Chapter 13
Outline
Learning & Memory

I. Classical conditioning (Pavlovian Conditioning)

   1. example:

 Neutral -------------> Unconditioned ------------>Unconditioned
 Stimulus (bell)            Stimulus (meat powder)          Response (salivation)
 

Conditioned------------------->Conditioned
Stimulus (bell)                          Response (salivation)

  2. Pavlov: thought classical conditioning reflected an increase in strength in brain
      connections between NS brain areas & UCS brain areas.

  3. Lashley: attempted to find the strengthened connection (Engram) that would
      develop after classical conditioning

  4. Thompson et al: has implicated the cerebellum (lateral interpositus N.) as being
       important for classical conditioning of the eye puff response in rabbits

             NS            UCS                UCR
     A.   tone------>air puff-------->blink

       CS       CR
                tone--------->blink
 

II. Short-Term Memory (STM): This is how we store the information that we are currently using
(also called working memory).
  1. attention:

  2. Rehearsal:

  3. Problem Solving:

  4. Communicating with LTM:

  5. Limitation of STM:

  6. Damage to areas of the prefrontal cortex impair STM
 

III. Long Term Memory (LTM):
LTM is our link with the past.  It is an essentially permanent storehouse of information about the world.
There appear to be several types

1. declarative memory: all the facts that you can describe verbally
  A. episodic memory:

  B. semantic memory:

2. nondeclarative memory: nonverbal memories
  A. procedural memory:

3. Consolidation: LTM become more secure with time
 
 

Amnesia (loss of long term memories)

I. Types of amnesia:
  1. anterograde amnesia: difficulty learning new information
  2. retrograde amnesia: can not remember event before the brain damage
 

II. The case of HM: HM also had severe anterograde amnesia after removal
     of both temporal lobes in 1953.
  1. HM also had some retrograde amnesia for events that occurred in the few
      years before his surgery.
 

III. What sort of damage causes anterograde amesia in humans?.
      Evidence for hippocampal involvement include.

  1. R.B. had a heart attack which deprived his brain of oxygen & resulted in
      anterograde amnesia.

  2. Korsakoff’s disease: results from thiamin deficiency & is usually caused
      by long term alcohol abuse.

  3. HM lost his hippocampus

  4. Alzhiemers disease: is associated with cell loss in the hippocampus as
     well as the amygdala and throughout the cortex.
     A. Kalat argues that abnormal protein develops (amyloid protein) due at least in
           some cases to genetic problems
 

IV. Animal research inplicating the hippocampus:
The hippocampus is important for spatial memory in animals (radial arm maze and milk maze).

1. Specific hippocampal neurons have been shown to fire when an animal is in a
    particular location (place cells).

2. Hippocampal neurons alter their rate of firing in other memory related activities
     (not just spatial).

3. Hippocampal lesions do the following in animals
  A. disrupt radial arm maze performance.  Thus, spatial (or relational
       memory) was disrupted.

  B. disrupt Morris milk maze performance.  The rats are released into
       different areas of the maze but the platform stays constant.
 

V. Thus, the hippocampus appears to be important for
  1. establishing connections (or at least strengthening connections) within and
       between regions of the association cortex.

  2. It also makes if possible to retrieve this information (relatively recent memories)  by
       activating circuits formed by these connections.

  3. It is also important for distinguishing one context from another.
 
 

What kinds of changes occur in the brain during learning?

I. early work:

1. In 1949 Hebb proposed that if a synapse repeatedly becomes active at about the same time that the postsynaptic neuron fires, changes will take place in the structure & chemistry of the synapse.
 

II. long-term potentiation (LTP):
 1. basic facts
   A. refers to an increase in synaptic efficiency after high levels of activity
        in the presynaptic areas (cooperativity)
   B. presynaptic cells & postsynaptic cell must be active together
       (associativity)
   C. the weaker synapses become stronger (e.g., less neurotransmitter
        needed to depolarize the postsynaptic cell).

 2. this activity has been observed in hippocampal formation neurons & the
     cerebellum

 3. this increased efficiency last for a long time & leads to permanent changes at
     the synaptic level

 4. thought to be an initial step in the process of learning & memory

 5. glutamate & nitric oxide may be involved in this process

 6. important for transferring information from STM to LTM (memory
     consolidation) remember HM

 7. long-term depression (LTD): is the opposite of LTP & thus may be
     implicated in forgetting

III. remember the brains of rats raised in an enriched environment were much
      different than those raising in an impoverished environment.
  1. a thicker cortex
  2. better capillary supply
  3. more glial cells
  4. more protein content
  5. more ACHE (which means more ACH terminal buttons).
  6. Also more synapses per neuron and more dendritic trees have been found

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