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Pinel basics ch09

Pinel basics ch09






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    Pinel basics ch09 Pinel basics ch09 Presentation Transcript

    • 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
    • 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
    • Assessing H.M.
      • 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
    • Assessing H.M.
      • 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
    • Korsakoff’s Syndrome
      • Most commonly seen in who?
      • Alcoholics
      • Also seen in individuals with a thiamine-deficient diet
      • Alcohol causes a disruption in the body’s ability to use thiamine
    • Korsakoff’s Syndrome
      • Characterized by amnesia, confusion, personality changes, and physical problems
      • Typically damage in the medial diencephalon – medial thalamus + medial hypothalamus
    • Korsakoff’s Syndrome
      • 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?
      • Decreased acetylcholine
        • 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
    • Posttraumatic Amnesia
      • 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
    • Object-Recognition 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.
    • A Paradox
      • 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?
    • A Hypothesis
      • 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.
      • Evidence?
    • A Hypothesis
      • Ischemia-induced hyperactivity leads to extrahippocampal damage that explains ischemia-induced object recognition deficits
        • Bilateral hippocampectomy prevents ischemia-induced deficits
        • Supported by functional brain-imaging studies
    • The Hippocampus
      • Rhinal cortex plays an important role in object recognition
      • Hippocampus plays a key role in memory for spatial location
        • Hippocampal lesions producesdeficits on Morris water and radial arm mazes
        • Many hippocampal cells are place cells – responding when a subject is in a particular place
    • Comparative Studies of the Hippocampus
      • Hippocampus seems to play a role in spatial memory in many species – not just rats
      • Food-caching birds - caching and retrieving is needed for hippocampal growth
      • Primate studies are inconsistent – no place cells
      • Differences may be due to differences in testing paradigms
        • Navigating through the environment Vs location on a computer screen
    • Theories of Hippocampal Function
      • Cognitive map theory – constructs and stores allocentric maps of the world
      • Configural association theory – involved in retaining the behavioral significance of combinations of stimuli
      • Involved in recognizing spatial arrangements of objects
    • Where Are Memories Stored?
      • Each memory is stored diffusely throughout the brain structures that were involved in its formation.
      • Hippocampus – spatial location
      • Rhinal cortex – object recognition
      • Mediodorsal nucleus – Korsakoff’s
      • Basal forebrain – Alzheimer’s disease
      • Damage to a variety of structures results in memory deficits.
    • Where are memories stored?
      • Inferotemporal cortex – visual perception of objects – changes in activity seen with visual recall
      • Amygdala – emotional learning – lesion leads to lack of learned fear
      • Prefrontal cortex – temporal order of events and working memory
    • Where are memories stored?
      • Prefrontal cortex – damage leads to problems with tasks involving a series of responses
      • Different part of this structure may mediate different types of working memory – some evidence from functional brain imaging studies
    • Where are memories stored?
      • Cerebellum and striatum – sensorimotor tasks
      • Cerebellum – stores memories of sensorimotor skills – conditioned eyeblink, for example
      • Striatum – habit formation – associations between stimuli and responses
    • Synaptic Mechanisms of Learning and Memory
      • What is happening within the brain structures involved in memory?
      • Hebb – changes in synaptic efficiency are the basis of long-term memory
      • Long-term potentiation (LTP) – synapses are effectively made stronger by repeated stimulation
    • LTP as a Neural Mechanism of Learning and Memory
      • Consistent with the synaptic changes hypothesized by Hebb
        • LTP can last for many weeks.
        • LTP only occurs if presynaptic firing is followed by postsynaptic firing
      • Hebb’s postulate for learning
        • Co-occurrence is necessary for learning and memory
    • LTP as a Neural Mechanism of Learning and Memory
      • Elicited by levels of stimulation that mimic normal neural activity
      • LTP effects greatest in brain areas involved in learning and memory
      • Learning can produce LTP-like changes
      • Drugs that impact learning often have parallel effects on LTP
    • LTP as a Neural Mechanism of Learning and Memory
      • Much indirect evidence supports a role for LTP in learning and memory
      • LTP can be viewed as a three-part process:
        • Induction (learning)
        • Maintenance (memory)
        • Expression (recall)
    • Induction of LTP: Learning
      • Usually studied where NMDA glutamate receptors are prominent
      • NMDA receptors do not respond maximally unless glutamate binds and the neuron is already depolarized
      • Calcium channels do not open fully unless both conditions are met
    • Induction of LTP: Learning
      • Calcium influx only occurs if there is the co-occurrence that is needed for LTP, leading to the binding of glutamate at an NMDA receptor that is already depolarized
      • Calcium influx may activate protein kinases that induces changes causing LTP
    • Maintenance and Expression of LTP: Storage and Recall
      • Pre- and postsynaptic changes
      • LTP is only seen in synapses where it was induced
      • Protein-synthesis underlies long-term changes
      • Long-lasting changes in extracellular glutamate levels
    • Maintenance and Expression of LTP: Storage and Recall
      • How are presynaptic and postsynaptic changes coordinated?
      • Nitric oxide synthesized in postsynaptic neurons in response to calcium influx may diffuse back to presynaptic neurons
      • Structural changes are now a well-established consequence of LTP
    • LTP – A Final Note
      • Most LTP research has focused on NMDA-receptor-mediated LTP in the hippocampus, but LTP is mediated by different mechanisms elsewhere.
      • LTD, long-term depression, also exists
      • Why should there be a variety of mechanisms and places that underlie learning and memory?