Chapter 13: The Biology of Learning & Memory

Chapter 13: The Biology of Learning & Memory

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  The Biology ofLearning & Memory
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  Localized Representations ofMemory Classical Conditioning UCS = UCR after repeated pairings of a CS CS + UCS = CR Operant Conditioning Following a behavior with a reward increases the possibility of a repetition of that behavior Punishment supresses the frequency of a response The ABCs of Operant Conditioning Anticedents Behavior Consequences
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  Localized Representations ofMemory Engram A physical representation of learning There are 2 principles regarding the nervous system: Equipotentiality – all parts of the cortex contribute equally to complex behaviors like learning Any part of the cortex can substitute for any other Mass Action – the cortex works as a whole The more of the cortex that is involved, the better The engram of memory is found in the cerebellum Lateral interpositus nucleus is implicated in conditioned responses
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  Memory Short-term MemoryWorking memory, present conscious memory Memory of events that have just occurred Long-term Memory Memory of past events Types of LTM: Declarative (explicit) memory- the ability to state a memory in word; material deliberately committed to memory and data deliberately recognized as memory Implicit (non-declarative) memory- material not deliberately committed to memory; recent experience on behavior not recognized as memory is being used LTM Explicit Memory Implicit Memory Episodic Memory Semantic Memory Procedural Memory Motor Skills Habits Simple Classically Conditioned Responses
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  Memory Working MemoryTemporary storage of memories about a task that is being attended to at the moment 3 components: Phonologogical loop – the process which stores auditory information Visuospatial sketchpad – stores visual information Central executive – directs attention toward one stimulus or another & determines what information will be stored in working memory
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  Memory Loss Amnesia2 types: Retrograde amnesia – loss of memory for events that occurred shortly before brain damage Anterograde amnesia – loss of long-term memories for events that happened after brain damage Damage to the hippocampus results in elevated levels of adrenal hormones It may be that memory impairment is due to increased levels of adrenal hormones
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  Memory Loss Korsakoff’sSyndrome Caused by prolonged thiamine deficiency mainly due to chronic alcoholism Thiamine deficiency leads to brain cell loss in the mamillary bodies of the hypothalamus projecting into the prefrontal cortex Have both anterograde & retrograde amnesia Have better implicit than explicit memory Confabulation – making up an answer to a question & accepting it as being true is a common behavior pattern Normal Brain Alcoholic Brain
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  Memory Loss Alzheimer’sDisease A dementia that becomes more prevalent with age Symptoms: STM & LTM memory loss, confusion, restlessness, hallucinations, disturbances in sleeping & eating Have better procedural than declarative memory; better implicit than explicit memory Down’s syndrome patients get Alzheimer’s in middle age Abnormal genes in several chromosomes lead to an accumulation of amyloid deposits in the brain causing neuronal degeneration & the dying axons & dendrites form plaques in many areas of the cerebral cortex & hippocampus, etc. Tau protein accumulates & produces tangles from the dying cell bodies Normal Brain Alzheimer's Brain
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  Storing Information HebbianSynapses A synapse that increases in effectiveness because of simultaneous activity in the presynaptic & postsynaptic neurons Habituation A decrease in response to a stimulus repeatedly presented & accompanied by no change in other stimuli Sensitization An increase in response to a amild stimulus after an intense stimulus has been presented; a prolonged release of a neurotransmitter
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  Storing Information Long-termPotentiation Increased responsiveness to axonal input as a result of repeated stimulation 3 properties make it the cellular basis for learning Specificity – only activated synapses become strengthened Cooperativity – nearly simultaneous stimulation by 2 or more axons produces LTP Associativity – paring a weak input with a strong one enhances later responses to the weak input
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  Storing Information Long-termDepression Prolonged decrease in responsiveness to synaptic input after repeated pairing with some previous input, generally of a low frequency Occurs in the cerebellum & hippocampus Almost all cases of LTP depend on NMDA & AMPA type glutamate receptors Once LTP has been established, it no longer depends on NMDA synapses LTP causes presynaptic changes through the release of a retrograde neurotransmitter from the postsynaptic cell The relationship between LTP & learning is unknown