Single stimulus learning lecture

Stimulus preexposure effects potential outcomes

sensitization, nochange, habituation

ex: startle, perceptual learning, infant looking time, imprinting, recognition of a conspecific, emotions, pain (analgesia and hyperalgesia)

Criteria for stimulus preexposure effects

1. The behavioral modification depends on a form of neural plasticity.

2. The modification depends on the organism's experiential history.

3. (a) The modification outlasts (extends beyond) the environmental

contingencies used to induce it. (b) The experience has a lasting

effect on performance.

4. Exposure to a stimulus alters the response elicited by the target

event, causing a decrement (habituation) or an enhancement

(sensitization) in its behavioral and/or psychological consequence

Formal properties of stimulus preexposure effects

Criteria

inference

direct: Change in R magnitude… ruling out sensory adaptation and motor fatigue, variation in outcome across response systems

Indirect: inferred through its impact on another process Impact on acquisition of a Pavlovian CR

Latent inhibition (CS habituation)

Perceptual learning (CS sensitization)

US preexposure effect (US habituation)

US enhancement (US sensitization)

Indirect impact of stimulus preexposure effects

Impact on an acquired response

Weaking a CS-elicited response (extinction)

Impact on instrumental learning

Neophobia

Learned helplessness

Phenomena

Dishabituation & spontaneous recovery

Short & long-term

Dual process theory

Habituation w/in a S-R pathway

Extrinsic sensitization via the state system

Account of dishabituation

Habituation

Sensitization

Dishabituation

Opponent process theory of acquired motivation (solomon)

Standard pattern of affective dynamics

a-process

b-process

Grows with experience

Neurobiological mechanisms

Learning from an invertebrate

Aplysia

Advantages: simple nervous system, large

neurons, invariant neural anatomy

Key components: gill, siphon, mantle shelf

Touch gill or siphon → gill withdrawal response

Nonassociative learning

Habituation and sensitization

Neural circuit

Sensory neuron (SN), motor neuron (MN),

facilitatory interneuron (FI)

Changes in amount of transmitter released from sensory neuron

With habituation observe a decrease

With sensitization observe an increase

basic neural function

Resting potential (Na, K)

Action potential

Initiated by depolarizing the cell

Rising phase: Na flowing into the cell

Re-establishing the resting potential:

K flowing out

Synaptic transmission

Ca channel, vesicles, neurotransmitter

Biochemical mechanisms

Habituation

Observe reduction in quantal release

Due to an inactivation of calcium channels

Revealed using voltage clamping

Long-term form leads to a structural modification

What reduces transmitter release?

Habituation

Biochemical cascade

Serotonin, serotonin receptor, G-protein, adenylate

cyclase, ATP-->cAMP, protein kinase,

K channel, Ca channel

Increases the duration of the action potential

Long-term sensitization

MAP+PKA engage gene expression via CREB-1 & CREB-2

Nociceptive plasticity

Nociceptive sensitization: In Aplysia and vertebrates

Studying central sensitization within the vertebrate spinal cord: Electrophysiological observations, Similarity to long-term potentiation (LTP)

Neurochemical mechanisms

AMPA and NMDA receptors

NMDA receptor acts like a gated channel: Allows Ca entry, Activates Ca-calmodulin dependent protein kinase (CaMK II), Modifies AMPA receptors (increases Na conductance), Awakens silent AMPA receptors

Long-term modifications require gene expression: Involves PKA, MAP kinase, CREB signaling pathway