Learning and Memory - Amnesia and brain functioning

life without memory means no sense of existing over time. what happens in the brain during learning and memory? EARLY IDEA was that a connection grew between two brain areas. PAVLOV - CLASSICAL CONDITIONING, pairings of CS and UCS create a new learned response called a Conditioned Response. INSTRUMENTAL / OPERANT conditioning leads to a reinforcer or punishment. reinforcer increases, punishment decreases likelihood of behaviour happening again.
1. HOWEVER some behaviours cannot be classified as classical or operant conditioning, such as when a songbird hears its species song and then repeats it the following year, this isn't paired with another stimulus or rewarded or punished. it is IMITATED (BANDURA)
LASHLEY - tried to prove PAVLOV'S theory, aimed to see if disrupting connections in the brain disrupted associations. he found not a single area of the cortex involved in learning, but the CORTEX WORKS AS A WHOLE. LASHLEY'S SEARCH FOR THE ANGRAM, ENGRAM is the PHYSICAL REPRESENTATION of what has been learned, for example, connections between two areas..
1. he suggested that a KNIFE CUT would significantly impair the rats performance, HOWEVER it did NOT impair performance. THEREFORE - EQUIPOTENTIALITY - all parts of the cortex contribute equally to complex behaviours AND MASS ACTION - the cortex works as a whole
2. MODERN SEARCH FOR THE ENGRAM - THOMPSON suggested that the engram for classical conditioning is in the cerebellum NOT cortex. they found this through investigating the conditioning of eye blinks in rabbits. THOMPSON identified one nucleus in the cerebellum, the LATERAL INTERPOSITUS NUCLEUS (LIP) as essential for learning. as learning proceeded, response in these cells increased. when the LIP was suppressed, the training had no effect. researchers therefore concluded that learning occurred in the LIP. HOWEVER learning could have depended on an area before the LIP.
  1. PET SCANS of young adults, when pairing a stimulus with an airpuff produces an eyeblink, activity increases in the cerebellum, red nucleus and several other areas. CEREBELLUM critical for many other instances of learning.
TYPES OF MEMORY - HEBB (1949) - no one mechanism can account for the phenomena of learning. some memories form quickly, some will last a lifetime. HEBB therefore proposed a distinction between short term memory and long term memory.
1. differences between the two - ST and LT memory differ in their capacity. short term memory depends on rehearsal, whereas you can recall long term memories not thought about in years. with short term memory once you've forgotten something, it's lost.
  1. it was proposed that all information initially entered a short-term storage where it stayed until the brain had time to CONSOLIDATE it into long-term memory
VIEWS OF CONSOLIDATION - LATER VIEWS found the distinctions between short term and long term more problematic. ST NOT JUST WAITING TO BE LT. e.g. football scores remain in our head for an hour before the score changes again and then it's lost.
1. the EARLY VIEW was that the brain held onto something in short-term memory for whatever time it needed, in order to establish a long term memory, then it became permanent. HOWEVER THIS IDEA FAILED BECAUSE the time for consolidation varies enormously, e.g. memorising facts takes hours, but remembering if a snake bit you isn't hard. EMOTIONALLY SIGNIFICANT MEMORIES FORM QUICKLY.
  1. STRESSFUL or emotionally significant memories increase the secretion of epinephrine and cortisol. CORTISOL ACTIVATES THE AMYGDALA and HIPPOCAMPUS, where storage and consolidation is enhanced.
    1. HOWEVER PROLONGED STRESS INCREASES CORTISOL even more which IMPAIRS memory
  2. THE CONSOLIDATION IDEA also failed as a consolidated memory is NOT SOLID FOREVER, for example, memory that is reactivated becomes liable to change, someone may add to your memory falsely. also if the reminder of a memory is followed by a similar experience then the memory is RECONSOLIDATED.
WORKING MEMORY - BADDELEY AND HITCH - the way we store memories when we are working on them. TEST for working memory is the DELAYED RESPONSE TASK, which requires responding to something you heard a short while ago.
1. PREFRONTAL CORTEX is the location for this storage. damage to the prefrontal cortex impairs performance. deficits can be very precise.
  1. OLDER people have deficits in memory due to changes in the prefrontal cortex. declining memory shows declining activity in the prefrontal cortex.
    1. stimulant drugs that improve memory enhance activity in the prefrontal cortex.
TYPES OF MEMORY
1. LONG TERM
  1. DECLARATIVE MEMORY / explicit - facts, conscious awareness
    1. EPISODIC - personal experiences
    2. SEMANTIC - world facts
  2. NON- DECLARATIVE / IMPLICIT
    1. PROCEDURAL MEMORY - skills, how, e.g. motor skills, unconscious
AMNESIA
1. AMNESIA IS MEMORY LOSS, no one loses all type of memory equally, e.g. may forget what happened 5 minutes ago but still knows skills
  1. 1953 - H.M. - suffered seizures, his hippocampus and some areas of medial temporal cortex removed, it reduced H.M's seizures however he suffered severe memory impairment.
    1. H.M. had deficits in forming long-term memories, short term and working memory were intact.
    2. even though normal working memory, as soon as he was distracted the memory was gone.
    3. H.M. had severe impairments in episodic memory, he could recite facts he learned before his damage but could not recall personal experiences.
2. RETEROGRADE AMNESIA - loss of memories BEFORE brain damage. loss of memories most severe nearer the time of the damage.
3. ANTEROGRADE AMNESIA - difficulty reforming new memories after brain damage
4. fMRI results show that describing past events and imagining future events activate the same areas, the hippocampus (ADDIS ET AL., 2007). people with amnesia are just as poor at imagining future events as they are at describing past ones.
5. nearly all patients with amnesia have better implicit (unconscious) memory than explicit.
  1. TRANEL + DAMASIO (1993) - three hospital workers acted in three different ways towards a patient with amnesia, either nicely, neutral or stern. the patient looked at photos of all three and said he did not recognise them, but said he would prefer to be friends with the pleasant one, despite the stern one being a beautiful woman.
  2. STICK-GOLD ET AL., 2000 - study of amnesic patients playing TETRIS. normal people improve skill over a few hours, even after playing for a few hours, patients with amnesia cannot describe the game and say they don't remember playing it.
ROLE OF THE HIPPOCAMPUS
1. hippocampal damage patients acquire new skills but have enormous trouble learning new facts.
2. SQUIRE (1992) - HIPPOCAMPUS critical for declarative memory, particularly episodic memory
3. MAGUIRE (2000) - TAXI DRIVERS, larger posterior hippocampus in london taxi drivers and larger the longer they had been taxi driver.
4. HIPPOCAMPUS important for remembering DETAILS, e.g. a recent memory, much detail, more dependent on hippocampus.
BASAL GANGLIA
1. playing against someone in a team sport, you will learn the other players moves after time. this GRADUAL LEARNING depends on the BASAL GANGLIA. IMPLICIT LEARNING OR HABIT LEARNING.
  1. PARKINSON'S DISEASE patients do not show this gradual learning, as they have impaired basal ganglia, but INTACT hippocampus,
    1. HIPPOCAMPUS - DECLARATIVE, BASAL GANGLIA - PROCEDURAL.
KORSAKOFF SYNDROME - prolonged THIAMINE DEFICIENCY IN CHRONIC ALCOHOLICS. leads to loss or shrinkage of neurons in the brain. SYMPTOMS - memory loss, confusion etc. symptom is CONFABULATION - fill in memory loss gaps, they fill them with ones that were once true or would like to be true.
1. ALZHEIMERS - progressive, impaired memory and attention, related to deposition of amyloid-B protein.

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