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Summary Theme 2 - Neuroplasticity
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A summary for the second meeting of the course.
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Carlson-Chapter 13: Learning and memory The Nature of Learning
o Learning= the process by which experiences change(=memories) nervous system (NS) +
behavior
o Learning can be:
perceptual= ability to identify and categorize objects (e.g. other members of own species) and
situations;
o each sensory system is capable of it
o primarily in the sensory association cortex, e.g. auditory info in auditory cortex
stimulus-response learning = ability to learn to perform a particular behavior for a particular
stimulus classical + instrumental/operant conditioning
o classical conditioning = learning procedure; when a stimulus that initially produces no
particular response is followed several times by an unconditional stimulus (US) that produces a
defensive or appetitive response (the unconditional response—UR), the first stimulus (now called a
conditional stimulus—CS) itself evokes the response (now called a conditional response—CR).
o Hebb rule= the hypothesis proposed by Donald Hebb that the cellular basis of learning
involves strengthening of a synapse that is repeatedly active when the postsynaptic neuron fires
explain how neurons are changed by experience in a way that would cause changes in behavior
o Instrumental/operant conditioning = learning procedure whereby the effects of a particular
behavior in a particular situation increase (reinforce) or decrease (punish) the probability of the
behavior;
o reinforcing stimulus = appetitive stimulus that follows a particular behavior and thus makes the
behavior become more frequent
o punishing stimulus = aversive stimulus that follows a particular behavior and thus makes the
behavior become less frequent.
motor learning= learning to make a new response, cannot occur without sensory guidance
from the environment a need of interaction + feedback; the newer the motor skill, the more
neural circuits involved
relational learning= learning the relationships among individual stimuli; activates the
association cortex
o spatial learning =perception of spatial location+ learning about the relationships
among many stimuli
o episodic learning=remembering sequences of events (episodes) that we witness
Synaptic Plasticity: Long-Term Potentiation and Long-Term Depression
o learning must involve synaptic plasticity: changes in the structure or biochemistry of
synapses that alter their effects on postsynaptic neurons
o Induction of Long-Term Potentiation
long-term potentiation (LTP) = long-term increase in the excitability of a neuron to a
particular synaptic input caused by repeated high-frequency activity of that input.
hippocampal formation = forebrain structure of the temporal lobe, it’s an important part
of the limbic system; includes the hippocampus proper (Ammon’s horn), dentate gyrus,
and subiculum; has an orderly structure a slice taken anywhere perpendicular to its
curving long axis contains the same set of circuits;
o it’s input comes from the entorhinal cortex (EC)
o The axons in EC pass through the perforant path
o It then forms synapses with the granule cells of the dentate gyrus.
o a single pulse of el. stimulation is delivered to the perforant path, and then the
resulting population EPSP is recorded in the dentate gyrus.
population EPSP = evoked potential that represents the EPSPs of a population of
neurons.
, o The size of the first population EPSP indicates the strength of the synaptic
connections before long-term potentiation has taken place.
o Long-term potentiation can be induced by stimulating the axons in the perforant
path with a burst of approximately one hundred pulses of el. stimulation, delivered within a few
seconds; when the response is > than it was before the burst of pulses was delivered, long-term
potentiation occurred.
o Long-term potentiation can be produced in other regions of the hippocampal
formation &the brain+ can last for several months
o can be produced in isolated slices of the hippocampal formation
o Longterm potentiation in hippocampal slices can follow the Hebb rule =
associative long-term potentiation produced by the association (in time) between the activity of
the two sets of synapses.
Role of NMDA Receptors
o Nonassociative LTP requires high-frequency stimulation (as opposed to slow-frequency
which can lead to depression)
o each successive EPSP occurs before the previous one has dissipated
o rapid stimulation depolarizes the postsynaptic membrane much more than slow stimulation
o synaptic strengthening = molecules of the neurotransmitter bind with postsynaptic receptors
located in a dendritic spine that is already depolarized BUT the the stimulation of the
synapses + the depolarization of the neuron have to occur together cuz then NO EFFECT!!!
o NMDA receptors controll the entry of calcium ions through the ion channels which is an
essential step in LTP
o NMDA receptor is found in the hippocampal formation (in CA1)
o a magnesium ion (Mg2+) blocks the calcium ion channel BUT if the postsynaptic membrane
is depolarized, the Mg2+ is ejected from the ion channel, and calcium ions (Ca2+) can enter
o the ion channel controlled by the NMDA receptor is a neurotransmitter- and voltage-
dependent ion channel!!!!
o the activation of NMDA receptors is necessary for the first step in the process events that
establishes LTP
o axons are capable of producing action potentials+ can occur in dendrites of some types of
pyramidal cells, including those in field CA1 of the hippocampal formation= dendritic spike
o AP5 2-Amino-5-phosphonopentanoate= a drug that blocks NMDA receptors
o when individual synapses became active at the same time that a dendritic spike had been
triggered, calcium “hot spots” occurred near the activated synapses+ the size of the excitatory
postsynaptic potential became larger=strengthened
o the dendritic spikes are necessary for the synaptic potentiation cuz tetrodotoxin (TTX)
prevents the formation of dendritic spikes by blocking voltage-dependent sodium channels&
LTP did not occur
o If weak synapses are active by themselves, nothing happens cuz the membrane of the
dendritic spine does not depolarize sufficiently for the calcium channels controlled by the
NMDA receptors to open BUT the activity of strong synapses does
o IF THEN some weak synapses become active, calcium will enter the dendritic
spines and cause the synapses to become strengthened.
NMDA receptors important for LTP + has associative nature.
, Mechanisms of Synaptic Plasticity
o Dendritic spines on CA1 pyramidal cells has 2 types of glutamate receptors:
1. NMDA receptors
2. AMPA receptors
o Strengthening of an individual synapse is done by inserting additional AMPA receptors
into the postsynaptic membrane of the dendritic spine
o AMPA receptors = ionotropic glutamate receptor that controls a sodium channel; when open
(thanks to glutamate), it produces EPSPs
o More AMPA receptors present larger release of glutamate by the terminal button the
synapse becomes stronger
a) LTP causes movement of AMPA receptors into the postsynaptic membranes of
dendritic spines from adjacent nonsynaptic regions of the dendrites
b) Minutes later, AMPA are carried from the interior of the cell to the dendritic shaft,
where they replace the AMPA inserted in the postsynaptic membrane of the spines
o The entry of calcium ions into the dendritic spine cause AMPA receptors to move into the
postsynaptic membrane due to CaM-KII (type II calcium-calmodulin kinase) = enzyme found
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