Neural Bases of Learning and Memory

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Neural Bases of Learning and Memory
2013-12-08 22:18:06
SLP Neuro meymory learning
Brief description of the neural bases of learning and memory
Show Answers:

  1. What is learning?
    the acquisition of new information
  2. What is memory?
    The storage and retrieval of learned information (how learning is stored/retrieved)
  3. How is memory stored?
    The initial connection is ________ by synaptic function. The strength and effectiveness of the connection is not ___________. Memory is the process of changing _____ _________.
    • Predetermined
    • Predetermined
    • synaptic connections
  4. What is short-term memory (STM)?
    Lasts only a few short seconds, rehearsal is necessary to recall this information. It is fleeting as events are continually happening, and it is limited (about 7 to 8 pieces of information) and lasts about 30 seconds. TBI and electric shock can affect STM
  5. What is working memory (WM)?
    This holds memories available for ready access during performance of a task. This allows you to keep information in your mind for a longer amount of time, like a phone number. It is different from STM because it allows you to perform an activity while recalling the information.
  6. What is long-term memory (LTM)?
    An enduring form of memory that lasts from days to years and has an unlimited capacity, it can last for weeks to months to years.
  7. What is the process of putting STM to LTM?
    This process is called consolidation. Different types of memory are mediated by different parts of the brain.
  8. Model of Memory Processes
    What is Encoding?
    • Information entering sensory channels is passed into STM
    • Converting STM or ITM into LTM
    • A process in which a stored memory is used by an organism
    • These processes are vulnerable to disruption (forgetting)
  9. The cortex and WM
    What has the prefrontal cortex been identified for in WM (4)?
    What happens when the PFC is damaged?
    • Object Identification (inferior temporal cortex, PFC)
    • Spatial Location (right H. posterior parietal cortex, hippocampus, premotor cortex, PFC)
    • Verbal information (Broca's/Wernicke's, anterior cingulate cortex, left premotor cortex, PFC)
    • Problem solving and planning behavior (PFC)
    • Results in issues with working memory, planning, and reasoning.
  10. What are the two types of LTM?
    What are their differences?
    • Declarative (explicit):involves memories of individual's previous experience. The LH deals with facts/knowledge and is semantic. The RH is more emotional and deals with events (episodic). It is formed rapidly, and starts as STM. The storage depends on where the memory was 1st formed (e.g. visual info). it involves the medial temporal lobe and the diencephalon
    • Nondeclarative (implicit/procedural): memory for learned behaviors (riding a bike, responding to stimuli, habit learning) this develops more slowly than declarative. The Basal Ganglia, Cerebellum, and Amygdala are involved in this.
  11. Amnesia
    The loss of ________ _______
    The process of forgetting is _________ to create more space
    What are the two types?
    Where is the damage?
    What may occur in TBI?
    • declarative memory
    • adaptive
    • Retrograde and Anterograde 
    • Hippocampus
    • damage to new declarative memories, but LTM stays intact
  12. Medial Temporal Lobes and Declarative Memory Formation
    Assists in the formation of ____ ________ memories
    What parts are involved?
    • new declarative
    • Coritcal Association areas
    • parahippocampal and rhinal cortical areas
    • hippocampus
    • fornix
    • thalamus, hypothalamus
  13. The Diencephalon and declarative memory formation
    Which parts of the diencephalon are important in this?
    A lesion of the dorsomedial thalamus, mamillary bodies or basal forebrain may cause:
    A type of syndrome caused by this is called:
    • Anterior & dorsomedial thalamic nuclei, mamillary bodies
    • confabulations/poor insights
    • Wernicke-Korsakoff's syndrome
  14. Wernicke-Korsakoff's syndrome
    disease is seen in:
    • Profound anterograde amnesia (STM impairment), lack of awareness, confabulations, confusion, flat affect, impaired insight, apathy
    • alcoholics (thiamin deficiency), eating disorders, obesity surgery
  15. The striatum and non declarative memory formation
    the striatum is implicated in the memory of _____ and _____. 
    Proof of this is seen in these two diseases ____ & ____ in which there is an impairment of ______ memory. 
    Other structures involved with this are (4):
    • skills
    • habits
    • parkinson's 
    • huntington's
    • procedural
    • prefrontal cortex, premotor cortex, posterior parietal lobe, cerebellum
  16. Alzheimer's (AD)
    Stage 1:
    Stage 2:
    Stage 3: 
    What two other things change?
    What %?
    • forgetful, disoriented, careless, anomia
    • forget recent events, impaired math skills, comprehension deficits
    • no recent memory, past memory impaired, language is lost
    • Personality/judgement
    • 11% over 65, 50% over 85 have some dementia
  17. Alzheimer's (AD) Continued
    What's is linked to?
    People with AD have ___ instead of ___ amino acids for ______. This creates a build up of this protein. This build up causes the growth of ________ _______ and _______ as neurons die/shrink. The microglia and astrocytes clean up the dead neurons, leaving only _______ ______. The areas most affected by this are (3):
    • 42
    • 40
    • amyloid
    • neurofibrillary tangles
    • plaque
    • amyloid deposits
    • temporal lobe, hippocampus, frontal lobe
  18. Cellular Mechanisms for short term memory
    What is the difference between long term potentiation and long term depression? 
    What structure does long term potentiation involve?
    How are memories formed?
    • potentiation: long lasting enhancement in strength of stimulated synapse
    • depression: decrease in strength of synapse 
    • the hippocampus
    • synaptic modification
  19. Long term potentiation 
    A brief __________ __________ (tetanus) to one pathway in the ____________ results in a LTP of the response to a single test stimulus. LTP also occurs in other parts of the brain. A tetanus creates a greater chance that an ____ will occur. The tetanus modifies the ______ of the synapse.
    • high-frequency stimulation
    • hippocampus
    • Action Potential
    • strength
  20. Biochemical mechanisms of LTP
    LTPs are regulated by _______ which is _______. Normally the NMDA channel is blocked by _________ and only the AMPA channel functions. With ________ activation of AMPA receptors, __________ drives _____ out of the NMDA receptor and ______ can enter.
    The rapid _______ of ____ ions triggers processes that lead to LTP. Once this occurs, activation of _______ ________ changes the structure of the postsynaptic membrane, allowing for LTP and an increase in ________ ________. A LTP can also result from changes in the presynaptic _____ release. Retrograde messengers, such as ______ ______ are sent from the postsynaptic to presynaptic membrane to increase ______ ______
    • Glutamate 
    • excitatory
    • Mg2+
    • repeated
    • depolarization
    • Mg2+
    • CA2+ 
    • increase 
    • CA2+ 
    • protein kinases
    • synaptic reactivity
    • NT
    • nitric oxide
    • NT release

    Although LTP is important in memory formation, it's most probably not the only player in learning