1
Q
What is Habituation?
A
- response to stimulus gradually gets smaller over time
- ex) if you turn on the fan in a room, you will initially hear it and eventually you don’t hear it anymore
2
Q
What is sensitization?
A
- the opposite of habituation
- response to a stimulus increase over time
- ex) after a bumpy plan ride, you may be a little jumpy for a while
3
Q
Neural Mechanisms of learning
A
- larger neurons and fewer neurons make it a good animal to study
- largely studied in aplysia californica
4
Q
What is the gill-withdrawal reflex?
A
- the gill is used for breathing
- the gill is covered with the mantle shelf
- waste and seawater are released through siphon
- touching the siphon leads to a retraction of the gill
5
Q
What is the habituation in the gill-withdrawal reflex?
A
- touching the siphon repeatedly leads to less of a reflex/retraction of the gill
- what would this be?
- either sensory neurons are becoming less responsive
- motor neurons are becoming fatigued or changes occur between the sensory and motor neurons
6
Q
What is habituation explained?
A
- single cell recordings show that sensory neurons do not decrease activity with each touch of the siphon
- electrical stimulation of the gill’s motor neurons show that it can still contract after being habituated
7
Q
Changes in hibituation explaned
A
- so, changes must be occurring between the sensory and motor neurons
- repeated siphon touches leads to less calcium into the sensory neurons which means less neurotransmitter is being released into the synapse
- smaller EPSP’s occur in interneurons and motor neurons ~ leads to a smaller gill withdrawal
8
Q
What is sensitization in siphon?
A
- after an electrical shock to the head or tail, aplysia show an increased gill-withdrawal response
- sensory neurons release more neurotransmitter onto the interneurons and motor neurons which to leads to the larger response
9
Q
Long term changes observed
A
- normal aplysia showed 1300 axon terminals synapsed with sensory neurons
- those that experienced sensitization had 2800 terminals
- those that experienced habituation had 800 terminals
10
Q
long term potentiation
A
- a long lasting strengthening of a synapse
- more NT is released with any input
- thought to be associated with memory formation
LONG TERM DEPRESSION: a weakening of a synapse that lasts hours or days ~ thought to be associated with learned
11
Q
What are the cellular mechanism for LTP?
A
- NMDA and AMPA receptors
12
Q
What does NMDA and AMPA receptors do?
A
- they both are receptors for glutamate
- normally just NMDA receptors are available to depolarize the postsynaptic membrane
- when the connection is strengthened, AMPA are added to the membrane
- allows for the postsynaptic membrane to be depolarized easier ~ leads to LTP
13
Q
Is LTP the mechanism for long term memory?
A
- both can last indefinitely
- both can result from very brief input
- LTP is consistent with models proposed by Donald Hebb
- LTP is found in cells thought to be associated with memory formation like the hippocampus and the cerebellum
- MNDA receptors (that have been linked to memory) are also linked to LTP
14
Q
What about brain structures in learning?
A
- Hippocampus and the temporal lobe
- thalamus ~ Papez’s Circuit
- prefrontal cortex
- basal ganglia
- cerebellum
15
Q
What happened with patient H.M.?
A
- large areas of H.M.s hippocampi and temporal lobes were surgically removed
- personality and IQ were not impacted and experienced profound anterograde amnesia
16
Q
- What is amnesias?
A
- retrograde: loss of memories of the past
- anterograde: inability to form new memories
- H.M. had issues with both
17
Q
What else happened with patient H.M?
A
- His short term memory was ok ~ “working memory”
- he could learn procedural tasks ~ mirror drawing
- his deficits were in explicit memory tasks
18
Q
What were the conclusions of H.H?
A
- the ability to store memories and the ability to access previously stored memories are in different brain areas
- procedural memories are dealt with in different brain areas than explicit memories
19
Q
What are the different parts of the hippocampus?
A
- the right hippocampus is active during spatial memory processing
~ may include a 3D representation of the world around - the left hippocampus is more active during verbal memory tasks
20
Q
What is Korsakoff’s syndrome?
A
- caused by a thiamine deficiency due to alcoholism
- damage to the thalamus and the mammillary bodies
21
Q
What else about the thalamus?
A
- patient N.A. : a fencing foil produced a lesion to their left thalamus ~ N.A’s amnesia was similar to H.M’s
22
Q
What is the DNMS task?
A
- delayed non-matching to sample task
- requires the ability to transfer memories from short term systems into long term systems
23
Q
What is the Papez’s Circuit?
A
- a network that connects the thalamus, mammillary bodies, and hippocampus
~ it is believed to be key to forming long term memories
24
Q
What about the prefrontal cortex?
A
- patients with PFC damage have issues with the Wisconsin card-sorting tasking ~ short term memory issues
- object permanence studies: adult monkeys with prefrontal damage don’t seen to grasp object permanence
~ prefrontal cortex is constantly developing throughout youth/childhood - object permanence usually develops in the first year of life
25
What about the bsala ganglia?
- lesions of the basal ganglia impact procedural memories, but not explicit memories ~ the opposite of H.M's problems
- diseases that lead to damage to the basal ganglia typically also have procedural memory deficits like Huntington's and Parkinson's Disease
26
What about the cerebellum?
- possibly key to procedural memories as well ~ motor learning
- unclear if damage upon the cerebellum leads to deficits in motor learning or simply the performance of that learned task
27
What about stess and memory?
- that stress impacts the amygdala ~ has connections to the hippocampus
- cortisol may damage the hippocampus ~ repression and flashback/flashbulbs memories
