test?
How does it work? |
Tests implicit skill learning
Person presses keys as fast as possible in response to visual cue on screen, person tends to do better when order is fixed sequence than when random -- indicating implicit learning as they aren't aware there was a fixed sequence |
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Is implicit learning more likely to occur during perceptual-motor skills, or cognitive skills? Explain why the learning process isn't sharply either implicit or explicit, but instead a continuum of awareness Despite the ambiguity, what does evidence suggest? |
Don't know Hard to identify the threshold point where an unaware learner becomes an aware learner. Conscious awareness may be a prerequisite for acquiring skills to expert levels [can learn skills accidentally/implicitly, but won't become an expert without explicitly learning] |
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What is a motor program? How does it differ from a reflex? Give an example of testing if a skill has become a motor program Can cognitive skills become motor programs? |
Learned/inborn movements an organism can do automatically [w/minimal attention] Reflex is inborn/involuntary response to stimuli Interrupting an action sequence, ex. grabbing a ball in mid air and seeing if the person still tries to catch and throw the non existent ball Yes - ex multiplication tables |
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What are the three stages of Fitts's three-stage model of skill learning? Ex of each That skill memories rely on different memory processes as practice progresses |
1 - Cognitive stage - performance based on rules that can be verbalized [observation/instruction/trial and error] - using written instructions to set up a tent 2 - Associative stage - actions become stereotyped [less emphasis on actively recalled memory of rules] - setting up a tent in fixed sequence w/out instructions 3 - Autonomous stage - movements seem automatic [motor programs] - setting up a tent while carrying on a discussion about politics |
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How do chess players' skill level correlate to their implicitly learned visual scanning patterns? How does visual processing correlate to expert athletes? What does this suggest? |
Noobies scan more areas and do so slowly Experts scan less areas and do so faster; more likely than noobies to focus on empty square/strategically relevant chess pieces Noobies watch ball and player passing Experts focus on players who don't have ball Perceptual learning may contribute to superior abilities of experts |
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What does the rotary pursuit task measure? What happens in it? What has been found in twins vs fraternal twins? What does this suggest? |
Perceptual-motor skill learning Person keeps a stylus above a fixed point on a rotating disk Twins become more identical as they practice, fraternal twins become more dissimilar Practice decreases effects of previous experience [ex. nurture] on motor performance and increases effects of genetic influences [nature] -- more practice = more performance differences are due to genetic differences |
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What is transfer specificity? This led Thorndike to create the identical elements theory, what does this say? What is learning set formation/learning-to-learn? |
The restricted applicability of learned skills to specific situations Learned abilities transfer to novel situations, dependent on how much the novel situation is the same as the situations where the skills were encoded. Acquisition of the ability to learn new tasks rapidly based on frequent experiences w/similar tasks |
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Memorability of a skill, how well the skill is performed on a later occasion, is dependent on what four things? Loss of a skill through non-use is called ______ _______ In what two ways is it similar to learning in reverse? |
Complexity of the skill/how well it was encoded in first place/how often it has been performed/conditions in which recall is attempted Skill decay Not performing = lose it; forgetting curve is similar to learning curve [forget most of it soon after last using it] |
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How else can forgetting occur? |
Interference - new skill learning can replace old ones [ie new dances make you forget old ones]; practicing two skills on same day can interfere w/retention of first one; reviewing a recently learned skill before beginning to practice a new one can interfere w/subsequent recall of skill being reviewed |
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How do the spinal cord and brain stem help perceptual-motor skills? What two systems dedicated to sensation and perception, including sensory cortices, are important for learning perceptual-motor skills? What 3 other areas of the brain are core to cognitive and perceptual-motor skill learning? |
By controlling & coordinating movements Somatosensory and visual systems Basal ganglia, cerebral cortex, cerebellum |
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The basal ganglia gets inputs from cortical neurons, what do these do? Many of the cortical inputs are initially processed by the dorsal striatum [helps in operant conditioning]. The basal ganglia sends outputs to what 2 places? By modulating these motor control circuits, the basal ganglia plays a roll in? |
Give info about sensory stimuli the person is experiencing Thalamus [affects interactions between neurons in thalamus and motor cortex] and to brainstem [influencing signals sent to spinal cord] Initiating and maintaining movement |
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What parts of movement is the basal ganglia especially important for? Disruption of the basal ganglia will affect skill learning, but not affect...? |
Velocity, direction, amplitude of movements, and preparing to move Recall of memories for events and facts |
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Rats with basal ganglia damage can learn the radial maze task as easily as rats w/no brain damage. What does this suggest? Why do rats w/basal ganglia damage perform poorly on a simpler radial maze task where they have to search for illuminated arms with food in them? |
Suggests basal ganglia damage doesn't disrupt rats' memories for events, nor prevent them from performing skills necessary to find food in radial maze Basal ganglia damage prevents them from learning the perceptual-motor skill of avoiding dark arms and entering illuminated arms |
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If experimenters move a visible platform in the Morris water maze to a new location during testing, rats with hippocampal damage (or no damage) swim directly to the platform to escape the water. Rats with basal ganglia damage, however, swim to where the platform used to be and only afterward do they find the platform in its new location. How can these findings be interpreted? What does this illustrate? |
Rats w/basal ganglia damage have difficulty learning to swim toward a platform to escape water [even when it's visible] and instead learn to swim to a particular location in the tank to escape the water Just because two animals seem to perform a skill the same way, doesn't mean their skill memories and ability to use those memories in novel situations are the same |
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These rat experiments have let researchers conclude what about the basal ganglia? |
The basal ganglia are important in perceptual-motor learning that involves making motor responses based on specific environmental cues |
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Researchers can train rats to turn left or right in response to a tone in a T maze. What are four basic patterns of neural activity in the basal ganglia that have been found? |
1 - Some neurons fired at the start of a trial, when the rat was first put in the maze 2 - Some neurons fired most when the instructional sound was given 3 - Some responded strongly when the rat turned right or left 4 - Some fired at the end of a trial, when the rat received food |
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What was found in rats' basal ganglia firing when comparing the early stages of learning to when they were more competent? What does this suggest? What does the majority of firing in the beginning and ending of the task suggest? |
50% of basal ganglia neurons fired during task-related activity, other 50% fired in ways not related to the rats' movements/experiences in the maze When they got better, 90% fired with task-related activity [w/most firing in beginning and end of task] Suggests encoding/control of skills by basal ganglia changes as learning progresses Suggests the basal ganglia made a motor plan initiated at the beginning of each trial that directed the rat's movements until the trial ended |
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What task is used to show the basal ganglia are active when participants learn cognitive skills? |
Weather prediction task where participants predict weather based on cards, and participants improve on this task w/practice
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Where does cortical expansion occur? What is musician's dystonia? |
In areas where it is trained [ex. hand that controls note sequences in violinist is more extensive than bow hand] Too much cortical expansion leading to reduction/loss of motor control due to excessive reorganization of motor cortex |
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What do structural MRIs show about the physical changes during practice? What do neuroscientists believe that representational expansion reflects? |
More cortical gray matter from practice Reflects the strengthening and weakening of connections within the cortex resulting from synaptic plasticity |
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Behavioural stages of skill acquisition are paralleled by changes in cortical activity, give an example What does the period of 'fast learning' involve? Slower learning? |
Parts of the motor cortex activated during a task requiring motor skill expand rapidly during the first training session and more gradually in later training sessions Processes that select/establish optimal plans for performing a task Long-term structural changes of basic motor control circuits in the cortex |
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What does Parkinson's disease result from? What is the main brain damage in Parkinson's? |
Disruptions in normal functioning of basal ganglia, progressive deterioration of motor control, perceptual-motor skill learning Reduction in dopaminergic neurons in the SNc that control dopamine levels in basal ganglia; when these neurons are gone, dopamine levels drop |
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In addition to muscular rigidity and muscle tremors, people w/Parkinson's find it harder to learn what types of tasks? Parkinson's disease selectively disrupts circuits in the basal ganglia that contribute to learning and performance of..? |
Perceptual-motor [ex. serial reaction time task/tracking tasks] Closed skills, especially those that have reached the autonomous stage of learning, where movement normally would be automatic |
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Parkinson's is treated by drug therapies that counteract the lower dopamine levels, and surgical procedures to counteract disruption by lack of dopamine in basal ganglia. What occurs during the surgical technique of deep brain stimulation? What are two theories why deep brain stimulation works? |
Delivers an electrical current into a patient's brain to neurons that connect basal ganglia neurons with cortical circuits, through one or more implanted electrodes W/out proper dopamine levels, interactions btwn neurons in the cerebral cortex and basal ganglia are locked in fixed patterns - this quiets both regions and allows normal activity Could replace disruptive activity in basal ganglia and cerebral cortex w/new pattern of activity that is less disruptive |
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What is a consolidation period of semantic & episodic memories? How was this tested in rats? |
Period of time where new episodic & semantic memories are vulnerable and easily lost/altered; each time a memory is recalled, it may become vulnerable again until it is reconsolidated Gave electroconvulsive shock right after training and found it highly disrupted the conditioned response, whereas if it was an hour+ after training, it didn't disrupt |
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What can electroconvulsive therapy [ECT] be used for? What happens to memory? |
Treating mental illness, including depression Recent memories [autobiographical memories] within three years are affected, but older ones are not |
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What is reconsolidation? What happens to memories when using transcranial direct current stimulation [tDCS] during memory reactivation? |
A process where each time an old memory is recalled, it can become vulnerable to modification Later recall of information is stronger |
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People with head injuries can get retrograde amneisa or anterograde amnesia, what happens in each? Retrograde amnesia follows a pattern called Ribot gradient, what is this? |
Retrograde = loss of memories that occurred before an injury Anterograde = can't form new memories after injury Retrograde memory loss being worse for events that occurred shortly before the injury than for events long ago [like how electroconvulsive shocks screw with new memories but not old] |
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People with bilateral temporal lobe damage show retrograde amnesia and anterograde amnesia -- to what extents? |
They don't forget their identity, but they lose memories for events that happened days/months before the brain damage, and this retrograde amnesia can affect information acquired decades earlier |
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What does the standard consolidation theory say? What does multiple memory theory say instead? |
Says the hippocampus and related medial temporal lobe structures are required for storage and retrieval of recent episodic memories, but not older ones A - episodic memory is many components [sight/sound/texture/etc. stored in sensory and association cortex] B - Initially the hippocampal region helps link these components into a single episodic memory C - Over time, the components link to each other directly, and hippocampal activity isn't needed Says part C never happens, so all episodic memories are partially dependent on hippocampus |
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What does multiple trace theory say? |
Memories are encoded by hippocampal and cortical neurons and that both hippocampus and cortex are normally involved in storing and retrieving even very old memories
When an event is experienced, it is stored as an episodic memory by neurons in the hippocampus and neocortex. Each time the memory is retrieved, the retrieval itself is a new episodic memory. So even old memories can have multiple memory traces in the brain. Overtime, the general content of the memories can become a semantic memory which can be stored in the cortex, independent of the hippocampus. But the initial episodic memory, with specific details of the spatial and temporal context that it occurred, remains dependent on the hippocampus People w/damage to hippocampus lose episodic memory, but rehearse autobiographical information so much it becomes a semantic memory. Therefore they lose the ability to mentally time travel |
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What types of memories are especially vulnerable for reconsolidation? What does this lead to? |
Emotional memories Flashbulb memories where the memory is initially accurate, but each time it is recalled, details are forgotten/altered |
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How has reconsolidation been shown in rats using conditioned avoidance procedures? Why does this experimental result occur? |
Control = give rat shock in dark chamber, it waits 60 seconds before going in again Experimental = give injection of epinephrine right after shock, delay sky rockets Epinephrine stimulates norepinephrine release to basolateral amygdala, stimulated learning in cortex and hippocampus = rat remembers better that dark chamber is bad |
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At what gestational age has the fetus's brain and sense organs developed for it to start perceiving and learning about the sounds it hears? How is fetal learning about sounds tested? What evidence is there that prenatal infants learn and this info persists after birth? Why do they do this? |
25 weeks Use habituation - ex. play a sound and a 34-36wk old fetus will respond by moving, but after several trials it stops Infant will change suck rate to hear familiar story they heard while prenatal Fetal exposure to mother's language can help encode language-relevant speech sounds/give head start on acquiring language after birth |
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In the operant conditioning task on two month old infants, where they learn to kick their feet to move a phone, what is the most interesting features of this task? How do infants respond to classical conditioning tasks? What else do infants use to learn? |
It is context-dependent -- baby will not do this is if the crib liner is changed They can be classically conditioned, but the capacity continues to develop as they mature, allowing for more efficient learning under more difficult circumstances Generalizations |
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What does 'elicited imitation' test for in infants? Once they grow older, what evidence is there that they're accumulating semantic knowledge? |
Tests memory by observing their ability to mimic actions they saw earlier Start imitating sounds they hear.. learn words.. syntax.. keep asking 'why' about things |
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Give two reasons why episodic memory takes longer to form than semantic memory |
1 - Hippocampus/PFC which encode/recall memories are immature 2 - Young kids don't show evidence of cognitive self [fail rouge test until 24 months old, which could be a prerequisite to making autobiographical memories |
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Give evidence that children as young as three years old have episodic-like memory |
Failure is just failure to communicate episodic memories effectively 3 & 4 can remember what objects are hidden where [although three year olds aren't great at remembering the temporal order] |
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What is the sensitive period? What is an example period of this? What is the sensitive period for vision? How does the sensitive period work for language learning? How does adults learn second languages compared to children? Given equal amounts of time, do children or adults learn a second language faster? |
Time in early life where a certain kind of learning is most effective Imprinting - forming attachments to first individual they see after birth Within a few months of birth, otherwise vision will never develop Perceptual learning via phonetic discrimination - 6-8 month olds can discriminate phonemes in different languages, but lose this ability by 10-12 months Adults = semantic memory [strategies like memorizing vocabulary] Children = social imitation Adults due to perceptual-motor & cognitive skills |
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Puberty is the process of physical change during which the body transitions to sexual maturity -- when does it occur in males, females?
Adolescence is the transitional psychological and social stage between puberty and adulthood -- when does it occur? Which learning and memory abilities are enhanced during adolescence? How are they tested & what are the results, why? |
Males = 12; females = 10 Teen years [13-19] Working memory and executive function Digit span - by age 14/15 same as adult's - kids don't have as much exposure to numbers/words/patterns and adults can encode those items into working memory [thus why 10 year old chess experts could memorize more pieces than adults] 2-back test - linear improvement from kids to young adults |
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Why do males and females have differences in learning and memory? How do we know its not attributable to cultural stereotyping? |
Due to hormonal changes of estrogen and androgen during puberty as differences only become apparent during/after puberty.
Ex. men better at spatial learning, women better at language/verbal memory Differences are observed in rats as well |
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When do cognitive abilities like verbal memory start to decline? When does working memory start to decline? When do semantic and verbal ability start to decline? Why is one reason why working memory degrades so early? What two other types of learning are hindered in older adults? When? |
60 years old; mid thirties; don't really decline Proactive interference - old information interferes w/ability to learn new information Conditioning is slower by 40-50 Skill learning is slower by 60+ |
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How are semantic and episodic memories affected by old age? Old people do worse on paired associative learning [studying a list of word pairs then given the first word of each pair and recall the second part]. Why are they worse? What are the two ways performance is enhanced? |
Previous semantic and episodic memories stay, but older people are worse at making new episodic and semantic memories Encoding difficulties and not retrieval difficulties Items being presented more slowly so they can encode the information; and if the words have meaning |
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How do older adults perform in direct forgetting? How do older adults perform in remembering items relating to emotion? Why? |
Are less able to do so compared to younger adults, but become much better if they're given instructions on how to forget Young adults remember equally negative and positive images, whereas older adults remember positive images more often Levels of processing - younger adults process negative images more deeply than older adults either consciously or due to age-related changes |
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Why do older adults report having lots of tip-of-the-tongue [TOT] experiences? |
A defining feature of TOT is a feeling of knowing [FOK], which is a feature of metamemory [knowledge and beliefs of our own memory]. Research says their metamemory declines with age, so age-related increases in TOT isn't failures of memory retrieval, but failure to assess what information they actually have |
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What does the BDNF gene on human chromosone 11 help regulate? What is this protein responsible for? How does this protein affect learning and memory? Like many genes, the BDNF gene comes in several naturally occurring variants, called ________. The most common version is the? However 1/3 of people have a different one, called _____ _________ that produces less effective form of BDNF |
![Production of brain derived neutrophic factor [BDNF]
The BDNF protein is responsible for neuron health
Enhances long-term potentiation [LTP]
Alleles; Val allele; Met allele](https://images.cram.com/images/upload-flashcards/26/53/67/25265367_m.png)
Production of brain derived neutrophic factor [BDNF] The BDNF protein is responsible for neuron health Enhances long-term potentiation [LTP] Alleles; Val allele; Met allele |
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5-HT2AR is another gene that helps learning and memory behaviour, how? How does the WWC1/KIRBA gene help? How does the SNC1A gene help? |
Encodes instructions for building receptors for the neurotransmitter serotonin and therefore can determine the effectiveness of neural transmission. Modifies synaptic plasticity & associated w/rate we forget new information Governs how action potentials go down the axon, which determines whether the message passes on to the next neuron |
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What does epigenetics study? One such mechanism is methylation, when does it occur? Genes are inherited at conception and fixed for life, but epigenetics are flexible and react to outside factors like? How can epigenetics affect learning/memory? What is the most striking feature of epigenetic changes? |
Mechanisms [chefs] by which gene expression [recipes] can be modified When a certain group of atoms attaches to a gene, tagging that gene and altering its activity Diet/environmental chemicals/stress Stress can reduce BDNF gene activation, and impair memory They can be passed down from parent to offspring, like genes |
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Neurogenesis is the creation of new neurons in the brain, what areas of the brain are nearly fully developed by 25 weeks? Given an example of neurogenesis not being uniform through the brain? |
Lower-brain centers for breathing/digestion/reflexes Purkinje cells in cerebellum form early in gestation, making the eyeblink condition possible for young infants; but cerebellum continues to develop after birth, making conditioning faster/better in older children and adults than infants |
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Apoptosis is where natural cell death occurs, instead of cell death caused by accident or disease. Explain how this occurs. Explain how apoptosis is like the brain's version of Darwinian natural selection |
Normally neurons need neurotrophic factors, like BDNF, to thrive. Neurons get neurotrophic factors from neighbours, so when a neuron is deprived of neurotrophic factors, genes become active that cause the neuront o die If many neurons are competing for a limited amount of neurotrophic factor, only some survive. Neurons densely connected to their neighbours, and therefore probably play vital roles in brain function, are more likely to get neurotrophic factors and win the competition. |
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Synaptogenesis is the creation of new synapses and starts at 5 months.
What part of the brain is completed by 3/4 months? What part continues until 6 years? How is synaptic pruning determined? Synaptogenesis continues throughout life, mainly where? |
Visual cortex PFC Darwinian-esque - synapses frequently used [therefore important to neuron function] are strengthened, those not frequently used are weakened/die On coritcal neurones on spines [tiny protrusions from dendrites] |
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Sensitive periods in learning may reflect sensitive periods in neuronal development, when environmental inputs (such as visual stimulation) can easily alter brain organization by changing local cortical connectivity.
Give an example using vision. |
Normally, visual stimulation activates sensory neurons in the retina of the eye that project to neurons in V1. Neurons that fire together wire together in normal eyes, but if an eye is deprived of sight, there is no activity along the pathway from that eye to V1 -- making the inactive synapses weakened/eliminated When the deprived eye is reopened, visual activity in that eye will no longer elicit activity in V1, and the weak activity won't be able to compete for synapses with strong pathways from the never closed eye |
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Why are sensitive periods restricting later learning a good thing for the developing brain? |
Early in life it makes sense for the brain to be maximally open to new experiences and change accordingly. But once the basic system is set, the brain shouldn't change dramatically with each new experience, or else it could overwrite critical old information |
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Where do most profound brain changes occur during adolescence? During childhood, the PFC has lots of synaptogenesis; and lots of synaptic pruning in adolescence; until the number of synapses plateaus at the adult level. At the same time, what do neurons in the PFC do? What do the neuronal axons do? |
PFC [working memory/judgement/planning] Begin to branch complicatedly which allows for more complex patterns of information flow Develop myelin sheaths to insulate signals going down the axon, speeding neuronal transmission |
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Myelin sheaths are made by glia, what do these glia cells do? How does myelination relate to working memory being the last type of learning and memory to fully mature? What happens to the neurotransmitter in the PFC, dopamine, during adolescence? |
Give support to neurons and are critical to brain function M1 and S1 are fully myelinated early, but the frontal cortex isn't until late adolescence/early adulthood Dramatic increase [impulsive/risk-taking] then reward sensitivity drops at 18/19 yrs old |
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Why does the brain shrink 5% by age 80?
Where is this most? Where are the least? Where else is lost? Give an example of age-related loss in connectivity between existing neurons |
Neuron and synapse loss, and number of spine loss PFC [consistent w/working memory declining w/age]; V1 and hippocampus Cerebellum [consistent w/conditioning declining w/age] Neurons in cerebral cortex have fewer dendrites/less complex branching = less able to receive signals from other neurons & fewer dendrites = less space taken up |
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The PFC loses spines by 33%, but only where? What is this finding correlate with? |
Thin spines that encode new information [not the large/mushroom spines that help with long-term memories] Learning new info is impaired, but long term memories are kept |
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The total number of hippocampal neurons and synapses don't decline with aging, but what does? |
The ability to maintain changes in synapse strength [which is increased by LTP, where conjoint activity in two neurons strengthens synaptic connection between them; which is a way neurons encode new learning; if LTP happens but fades away, the new learning is lost] |
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Explain why this happened |
LTP in the old rat's hippocampal neurons was unstable and didn't last over the interval between session 1 and 2. This instability of hippocampal LTP contribute to age-related deficits in spatial learning and other things like episodic memory which requires remembering the context which an event occurred in |
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Why does LTP become less stable with age? What else could this explain? |
Epigenetics - epigenetic processes activate/deactivate genes that trigger synaptic changes and other processes to stabilize new memory
Major mechanisms of epigenetic control like methylation change with age Explain the wide differences in healthy aging as everyone has different life events and different epigenetic changes |
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How do we know neurogenesis occurs throughout life? Where? There's no known reason why neurogenesis continues throughout life, but some claim its for a renewed pool of fresh neurons available to encode new information. If so, then at least some kinds of learning and memory should be improved or impaired by increasing or decreasing the rate of neurogenesis. What evidence is there for this? |
Inject with thymidine, which is taken up by cells undergoing miotic division, and therefore can be used as a marker for newly born cells. Hippocampus & basal ganglia Rats w/inhibited neurogenesis in hippocampus are impaired at new hippocampal-dependent learning Rats undergoing new hippocampal-dependent learning show more neurogenesis [suggesting neurons are created on demand to encode the new info] Physical exercise & environmental enrichment increase neurogenesis, which could explain why exercise/environmental enrichment improves learning/memory |
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What are the negatives of adult neurogenesis? |
The new neurons die off within a few weeks, and the number that survive longer are less than 1% of the number of neurons that died.. meaning there aren't enough new cells to make up for the damaged/dead ones |
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Repeated visual experiences shape the organization of V1 during development, which determines an organism's perception of the visual world. What happens if stimulation from eyes is cut off [as in someone is born blind/loses sight right after birth]? |
Cortical plasticity - The areas of of V1 that usually respond to visual stimuli in normal people now respond to sounds/tactile stimulation [ex increases during Braille reading, whereas in normies it decreases during the same task] |
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What are the characteristics of cortical regions in regular possums? What happened to possums that were blinded? |
Have distinct cortical regions tuned to either V1/A1/S1, and receptive fields in other regions that are multimodal [neurons in those areas respond to inputs from more than on sensory modality (ex. V1 and A1 stimuli)] Cortical areas tuned to V1 stimuli in normal possums, had shrunk; within those areas, neurons responded to A1/S1 stimuli; A1/S1 had grown beyond normal; had a new cortical region w/unique anatomical/physiological characteristics that normal possums didn't have |
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What happens to memories when medial temporal lobes are damaged/destroyed? What happens to memories during electroconvulsive therapy [ECT]? |
The lost memories cannot be recovered Anterograrde amnesia for the events of the ECT session & retrograde amnesia for events that happened shortly before it |
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What is transient global amnesia [TGA]? Why does it occur? Describe its occurrence It includes severe __________ and some degree of _____________ amnesia for events within the past decade or so How does TGA work? |
Transient/temporary anterograde and retrograde amnesia Mexercise/swimming in cold water/emotional stress???; temporary interruption of blood flow to the brain from head injury/hypoglycemic episode/heart attack/stroke; hippocampus abnormalities Starts suddenly, persists for a few hours, then dissipates over a day or so Anterograde; retrograde Temporary disruption in neural activity erases unconsolidated memories of recent events but only temporarily limits access to fully consolidated older memories. Blood flow resumes, and brain function does too |
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What is functional amnesia/psychogenic amnesia? Dissociative amnesia and dissociative fugue are two types of functional amnesia, what happens in both? How can we predict when/whether a person recovers their memory |
Sudden, massive retrograde memory loss resulting from psychological causes and not physical causes like brain injury Dissociative amneisa = lose memory of specific, traumatic event Dissociative fugue = lose all memory of identity Can't |
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What have PET scans shown to be a possible cause of functional amnesia? What does this suggest? What have fMRI imaging shown to occur when people with functional amnesia fail to recognize people they know? When does this same pattern occur? Suggesting? What happens when amnesia resolves? What do these imaging results suggest? |
Abnormal activity in medial temporal lobes and diencephalon, these abnormalities disappeared when amnesia resolved Functional amnesia could be from malfunction of brain areas involved in episodic memory storage/retrieval Increased PFC activity, decreased hippocampus activity During direct forgetting - suggesting conscious/unconscious suppression of recall Abnormal PFC activity disappears Functional amnesia has dysfunction of same brain regions in organic amnesia |
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Down syndrome is a congenital disorder that causes mild-to-moderate intellectual disability. What are the three issues that come along with down syndrome? Average life expectancy was 25, but is now? |
Slow language/speech [IQ ~25-55] Physical growth delays [flattened nose/folds of skin over corners of eyes] Congenital heart defects 60 |
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Why does down syndrome occur? Which parent does this usually come from? What three parts of the brain are small in people with down syndrome? Alzheimer's disease is a form of dementia due to what? |
Trisomy 21 - Embryo gets three [instead of two] copies of chromosome 21 Mom -- especially older moms Hippocampus, frontal cortex, cerebellum [causes particularly worse memory] Accumulating brain pathology [specifically amyloid plaques & neurofibrillary tangles] |
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What things start to deteriorate during Alzheimer's? What memory processes last the longest in Alzheimer's? What happens at late stage Alzheimer's? |
First episodic memories [ex. forgetting recent conversations], then semantic memories Conditioning & skill memories [ex. making tea; mirror tracing; rotary pursuit] Complete memory failure; cognitive system failure Personality changes/disorientation/loss of judgement/confusion/loss of speech/inability to perform daily activities |
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Alzheimer's is not defined by behavioural symptoms like memory loss, but instead by the presence of what two things? |
Amyloid plaques - abnormal byproducts of amyloid precursor protein APP deposit of beta-amyloid protein, accumulating in brain and are toxic to neurons Neurofibrillary tangles - collapsed abnormal tau proteins that normally hold a neuron in place & send nutrients around the cell, but instead tangle during Alzheimer's |
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Where do amyloid plaques accumulate?
Where do neurofibrillar tangles accumulate? How does brain aging differ in Alzheimer's patients than regular people? |
Evenly in cerebral cortex, hippocampus spared First in hippocampus, then other areas Opposite of regular people, Alzheimer's patients hippocampus goes first, then frontal lobes |
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What are the three phases of Alzheimer's? How many phases do most people go through? |
Presymptomatic - accumulation of amyloid plaque/neurofibrillar tangles/shrinking of hippocampus Mild cognitive impairment [MCI] - deficits like impaired episodic memory Dementia - long enough second phase leads to this First two |
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How could behavioural methods detect early Alzheimer's? What are the four ways to test for Alzheimer's? |
Testing performance on tasks involving hippocampus [ie. generalization abilities]
Brain autopsy for plaque and tangles MRI scans of brain structure PET scans to image beta-amyloid deposits Symptoms/genetic history |
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What are the two types of medications for Alzheimer's? How effective are these? |
Cholinesterase inhibitors - reduce breakdown of unused acetylcholine in synapses between neurons Memantine - blocks receptors for neurotransmitter glutamate, which is produced too much in Alzheimer's patients Only really treat symptoms/not underlying brain damage |
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Mutations of what three genes are associated with early-onset Alzheimer's? |
APP gene on chromosome 21 Presenilin-1 [PS1] gene on chromosome 14 Presenilin-2 [PS2] gene on chromosome 1 |
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What gene is associated with more common, late-onset form of Alzheimer's in people 60+? It comes in several alleles, three of which are E2, E3, and E4 What is characteristic of E2? What is characteristic of E3? What is characteristic of E4? |
APOE on chromosome 19 E2 = one/two copies reduces risk of Alzheimer's E3 = normal/most common/many people have one from each parent E4 = People with one copy of it are 3x more risk of Alzheimer's; two copies = 15x |
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What are two possible reasons why these Allele's have these effects?
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E4 has fewer dendritic spines in hippocampus than E3 APOE may control how brain clears beta-amyloid, some alleles like E2 do this well, whereas some like E4 don't and allow plaque to build up |
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What links are there between down syndrome and Alzheimer's disease? |
Chromosome 21 - it is tripled in Down syndrome and also has the APP gene found in Alzheimer's Down syndrome people who live after 40, get plaques and tangles like Alzheimer patients 50% of adults w/Down syndrome have memory decline/similar cognitive impairments to those with Alzheimer's |
