Chapter 12 Flashcards
(43 cards)
1
Q
Lashley’s research
A
- searched for the physical representation of learned material (endogram)
- cut brains of rats to interrupt connections and let them go through a maze (not successful)
- proposed: equipotentiality and mass action
- unnecessary assumptions: engrams are in cerebral cortex and all kind of learning are basically the same
2
Q
lateral interpositus nucleus (LIP)
Thomson
A
- crucial for learning
- research with rabbits: cooled or drugged LIP does not send signals -> no learned CS
BUT: when LIP recovered from impact, learning was possible
3
Q
Thomson research brain regions
A
- research on learning/CC with rabbits
- lateral interpositus nucleus (LIP)
- red nucleus
4
Q
Red nucleus
A
- midbrain motor area
-receives input from cerebellum
-Thomson research: if suppressed, rabbits showed no reaction of learning CS BUT when recovered, they have been better than before
-> Prevented response, but not learning
-> Cerebellum plays important role in learning !
but also different brain areas (ex.learning tastes in the amygdala)
5
Q
Distinction long-term (LTM) & short-term memory (STM)
A
- Hebb: distinguished LTM and STM, when we hold an information long in the STM it consolidates into LTM
- > critic: information does not have to be stored in LTM even after rehearsing it for an hour
6
Q
Why can emotionally information be remembered more quickly?
A
- excitement = secretion of epinephrine and cortisol
- Cortisol activates amygdala and hippocampus
=> amygdala and hippocampus enhance storage and consolidation of recent experiences - Amygdala stimulates the hippocampus and cerebral cortex (both important for memory storage)
- stress (more cortisol) impairs memory, impact: consolidation can be faster or slower
7
Q
Working memory
A
- the way we store information while we are working with them
- common test :delayed response tasks =reacting to a stimulus delayed
- Prefrontal cortex is crucial for this storage
- during delay: cells in prefrontal cortex and parietal cortex increase activity
- old people with declining memory show decline in activity in the prefrontal cortex
- old people with intact memory show greater activity in prefrontal cortex than young people
- > Maybe prefrontal cortex has to work harder to compensate for impairments elsewhere in the brain
8
Q
brain areas involved in memory
A
- hippocampus
- amygdala
- prefrontal cortex
- basal ganglia (to some degree)
9
Q
patient HM
A
- got hippocampus removed
- No LTM, but WM
- form a few weak semantic memories
- severe impairment of episodic memory
- strong retrograde amnesia for episodic memory (knows information, but not where he got them from)
- retrograde as well as anterograde amnesia
10
Q
anterograde amnesia
A
- inability to form memories for events that happened after brain damage
11
Q
retrograde amnesia
A
loss of memory for events that occurred before the brain damage
12
Q
Both: retrograde and anterograde amnesia
A
- damage to hippocampus and surrounding medial temporal lobe
- retrograde is most sever for the time (couple of years) just before the damage -> usually remember childhood etc.
13
Q
recalling past / imagine future
A
- same brain areas active for both activities, incl. hippocampus
- > in anterograde amnesia: as impaired in imagine the future as they are in recalling the past
14
Q
implicit memory and amnesia
A
- patients with amnesia have better implicit memory than explicit/ declarative memory (experiment: friendly, unfriendly, neutral people)
- ## also procedrual memory (form of implicit memory) is intact even if the patient is not aware of his skills.
15
Q
Hippocampus and Declarative Memory
A
- Although patients with hippocampal damage acquire new skills, they have great trouble learning new facts
- > Hippocampus related to declarative and episodic memory
16
Q
delayed matching-to-sample task
A
animal sees an object (the sample) ,after a delay,gets a choice between two objects, from which it must choose the one that matches the sample.
17
Q
delayed nonmatching-to-sample task
A
animal sees an object (the sample) ,after a delay,gets a choice between two objects, from which it must choose the one that is different from the sample
18
Q
spatial memory
A
- hippocampus is involved in spatial memory,
- > taxi drivers have been found to have greater activation in hippocampus when ask for the shortest way
- > They also had bigger posterior hippocampus => Actual growth of adult human hippocampus in response to spatial learning experiences
19
Q
contextual memory
A
- hippocampus is important for contextual memory:
- > coordinator to create episodic memory, director of all experiences (sound, colour, series of events)
- > reconstructs the context!
20
Q
brain activity episodic memory
A
episodic memory: activity in and around hippocampus synchronize with several parts of the cortex
=> consistent with the idea of the hippocampus as providing the connections
21
Q
people remember better with …
A
... flashcards. and context (environment ) and detail for STM. This is less important for LTM.
22
Q
When time pass by…
A
- memories are not as detailed and lose context.
- > activity in the cortex is greater and in hippocampus becomes less
23
Q
Korsakoff’s syndrome/ Wernicke-Korsakoff syndrome
A
- Often in alcoholics
- caused by prolonged thiamine (vitamin B1) deficiency
- > Thiamine important to metabolize glucose
- > Thiamine deficiency leads to loss or shrinkage of neurons throughout the brain
- dorsomedial thalamus is mostly affected => main source of input to the prefrontal cortex
- Similar symptoms like patients with prefrontal cortex damage: Apathy, confusion, memory loss
- Overlapping symptoms with hippocampal damage: impairment of episodic memory, but spared implicit memory
- Confabulation
24
Q
Confabulation
A
- Filling memory gaps with guesses
- Not about semantic questions or nonsense questions, mainly about episodic questions
- Most answers are more pleasant than the actual present
- Try to act according to their confabulations
25
Alzheimer’s disease
- Better procedural than declarative memory
- increase in memory loss, confusion, depression, restlessness, hallucinations, delusions, sleeplessness, and loss of appetite
- becomes common in 5% of 65y-74y and 50% over 85y
- People with down-syndrome get it almost invariably (they have 3 copies of chromosome 21)
- > A gene on chromosome 21 is linked to early onset of Alzheimer’s which cause the protein amyloid-β to accumulate in- and outside neurons
- >amyloid damages dendritic spines, decrease synaptic input & decrease plasticity
- > damaged structures form into a cluster into structures named plaques
- > As plagues accumulate, cerebral cortex, hippocampus, and other areas waste away
- Amyloid-β causes more phosphate groups to attach to tau-proteins (= intracellular support structure of axons)
- > altered tau cannot bind to its usual targets within axons and starts spreading into cell body and dendrites
- > might also increase the production of amyloid-β, leading to a cycle of reinforcement
- Tau-proteins are responsible for tangles, structures formed from degenerated neurons
-Most common treatment are drugs that stimulate acetylcholine receptors or prolong acetylcholine release
Most medicaments seem to be ineffective when diagnosis is given too late
26
Basal Ganglia
- crucial for making educated guesses
- learning habits by integrating information over many trials
- often not possible to describe what have been learned (implicit)
- immediate reward or punishment is required for learning effect
- People with Parkinson’s disease have impairments of basal ganglia -> They do not acquire nonverbal habits
- in people with damage: loss of learned motor-pattern, impaired learning of habits/skills
- People learning under massive distraction get better because their basal ganglia forms habits
27
Hippocampus and Cerebral Cortex
- Can learn in a single trial
- More flexible responses
- Can connect information over time
- Can learn from delayed feedback
- Generally explicit; describable in words
- Damage impairs declarative memory, especially episodic memory
28
other brain areas involved in memory and their functions
- Amygdala: important for fear memories
- Parietal lobe: damage makes it not possible to elaborate on memory spontaneously, while still having an intact episodic memory
-> The ability to associate things with each other is impaired
-> important for memory since the start of a story reminds us of how things go on
- Anterior temporal lobe: damage leads to semantic dementia -> loss of ability to remember concepts
- Prefrontal cortex: learned behaviour and decision making
Immaturity of some areas explains why children / adolescents often have trouble inhibiting impulses
- other areas (including ventral prefrontal cortex) are important for learning rewards and punishments and making decisions based on them
- Basal ganglia also learns it, but more slowly and after a lot of repetition
->Prefrontal more quickly on the most recent events
-> the ventromedial prefrontal cortex responds based on the expected reward and sends this information to the orbitofrontal cortex
-> the orbitofrontal cortex responds based on how the reward relates to the other possible choices
29
List of all brain areas involved in memory
- hippocampus
- amygdala
- prefrontal cortex, ventromedial prefrontal cortex,
- basal ganglia
- parietal lobe
- anterior temporal lobe
- orbitofrontal cortex
30
researchers who went wrong with their assumptions
| storing information in the nervous system
1. Wilder Penfield: brief, weak electrical stimulus to brain
-> temporal cortex got stimulated, patients saw vivid pictures
- suggested that each neuron stores a particular memory like a video tape
- Instead of memory it evoked more like a dream state
2. Horridge : test whether captivated cockroaches learn via a test called yoked-control design
-> were given electrical shocks if their legs touched the water
->showed that captivated cockroaches can learn over the first 5 to 10 minutes by tucking their legs to avoid the shock ( But slow and results not significant)
3. 60s and early 70s: researcher thought that memories are stored in the RNA or protein
-> injected extracted RNA of trained animals into other animals and thought that they were better at the tasks the animals that got their RNA extracted were good at
(Inconsistent and couldn’t be replicated)
31
Hebb
Hebbian synapse: if a synapse is firing repeatedly or consistently some metabolic change or growth process takes place in one or both cells
- > successful stimulation in the past would contribute to the success rate afterwards
- > strongly connected to the ideas of classical conditioning, since responses get stronger
- ex. : neurons in the eye when synapses in both eyes fire at the same time the visual cortex increases response to both of them
32
Single-Cell Mechanisms of Invertebrate Behaviour Change
Invertibrate animals (ex Aplysia) have benefits to study :
-Fewer and larger neurons
-Neurons are nearly identical from individual to individual
-Often withdrawal behaviour is studied: When something touches an Aplysia, it withdraws the irritated structure
-> can be habituate (reduced reaction to repeated stimuli)
-> can be sensitize(strong reaction to normal stimuli as a result of exposure to intense stimuli)
- intense stimuli causes fascilitating interneurons of the Aplysia to excite serotonin onto a postsynaptic terminals of many sensory neurons
- > Serotonin blocks potassium channels in these membranes
-> After later action potentials the membrane takes longer than usual to polarise, because potassium is slow to flow out the cell
-> Presynaptic neuron continues releasing its neurotransmitter for longer than usual
-> Repeating this process causes the sensory neuron to synthesise new proteins that cause long-term sensitization
= behavioural plasticity in terms of molecular events
33
long-term potentiation (LTP)
- One or more axons connected to a dendrite
- > fire a rapid series of stimuli.
- > The intense stimulation leaves some of the synapses potentiated (more responsive to new input of the same type)
- can be for minutes, days, or weeks.
- reflects increased activity by the presynaptic neuron and increased responsiveness by the postsynaptic neuron
34
properties of learning and memory on cellular basis
| in vertebrates
- Specificity= If some of the synapses onto a cell have been highly active and others have not, only the active ones become strengthened.
- Cooperativity= simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by just one axon.
- Associativity= Pairing a weak input with a strong input enhances later response to the weak input.
- therefore LTP matches what we would expect of Hebbian synapses
- >In some cases, a synapse that was almost completely inactive before LTP becomes effective afterward
35
long-term depression (LTD)
- opposite of LTP
- longterm decrease in response at a synapse
- Like a compensatory process: For every strengthened synapse another synapse weakens
36
AMPA synapses
- have AMPA receptors that are excited by neurotransmitter glutamate, but can also react to the drug AMPA
37
NMDA synapses
- have NMDA receptors that are excited by glutamate, but can also react to the drug NMDA
38
ionotropic receptors
receptors that open channels to let ions enter the postsynaptic cell if they get stimulated
39
processes at AMPA and NMDA receptors l.
| open the gates
- glutamate excites ANPA receptor-> ANPA opens sodium channels
- NMDA opens only if besides glutamate a positive charge is inside the cell, otherwise channels are blocked by magnesium ions
- > magnesium ions are positively charged
- > when synapse is positively charged, the magnesium ions are not blocking the NMDA gates and let sodium and calcium enter
- If enough AMPA receptors open its gate and enough sodium gets into the synapse, magnesium ions are not blocking the gate and attached glutamate opens NMDA channels to let sodium and calcium flow through the gate
40
processes at AMPA and NMDA receptors ll.
| calcium made it inside
- through NMDA receptors, calcium is able to enter post synapse
-> activates a protein called CaMKII (α-calcium-calmodulin-dependent protein kinase II)
-> CAMKII releases a protein called CREB
-> CREB regulates in the nucleus the expression of some genes
-> altered gene expression lasts for month or years and accounts for long-term memory
(an example of epigenetic change)
If the dendrites builds new AMPA receptors or moves old ones into better positions
The dendrite makes more branches and spines, thus forming additional synapses with the same axon (recall from chapter 4, enriched experience leads to increased branching)
Phosphate groups attach to certain AMPA receptors to make them more responsive than before
In some cases, the neuron makes more NMDA receptors
41
LTP depends on...
1. ... CaMKII, CREB, BDNF
- > Those with the greatest production will undergo LTP
2. ... when dendrites build new AMPA receptors or moves old ones into better positions
3. ... The dendrite makes more branches and spines, thus forming additional synapses with the same axon
- > enriched experience leads to increased branching
4. .... Phosphate groups attach to certain AMPA receptors to make them more responsive than before
5. .... In some cases, the neuron makes more NMDA receptors
42
Presynaptic changes with LTP
- Extensive stimulation of postsynaptic cells causes release of a retrograde transmitter ( often nitric oxide (NO))
-> neurotransmitter travels back to presynaptic cell to modify it
=> changes:
- threshold to produce action potential is reduced (more AP)
-> increased elease of neurotransmitter
- expands its axon and releases its neurotransmitter from additional sites along its axon
=> LTP reflects increased activity by the presynaptic neuron and increased responsiveness by the postsynaptic neuron
43
improving memory
- Caffeine, amphetamine, or metamphetamine (Ritalin) drugs before or shortly after learning improve storage of memory by increasing arousal
- Emotionally stimulating experiences also help by activating the amygdala
- Cortisol just before the testing sometimes helps people access memory
