Chapter 12: Learning and Memory Flashcards
Who is Henry Molaison?
A young boy who cracked his skull while riding a bike and experienced frequent seizures. His case allowed for knowing more about how memory worked in the brain.
What was removed in Henry’s surgery?
Medial temporal lobe specifically hippocampus and amygdala
What happened after Henry’s surgery?
He functioned well and had fewer seizures but could not form new memories. He was only able to remember memories from before his surgery.
What is anterograde amnesia?
The inability to form new memories after an injury
What is retrograde amnesia?
The inability to recall old memories before the injruy
What is needed to form new declarative memories?
hippocampus
What is consolidation?
the process where the brain is forming a physical representation of memories
What is retrieval?
The accessing of memories
What is needed for consolidation and retrieval?
glutamate
What happens when glutamate receptors are blocked?
It prevents consolidation and retrieval for memories
Where are memories stored?
In the prefrontal cortex and hippocampus for consolidation and retrieval. Other areas in the brain are used to store physical memories.
What are place cells?
Cells that fire when in a specific environment. These cells are found in both humans and primates.
What is declarative memory?
knowing facts, people, and events
What is non-declarative memory?
knowing memories of behaviors, skills, procedures, emotions
What is needed for declarative memory?
the hippocampus
What is needed for non-declarative memory?
striatum (a part of the basal ganglia)
What memory was intact in Henry Molaison?
non-declaritive
What is a working memory?
Where memory is temporarily stored. Working memory matches old memory with new memory.
What is used in working memory?
the prefrontal cortex
What is Hebb’s rule?
When neurons fire together, the synapse strengthen together.
“cells that fire together, wire together”
What is long-term potentiation(LTP)?
synapses become stronger over time
What is long-term depression(LDP)?
decrease in synaptic strength due to weak pre-synaptic activity towards post-synaptic cell
What is associative LTP?
When a weak synapse is present when two strong synapses are together
What stimulates LTP?
high frequency
What stimulates LTD?
low frequency
What is LTP used for?
forming and recalling memories
What is LTD used for?
deleting memories, editing incorrect memories
What is associative LTP used for?
classical conditioning
How is learning measured?
theta waves from 4 to 7 Hz
What is necessary for LTP?
two glutamate synapses which are AMPA and NMDA. AMPA opens sodium channels and causes excitatory postsynaptic potential. As well as NMDA that opens calcium channels
What was concluded in the taxi study?
Drivers with more experience have large posterior growth in the hippocampus
What two enzymes are necessary for consolidation?
CaMKII for the establishment of LTP and protein kinase M theta for long-term memory
When does consolidation take place?
sleep
What happens to neurons during learning?
hippocampus adds neurons (neurogenesis) as seen in taxi driver study.
What is extinction?
The deleting of memories through learning requires the activation of NMDA. Similar to Pavlov’s dogs that will stop doing a behavior and is still learning
What is forgetting?
the active biological process of removing useless information through enzyme PP1 and rac protein
What is reconsolidation?
during memory retrieval that corrects errors and refines memories. Can create false memories in the process.
What was once believed about dementia?
Researchers believed that dementia was inevitable and was bound to happen
What can memory loss be attributed to?
myelin/neuron loss and impaired LTP
What can slow down memory loss?
enriched activities like crossword puzzles and even exercise
What is the reserve hypothesis?
an active lifestyle can promote neurogenesis like reading or exercising
What did the nun study conclude?
More elaborate writing journals can decrease memory loss
What is Alzheimer’s disease?
the deterioration of the brain that results in memory loss
Who is affected by Alzheimer’s disease?
10% of people who are over 65 and 50% of those over 85
What are the symptoms of Alzheimer’s disease?
aggressive, confused about environment and those around them, and loss of reason
What are some neural abnormalities?
amyloid plaques and neurofibrillary tangles
What are amyloid plaques?
an interference in neural transmission. Clumps of amyloid protein will cluster around axon terminals and interfere with transmission signals
What are neurofibrillary tangles?
An abnormal increase of tau protein causes neural death.
What happens to the brain when one has Alzheimer’s disease?
There is a loss of neurons in the temporal/frontal lobe, enlarged ventricles, and isolated hippocampus
How many genes are confirmed for Alzheimer’s?
4
What is the breakdown of genes for Alzheimer’s?
3 early onset for those less than 60 and 1 late on set for those older than 60
What gene has the highest risk and is related to neural abnormality?
APOE ε4 that causes 3-8x more risk
What are the 4 genes in Alzheimer’s?
APP, Presenilin 1 &2, and APOE ε4
What are some environmental factors that contribute to Alzheimer’s?
pesticides, lead exposure, and chronic stress
What are some treatments for Alzheimer’s?
Memantine for glutamate, drugs that remove tangles and plaques that are somewhat effective but not really. Most of the treatment can slow down but will not cure it
How is Alzheimer’s detected?
brain scans like PET and MRI
What is Korkasoff’s syndrome?
brain deterioration that is caused by alcoholism.
What is damaged in Korkasoff’s syndrome?
mamillary bodies, medial thalamus as well as abnormal frontal lobe
What deficiency is found in Korkasoff’s syndrome?
Low thiamine (B1) where calories are taken in through alcohol rather than food
What are the symptoms found in Korkasoff’s syndrome?
anterograde amnesia, confabulation(reality vs. memory), but intact non-declarative memory
What is confabulation?
the inability to distinguish what is real and a memory due to frontal lobe damage
What is some treatment for Korkasoff’s syndrome?
High thiamine intake but little treatment as it can’t be reversed
