Download Learning, Memory, and Amnesia

Learning, Memory, and Amnesia
1. Know what learning, memory and amnesia are.
a. Memory: the site and/or process where knowledge and experiences are stored.
b. Learning: the process of committing new knowledge and experiences into (semi-) permanent
storage. E.g.,: classical & operant conditioning and other neural mechanisms.
c. Amnesia: the inability to form or recall memories.
2. Know the various classifications of memory types.
a. Declarative or explicit (conscious): facts or events; easily formed, easily forgotten.
i. Semantic
ii. Episodic
b. Nondeclarative or implicit (unconscious): skills, habits, conditioning
i. Procedural: skills  how to do something e.g., ride a bike
ii. Classical / operational conditioning
1. involving skeletal muscles
2. involving emotional responses
iii. Requires repetition, but rarely forgotten.
c. Short-term (Working Memory):
i. 7 +/- 2 chunks of information
ii. Lasts seconds – hours, depending on rehersal/attention
iii. Easily disruptable
iv. Kept in right orbital cortex (frontal lobe) i.e., behind right eye.
d. Sensory Memory:
i. Kept in brain area of sense (e.g., auditory STM is in temporal lobes)
ii. If attention, sensory info moved to working memory; otherwise, it is lost.
3. Know the types of amnesias.
a. Retrograde: cannot access information that was previously accessible. Sometimes is time-limited,
where some older memories are still available.
b. Anterograde: cannot create new memories; can affect both short and/or long
c. Specific Deficits:
i. Prosopagnosia: cannot remember/recognize faces
ii. Anomia: cannot give names to objects.
4. Know the general brain areas involved in each type of memory.
a. Declarative: medial temporal lobe; diencephalon
i. Hippocampus: main site in forming episodic memories, spatial memory, and learning
ii. Thalamus: sensory relay
iii. Amygdala: emotional memory
iv. Rhinal cortex: (part of temporal lobe around hippo.) object and recognition memory
v. Fornix and mammilary bodies: pathways in/out of hippocampus
vi. Prefrontal cortex: short-term working memory
vii. Surrounding limbic structures.
b. Nondeclarative:
i. Procedural: Striatum (filters movements, suppresses unnecessary motor movements)
1. involved in procedural memories and conditioning
ii. Skeletal muscle responses: cerebellum (primary site of coordinated movement learning)
iii. Emotional responses: amygdala
c. Short-term Working: right orbital cortex
d. Sensory: kept in brain area of sense (e.g., hearing = temporal lobe; vision = occipital lobe)
5. Know how attention affects memory formation.
a. Sensory information without adequate attention is not transferred into short-term memory nor longterm memory.
6. Know Lashley’s theory of memory.
a. Lashley (1950) thought that memories were distributed throughout the cortex; eliminating part of the
cortex would not disturb the memory. This was found to be FALSE.
7. Understand the relation of clinical data to the importance of the hippocampus.
a. H.M. lost both hippocampi due to seizure surgery: severe ANTEROGRADE amnesia, little
retrograde amnesia or STM problems.
i. Suggests that hippocampus is necessary to create new memories, not access old ones.
b. Alzheimer’s disease: damage begins in medial temporal cortex (where hippo. is) – starts with
ANTEROGRADE amnesia.
c. Korsakoff’s Syndrome: Severe ANTEROGRADE amnesia – attacks the mamillary bodies (relay
info from the hippo. to the thalamus via the fornix).
d. R.B.: permanent ANTEROGRADE amnesia cause by anoxic ischemia of hippo.
8. Know what type of memories are formed in the amygdala, hippocampus and rhinal cortexes.
a. Amygdala: emotional memories
b. Hippocampus: spatial memories, learning
c. Rhinal cortex: object and recognition memory
9. Know Hebb’s Rule.
a. 1949: a synaptic connection will become stronger if a synapse repeatedly becomes active at the same
time or just after another post-synaptic nerve fires.
10. Know the two types of glutamate receptors, what controls them, how they operate, and what ions they
pass.
a. AMPA: Activated by glutamate – is an Na+ channel.
b. NMDA: activated by 2 keys: voltage and glutamate – is a Ca++ channel
i. Normally blocked by Mg++ ion, which is expelled when cell becomes depolarized.
c. How they work together:
i. On all dendritic spines, NMDA receptors exist, looking for simultaneous local activity.
ii. If local cell becomes depolarized at same time as post-synaptic glutamate is detected (i.e.,
Hey, look, that cell is firing (glutamate detection) at the same time that my cell is firing
(voltage detection)), then receptor opens, letting Ca++ in, which results in new AMPA
receptors.
iii. AMPA receptors enable cell to fire just from post-synaptic glutamate detection.
11. Know the native state of a new dendritic spine, and what changes it undergoes during learning and
forgetting.
a. New dendritic spines contain only NMDA receptors – silent synapse.
b. Learning occurs by addition of AMPA receptors.
c. Forgetting occurs by loss of AMPA receptors.
12. Understand the basic mechanism of long-term potentiation and long-term depression.
a. LTP:
i. NMDA receptors responsible for LTP.
ii. Ca++ acts as second messenger  creates new AMPA receptors
iii. Ca++ influx also causes post-synaptic cell to create and release NO (nitrous oxide), which
signals pre-synaptic neuron to release more Glutamate.
iv. Evidence also shows pre-synaptic terminal button extends a projection that causes dendritic
spine to divide = two buttons and two spines = greater surface area.
b. LTD:
i. AMPA receptors are dephosphorylated = less sensitivity to Glu.
ii. AMPA receptors decrease in number
iii. When CREB is turned off, no new AMPA receptors are made.
13. Know what role protein synthesis plays in long-term memories.
a. CREB1 and CREB2 invovled in long-term learning.
b. CREB2 = repressed memory formation
c. CREB1 = super memory.
d. Without CREB (or with wrong CREB), long-term memories cannot be formed.