Chapter 9 Learning, Memory, and Amnesia How Your Brain Stores Information
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The Brain Changes its Functioning in Response to Experience
Learning –how experience changes the brain
Memory –how changes are stored and subsequently reactivated
What brain structures are involved in processes of learning and memory?
Effects of Bilateral Medial Temporal Lobectomy
H.M. – an epileptic who had his temporal lobes removed in 1953
His seizures were dramatically reduced – but so was his memory
Mild retrograde amnesia and severe anterograde amnesia
Retrograde (backward-acting) – unable to remember the past
Anterograde (forward-acting) – unable to form new memories
While H.M. is unable to form most types of new long-term memories, his STM is intact
Digit span – H.M. can repeat digits as long as the time between learning and recall is within the limits of short-term storage
Mirror-drawing task – H.M. exhibits improvement with practice. He is able to show skill memory – demonstrating that he can learn some things (also rotary-pursuit and a drawing task) – although he is not aware of it
H.M. readily “learns” responses through Pavlovian (classical) conditioning
H.M. can learn some things, but has no memory of having learned them
Scientific Contributions of H.M.’s Case
Medial temporal lobes are involved in memory
Short-term memory (STM) and long-term memory (LTM) are distinctly separate
H.M. is unable to move memories from STM to LTM, a problem with memory consolidation
Scientific Contributions of H.M.’s Case
Memory may exist but not be recalled – as when H.M. exhibits a skill he does not know he has learned
H.M. forms new implicit memories, but not new explicit memories
Explicit Vs Implicit Memories
Explicit memories – conscious memories
Implicit memories – unconscious memories, as when H.M. shows the benefits of prior experience
Repetition priming tests – used to assess implicit memory – performance in identifying word fragments is improved when the words have been seen before
Medial Temporal Lobe Amnesia
Not all with this form of amnesia are unable form new explicit long-term memories – as was the case with H.M.
Semantic memory (general information) may function normally while episodic memory (events that one has experienced) does not – they are able to learn facts, but do not remember doing so (the episode when it occurred)
Effects of Cerebral Ischemia on the Hippocampus and Memory
R.B. suffered damage to just one part of the hippocampus (CA1 pyramidal cell layer) and developed amnesia
R.B.’s case suggests that hippocampal damage alone can produce amnesia
H.M.’s damage – and amnesia – was more severe than R.B.’s
Most commonly seen in who?
Also seen in individuals with a thiamine-deficient diet
Alcohol causes a disruption in the body’s ability to use thiamine
Characterized by amnesia, confusion, personality changes, and physical problems
Typically damage in the medial diencephalon – medial thalamus + medial hypothalamus
Amnesia comparable to medial temporal lobe amnesia in the early stages
Anterograde amnesia for episodic memories
Differs in later stages
Severe retrograde amnesia develops
Differs in that it is progressive, complicating its study
What damage causes the amnesia seen in Korsakoff’s?
Hypothalamic mammillary bodies?
No – Korsakoff’s amnesia is seen in cases without such damage
Thalamic mediodorsal nuclei?
Possibly – damage is seen here when there is no mammillary damage
Cause is not likely to be damage to a single diencephalic structure
Alzheimer’s Disease (AD)
Begins with slight loss of memory and progresses to dementia
General deficits in predementia AD
Major anterograde and retrograde amnesia in explicit memory tests
Deficits in STM and some types of implicit memory – verbal and perceptual
Implicit sensorimotor memory is intact
What damage causes the amnesia seen in AD?
Due to basal forebrain degeneration
Basal forebrain strokes can cause amnesia and attention deficits which may be mistaken for memory deficits
Medial temporal lobe and prefrontal cortex also involved
Damage is diffuse – resulting amnesia is likely a consequence of acetylcholine depletion and brain damage
Concussions may cause retrograde amnesia for the period before the blow and some anterograde amnesia after
The same is seen with comas, with the severity of the amnesia correlated with the duration of the coma
Period of anterograde amnesia suggests a temporary failure of memory consolidation
Gradients of Retrograde Amnesia and Memory Consolidation
Concussions disrupt consolidation (storage) of recent memories
Hebb – memories are stored in the short term by neural activity
Interference with this activity prevents memory consolidation
Blows to the head (i.e., concussion)
ECS (electroconvulsive shock)
The Hippocampus and Consolidation
What role does the hippocampus play in consolidation?
Some have proposed that memory storage structures store memories for as long as they exist and eventually an engram forms
Engram – a change in the brain that stores a memory
Early animal models of amnesia involved implicit memory and assumed the hippocampus was key
1970’s – monkeys with bilateral medial temporal lobectomies show LTM deficits in the delayed nonmatching-to-sample test
Like H.M., performance was normal when memory needed to be held for only a few seconds (within the duration of STM)
Testing object-recognition memory
Delayed Nonmatching-to-Sample Test for Rats
Aspiration used to lesion the hippocampus in monkeys – resulting in additional cortical damage
Extraneous damage is limited in rats due to lesion methods used
Bilateral damage to rat hippocampus, amygdala, and rhinal cortex produces the same deficits seen in monkeys with hippocampal lesions
Object-Recognition Deficits and Medial Temporal Lobectomy
Neuroanatomical basis of resulting deficits?
Bilateral removal of the rhinal cortex > object-recognition deficits
Bilateral removal of the hippocampus > no or moderate effects on object recognition
Bilateral removal of the amygdala?
No effect on object-recognition.
Removing the hippocampus has a moderate effect on object recognition while ischemia-induced lesions to a small part of it leads to severe deficits
How can this be?
Ischemia-induced hyperactivity of CA1 pyramidal cells damages neurons outside of the hippocampus
Extrahippocampal damage not readily detectable
Extrahippocampal damage is largely responsible for ischemia-induced object recognition deficits.
Ischemia-induced hyperactivity leads to extrahippocampal damage that explains ischemia-induced object recognition deficits