Learning and
memory -
Storing
Information in
the Nervous
System
we wouldn't call footprints
that we leave memories.
similarly, when a pattern of
activity passes through the
brain, it leaves a trace or
path of physical change. not
every change is a memory
EARLY THEORIES
PENFOLD suggested that
each neuron held a
specific memory, however
stimulation elicited
memories more like a
dream....
in the 1960s and 1970s it was proposed that
memory is coded as a specific molecule,
such as RNA or protein. found that when
rats were trained to approach clicking for
food and then RNA from their brains put into
another brain, the untrained rats will
approach the clicking
HEBB - proposed a
mechanism for a
change at a synapse.
he suggested that an
axon that had
successfully
stimulated a cell in the
past becomes even
more successful in
the future.
A HEBBIAN
SYNAPSE is a
synapse that
increases in
effectiveness
because of
simultaneous activity
in the pre and post
synaptic neurons.
such
synapses
may be
critical for
associative
learning.
simultaneous activity
increases
effectiveness. axon and
cell connection is
strengthened. synapse
strengthened, increased
effectiveness, post
synapse more sensitive,
more transmitters
released.
APLYSIA - animal like a slug, has less neurons and they are
large and easy to study. HABITUATION IS A DECREASE IN
RESPONSE TO A STIMULUS THAT IS PRESENTED
REPEATEDLY. e.g. respond less and less when clock
continues to chime.
HABITUATION in APLYSIA occurs when serotonin blocks
potassium channels in post synaptic neuron, and
prolongs neurotransmitter release from that neuron.
LONG-TERM POTENTIATION (LTP)
AXONS connected to a
DENDRITE, one or more axon
bombards a dendrite with
stimulation. synapse is
'potentiated' and neuron is
MORE RESPONSIVE for
minutes / days / weeks.
intense stimulation delivered to
a neuron, prolongs the
release of transmitter from
that neuron
three properties, SPECIFICITY -
only the active synapses
become strengthened.
COOPERATIVITY - simultaneous
stimulation by axons produces
LTP more strongly than
repeated stimulation by just one
axon. ASSOCIATIVITY - pairing
weak with strong input
enhances later response to the
weak input.
BIOCHEMICAL MECHANISMS - LTP depends on
changes at glutamate synapses.
GLUTAMATE RECEPTORS
AMPA RECEPTOR - excited
by neurotransmitter
glutamate and AMPA acid.
opens SODIUM channels,
depolarisation = excitation.
NMDA RECEPTOR - excited by
glutamate and NMDA. SODIUM
and CALCIUM channels open,
only when membrane is
already depolarised.
** Repeated glutamate excitation
of AMPA receptors depolarizes
the membrane, depolarisation
removes magnesium ions that
had been blocking NMDA
receptors, GLUTAMATE can then
excite the NMDA receptors,
opening a channel for calcium
ions to enter the neuron ** the
entry of calcium is key to
maintaining LTP.
drugs that block NMDA synapses prevent the establishment
of LTP but don't interfere with the maintenance of LTP
LTP reflects
increased activity in
the presynaptic
neuron as well as
increased
responsiveness by
the post synaptic
neuron
LONG-TERM DEPRESSION (LTD) - prolonged
decrease in response at a synapse for axons that
are less active than others, as one synapse
strengthens, another one weakens.
CONSOLIDATION
short term memory consolidated
into a long-term memory. LTP in
the hippocampus important for
certain types of learning, but as
time passes learning becomes
less dependent on the
hippocampus and more
dependent on the CEREBRAL
CORTEX. more activity in the
hippocampus after 15 minutes,
more activity in the cerebral
cortex after 24 hours.
IMPROVING MEMORY -
understanding the mechanisms
of LTP enable researchers to
understand what could impair or
improve memory. AT THIS POINT
IN TIME HOWEVER there are no
safe and effective procedures or
drugs that improve memory