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.
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..
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
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.
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.
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.
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.
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.
STRESSFUL or emotionally significant memories
increase the secretion of epinephrine and cortisol.
CORTISOL ACTIVATES THE AMYGDALA and
HIPPOCAMPUS, where storage and consolidation is
enhanced.
HOWEVER
PROLONGED
STRESS
INCREASES
CORTISOL even
more which
IMPAIRS memory
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.
PREFRONTAL
CORTEX is the
location for this
storage.
damage to the
prefrontal
cortex impairs
performance.
deficits can be
very precise.
OLDER people have
deficits in memory due to
changes in the prefrontal
cortex. declining memory
shows declining activity in
the prefrontal cortex.
stimulant drugs
that improve
memory
enhance activity
in the prefrontal
cortex.
PROCEDURAL
MEMORY -
skills, how, e.g.
motor skills,
unconscious
AMNESIA
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
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.
H.M. had
deficits in
forming
long-term
memories,
short term and
working
memory were
intact.
even though normal
working memory, as
soon as he was
distracted the
memory was gone.
H.M. had severe
impairments in
episodic memory,
he could recite
facts he learned
before his
damage but could
not recall personal
experiences.
RETEROGRADE
AMNESIA - loss
of memories
BEFORE brain
damage. loss of
memories most
severe nearer
the time of the
damage.
ANTEROGRADE
AMNESIA -
difficulty
reforming new
memories after
brain damage
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.
nearly all patients
with amnesia
have better
implicit
(unconscious)
memory than
explicit.
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.
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
hippocampal
damage patients
acquire new skills
but have enormous
trouble learning
new facts.
MAGUIRE
(2000) - TAXI
DRIVERS,
larger posterior
hippocampus in
london taxi
drivers and
larger the longer
they had been
taxi driver.
HIPPOCAMPUS important
for remembering DETAILS,
e.g. a recent memory, much
detail, more dependent on
hippocampus.
BASAL
GANGLIA
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.
PARKINSON'S DISEASE
patients do not show this
gradual learning, as they
have impaired basal ganglia,
but INTACT hippocampus,
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.
ALZHEIMERS - progressive,
impaired memory and
attention, related to
deposition of amyloid-B
protein.