Learning

What is Memory?

". . . memory is the process by which that knowledge of the world is encoded, stored, and later retrieved." Eric Kandel 2000

"Memory is a phase of learning . . .

1. Encoding-information for each memory is assembled from the

different sensory systems and translated into whatever form

necessary to be remembered. This is presumably the domain of the

association cortices and perhaps other areas.

2. Consolidation-converting the encoded information into a form that

can be permanently stored. The hippocampal and surrounding

areas apparently accomplish this.

3. Storage-the actual deposition of the memories into the final resting

places–this is though to be in association cortex.

4. Retrieval-memories are of little use if they cannot be read out for

later use. Less is known about this process.

What is Learning?

"Learning refers to a more or less permanent change in behavior which occurs as a result of practice," Kimble, 1961

“Learning is the process by which we acquire knowledge about the world.” Eric Kandel 2000

Learning is the strengthening of existing responses or formation of new responses to existing stimuli that occurs because of practice or repetition

Types of learning

Non Associative Imprinting

Habituation

Sensitization

Associative Classical Conditioning

Operant Conditioning

Emotional Conditioning

Observational Learning Play

Enculturation

Rote Learning

e Learning

Reflex : Basis of all Behavior

Imprinting

Trials

Response

Habituation

There is a decrease in behavioral response to a stimulus after repeated exposure to that stimulus over a duration of time

Sensitization

Progressive amplification of a response follows repeated administrations of a stimulus

Trials

Response

Ivan Pavlov: Classical Conditioning 1904

Phobias

Instrumental Learning Thorndike's (1911)

Law of effect

Thorndike’s theory that behavior consistently rewarded will be “stamped in” as learned behavior, and behavior that brings about discomfort will be “ stamped out.”

Operant conditioning (Skinner )

Individuals learn new behaviors that "operate on" the environment — behaviors that cause the individuals to experience environmental stimuli

A box often used in operant conditioning of animals; it limits the available responses and thus increases the likelihood that the desired response will occur.

Operant conditioning

Operant conditioning: the type of learning in which

behaviors are emitted to earn rewards or avoid

punishments.

Operant behavior: behavior designed to operant on the

environment in a way that will gain something desired or

avoid something unpleasant.

Reinforcer: a stimulus that follows a behavior and increases the

likelihood that the behavior will be repeated.

Punisher: a stimulus that follows a behavior and decreases the

likelihood that the behavior will be repeated

The antecedent stimulus, which is called the discriminative stimulus,

serves as a cue that signals the probable consequence of an operant

response

The Operant Conditioning of Drinking Alcohol

Emotional Conditioning

Hebb’s Rule 1949

“When an axon of cell A . . . excites cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells so that A’s efficiency as one of the cells firing B is increased.”

The Organization of Behavior: A Neuropsychological Theory

Aplysia californica

Aplysia has about 20,000

neurons in the nervous system

consisting of nine ganglia -- four

pairs of symmetrical ganglia and

one large abdominal ganglion

consisting of two lobes

Habituation Involves an Activity-Dependent Presynaptic Depression of Synaptic Transmission

Sensitization

Sensitization is produced by applying a noxious stimulus to the tail of the Aplysia's tail, activated sensory neuron 2. This, in turn activates a facilitating interneuron that enhances transmission in the pathway from the siphon to the motor neuron.

Short-term sensitization of the gill-withdrawal reflex in Aplysia involves presynaptic facilitation

A single shock to the tail triggers the release of the neurotransmitter serotonin at the terminals of the interneuron. Serotonin binds to receptors in the cell body and terminals of the sensory neuron in the siphon-gill pathway. These are G-protein-coupled receptors (GPCRs) that activate adenylyl cyclase which catalyzes the formation of the second messenger, cyclic AMP (cAMP). The rise in cAMP activates a cAMP-dependent protein kinase (PKA) which increases the release of transmitter at its synaptic connection to the motor neurons (red arrow pointing up). The result: a longer period of gill-withdrawal in response to a light touch to the siphon

Classical conditioning of the gill-withdrawal reflex in Aplysia

Persistent synaptic enhancement with long-term sensitization.

The level of cAMP in the cell

becomes still higher.

Some of the activated PKA moves

into the nucleus where it

phosphorylates and thus activates

CREB-1 (cAMP Response Element

Binding protein-1) which

binds the cAMP Response Element -

a DNA sequence in the promoters of

many genes whose transcription and

translation produce the proteins needed

for

forming new synaptic connections

between the sensory and motor

neurons in the siphon-gill pathway. (The

number may be more than doubled.)

Long-term habituation and sensitization in Aplysia

A. When measured 1 day or 1 week

after training, the number of

presynaptic terminals is highest in

sensitized animals (about 2800)

compared with control (1300) and

habituated animals (800).

B. Long-term habituation leads to a

loss of synapses and long-term

sensitization leads to an increase in

synapses.

Long-term potentiation (LTP)

A short high-frequency train of

stimuli to any of the three major

synaptic pathways in the

hippocampus increases the

amplitude of the excitatory

postsynaptic potentials in the target

hippocampal neurons

Long-Term Potentiation in the Mossy Fiber Pathway Is Nonassociative

The mossy fiber pathway consists of

the axons of the granule cells of the

dentate gyrus.

The mossy fiber terminals release

glutamate as a transmitter, which binds

to both NMDA and non-NMDA

receptors on the target pyramidal cells.

However, in this pathway the NMDA

receptors have only a minor role in

synaptic plasticity under most

conditions;

blocking the NMDA receptors has no

effect on LTP. Similarly, blocking Ca2+

influx into the postsynaptic pyramidal

cells in the CA3 region does not affect

LTP

Long-Term Potentiation in the Schaffer Collateral and Perforant Pathways Is Associative

The Schaffer collateral pathway

connects the pyramidal cells of the CA3

region of the hippocampus with those of

the CA1 region.

Like the mossy fiber terminals, the

terminals of the Schaffer collaterals also

use glutamate as transmitter, but LTP in

the Schaffer collateral pathway requires

activation of the NMDA-type of

glutamate receptor

Therefore, LTP in CA1 cells has two

characteristic features that distinguish it

from LTP in the mossy fiber pathway,

both of which derive from the known

properties of the NMDA receptor

Long-Term Potentiation Has a Transient Early and a Consolidated Late Phase

Mice that lack the NMDA receptor in the CA1 region of the hippocampus have a defect in LTP and in spatial memory

Long-Term Depression (LTD)

Slow, weak electrical stimulation of CA1 neurons also brings

about long-term changes in the synapses, in this case, a

reduction in their sensitivity. This is called long-term

depression or LTD. It reduces the number of AMPA

receptors at the synapse. .

Thank You