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147 Cards in this Set

  • Front
  • Back

Appetitive Stimulus

A pleasent stimulus:

Aversive Stimulus

An unpleasent stimulus:

Postive Reinforcement

Is a procedure in which the instrumental response produces an appetitive stimulus.


If response occures appetitive is present.


Postitive: Response produces an appetitive stimulus


Reinforcement: increase in response rate


Punishment



(aka: postitive punishment)

There is a postitive contingency between the intrumental response and the stimulus outcome (the response produces the outcome), but the outcome is aversive.


Positive: response produces an aversive stimulus


Punishment: decrease in response rate


-PRODUCES THE AVERSIVE EVENT


-INSTRUMENTAL BEHAVIOR IS DECREASED BY PUNISHMENT

Negative Reinforcement



(aka: escape or avoidance)

The instrumental response turns off an aversive stimulus.


Negative reinforcement produces increase instrumental responding.


Negative: response eliminates or prevents the occurrence of an aversive stimulus


Reinforcement: increase in the response rate


RESPONSE TERMINATES THE AVERSIVE EVENT


INSTRUMENTAL BEHAVIOR IS DECREASED BY NR

Omission Training or Negative Punishment



(aka: DRO, differential reinforcement of other behavior)

Results in the removal of a pleasant or appetitive stimulus.


Withdrawaling sources of positive punishment.


Negative response between the response and an environmental event and the result in a DECREASE IN INSTRUMENTAL RESPONDING.


Perferred over positive punishment.


Negative: response eliminates or prevents the occurence of an appetitive stimulus


Punishment: decrease in response rate

Instrumental Conditioning

Instrumental behavior is controlled by its consequences.


Three elements:


1. The instrumental Response


2. The outcome of the response (the reinforcer)


3. The relation or contingency b/w the response and the outcome

Triadic Design

The design involves two phases:


1. an exposure phase


2. a conditioning phase


Findings from the rat test:


The difference in the rate of learning between these two groups show that the animals are sensitive to the response- reinforcer contingency

Exposure Phase

One group of rats is exposed tp periodic shocks that can be terminated by performing an escape response.

The Triadic Design Used In Studies of the Learned-Helplessness Effect

Group Exposure Phase Conditioning Phase Result EEscapable ShockEscape- avoidance training Rapid- avodiance learning YYoked inescapable shock Escape- avoidance training Slow- avodiance learning RRestricted to apparatus Escape- avoidance training Rapid- avodiance learning

Conditioning Phase

All three groups recieve escape- avodiance

Group E



(aka: escaped)

Exposed to periodic response that can be terminated by performing an escape response


Findings:


Group Y



(aka: yoked)

Assigned a partner from group E, although animals cannot turn off the shocks.


The shocks are inescapable.


Findings:


Exposure to uncontrollable shock produces a severe disruption in subsequent escape- avodiance learning.


In conditioning phase, shows much poorer escape- avoidance performance.


Group R



(aka: restricted)

Recieves no shocks during the exposre phase but is restricted to the apparatus for as long as group E and Y

Learned-helplessness Effect

Interference with the learning of new instrumental responses as a result of exposure to inescapable and unavoidable aversive stimulation.

Learned-helplessness Hypothesis

The proposal that exposure to inescapable and unavoidable aversive stimulation reduces motivation to respond and distrupts subsequent instrumental conditioning because participants learnt that their behavior does not control outcomes.

What is a major symptom of PTSD?

Enhanced fear reactivity

What happens with an exposure to uncontrollable stimulation?

It induces a constellation of behavioral effects that undermine the subject's ability to cope; know as learned helplessness.

What happens with exposure to controllable stimulation?

Has a lasting protective effect that blocks induction of helplessness if the organism later encounters uncontrollable stimulations

What are the consequences of long-term uncontrollable stimulations?

Depends on the region of the midbrain known as the dorsal raphe nucleus (DRN). The DRN lies just ventral to another key region the PAG.

DRN



(aka: dorsal raphe nucleus)

The DRN can regulate neural activity in other regions of the CNS. It does this through neurons that release a neurotransmitter seritonin (5-HT). Because the 5-HT neurons project to regions implicated in stress and fear.

Does DRN have an effect on helplessness?

5-HT neurons have a sensitizing effect with the DRN. This enchances the amount of 5-HT released at distant sites. *These effects are not observed after an equivelant exposure to a controllable stimulus*


Maier and Watkins: showed that pharamacologically inhibiting the DRN during uncontrollable stimulation blocked the induced of learned helplessness.

DRN observations

The activation of the DRN is both nessecary and sufficient to produces learned helplessness

What regulates the DRN activity?

Through neurons that project from prelimbic to infralimbic regions in the ventral medial prefrontal cortex (vmPFC).


What do these excitatory neurons engage?

GABAergic interneurons within the DRN that have an inhibitory effect.

What does pharmacolgical activation of the vmPFC inhibit?

Inhibits the 5-HT neural activity within the DNR and blocks the development of learned helplessness.


Behavioral control inhibits the DNR through vmPFC.


Pharmacologically disrupting the vmPFC function should eliminate the protective effect of instrumental control. (controllable aversive stimulation should engage 5-HT neurons within the DNR and paradoxically produce the helplessness-like effect)


*IMPORTANT*

What does the aversive stimulation engage?

Lateral habenula


Locus coeruleus


Bed nucleus of the stria terminalis


What does this project to?

The forsal raphe nuclei (DNR)


What does the DNR engage?

Serotonergic (5-HT) fibers

What does the Serotonergic fibers then activate?

The neural regions implicated in defensive responding (PAG and amygdala) and reward (nucleus accumbens)

What does behavioral control activate?

Activates excitatory glutamatergic (Glut) neurons within the vmPFC. Then projects to the DRN.


After it projects to the DRN what does it engage?

They engage inhibitory (GABA) neurons that reduce 5-HT activity.

What happens when you activate vmPFC?

It will prevent uncontrollable shock from inducing helplessness.

What happens when you combine vmPFC activation with uncontrollable shocked?

Yeilded an effect equivalent to controllable stimulation, engaging a protective effect that blocked the subsequent induction of helplessness.

What effects does uncontrollable stimulation have on Pavlovian fear conditioning?

Generally enhances conditioning.

What effects does controllable stimulation have on Pavlovian fear conditioning?

It has an inhibitory effect.

What does input from the CS and US appear to be associated within?

The basolateral region of the amygdala.

What is the CR orchestrated by?

It is orchestrated by the central nucleus.


What happens with the output from the infralimbic area of the vmPFC?

It acts to inhibit the performance of fear-elicited CRs (within the central nucleus) rather than learning (within the basolateral nucleus).

What happens if you inactivate the infralimbic area by administering the GABA agonist muscimol, either before conditioning or before testing?

In rats that recieved the drug vehicle alone: the controllable shock reduced behavioral signs of fear. The prior exposure rats to uncontrollable shock enchanced conditioned freezing.

What happens if you inhibit the infralimbic region prior to conditioning?

No effect, suggesting it did not effect learning.


History of behavioral control reduces what?

The expression of fear, but not its acquistion.

Avoidance

An instrumental conditioing procedure in which the instrumental response prevents the delivery of an aversive stimulus.

Temporal Relation

The time interval between an instrumental response and the reinforcer.

Instrumental Conditioning


The three things to consider:


Stimulus contex (S)


Instrumental response (R)


Response outcome (O)


The instrumental response (R) occurs in the presence of distinctive stimuli (S) adn results in delivery of the reinforcer outcome (O)

S-R Association

The key to instrumental learning and central to Thorndikes law of effect.


Instrumental

Appetitive Reinforcers

Reward training (positive reinforcement)


Performing the response produces an appetitive stimulus


Schedule matter



Partial reinforcement principle



Omission (negative punishment)


Performing the response prevents/ eliminates the occurrence of the appetitive stimulus



Aversion Reinforcers

Punishment (positive punishment)


Performing a response leads to an aversive stimulus


(ex: going to jail for stealing)



Escape (negative reinforcement)


Response contingent shock



Performing a response eliminates/ prevent the occurrence of an aversive stimulus




(ex: opening an umbrella getting rid of the rain)


Hippocampus

Spatial learning


Involved in learning about complex relations, the stimulus configurations that encode particular locations and episodes in time.


(NB 8.2)

Caudate

Habit learning

Engram

The biological memory

Eyeblinking in the hippocampus

The cells in the region of the hippocampus reflect a CS-US association.


Removing the hippocampus did not eliminate the animals ability to acquire and retain conditioned eyeblink and response.


Removing all of the brain above the midbrain had little effect on conditioned eyeblinking

Where do the mechanisms for eyeblinking lye?

Within the lower neural sturcture of the brainstem and the cerebellum.

The UR elicited by an air puff to the eye is mediated by what?


By the neurons that project to a region of the brainstem known as the trigeminal nucleus.


What happens from the trigeminal nucleus?

Neurons travle along two routes, either directly or through the reticular formation to the cranial motor nucleus, where behavioral output is organized.

What three basic pathways were used to deine this pathway?

1. Electrophysiological recording to verify that neurons in the neural circuit are engaged in response to the US.


2. Inactivating nuclei within the circuit, either permanently (by killing the cells) or temporarily (by means of a drug or cooling) to show that the region plays an essintial role.


3. Specific nuclei were artifically stimulated to show that activity in these areas is sufficient to produce behavioral response.

Where do the mossy fibers and the climbing fibers meet?

The cerebellar cortex, this is where the coincident activity brings about a synaptic modification that alters the neural ouput from the cerebellum.

What do the climbing fibers act as?

They act as teachers, selecting a subset of connections to be modified.

What do these changes define?

The stimulus properites (the characteristic of the CS) that engage in discrete motor output.


What is the output mediated by?

Neurons that project from the interpositus nucleus to the red nucleus and then finally to the cranial motor nucleus.

What performs a type of negative feedback that decrease the effectiveness of the US?

Conditioned activity develops within the interpositus nucleus. Neurons from this project back to the US pathway and inhibit the US signal within the inferior olive.

When is the hippocampus necessary if the hippocampus is removed?

If a CS ends more than .5 seconds before the US then the hippocampus is needed

What happens with amnesic patients who have damage to their hippocampus?

These patients cannot consciously remember the CS-US relation.

What happens in the absence of this explicit memory?

They fail to learn with a trace- conditioning procedure.

What is our emotional reaction to stimuli modulated by>

A group of structures known as the limbic system.

What are the two components in this system that are important for learning?

Amygdala


Hippocampus

Amygdala

Plays a key role in linking new affective responses to previously neutral stimuli.


Regulation of fear.


It also mediates the conditioning of fear to signal danger.

What regions serve as distinct functions of the amygdala?

1. The lateral (side)


2. basal (lower)


3. central nuclei

What happens if you lesion the amygdala?

A fearless creature that no longers avods dangerous situations.


Also disrupts the learning about cues (CSs), that have been paired with an aversive event.


In fear conditioning where do the neural signals elicited by the CS and US converge?

Within the lateral amygdala

What provides a biological link that endows a CS with the capacity to elicit fear?

Neurons within the lateral and basal region (basolateral amygdala) provide a biological link.

What happens when you engage the NMDA receptors?

Can initiate a cellular process that enhances synaptic connectivity, allowing a previously neural cue (the CS) to elicit a new response.

Unlocking the NMDA gates

Requires a strong input, such as a shock.


Under these conditions, the cue- elicited input to the basolateral amygdala (the CS) may gain the capacity to drive the neural machinery that generates fear (the CR).

What blocks fear conditioning?

Chemically inactivating basolateral amgydala this region, or microinjecting a drug that disrupts NMDA receptors fucntion.

What is the output of fear channeled through?

The central nucleus of the amygdala, which organizes the expression of fear.


Where does one output pathwat project to?

A region of the midbrain known as the periaquenductal gray (PAG).



PAG



(aka: periaquenductal gray)

Two different regions:


1. portion that lies along the upper sides (dorsolateral PAG) organizes active defensive needed for fight or flight.


2. lower (ventral) portion of the PAG mediates CS-elicited freezing behavior.

What happens if you lesion the ventral PAG?

Rats exhibit other fear- elicited behaviors but do not freeze.

Sematic Memory

You can recongize objects and understand the meanings of words

LTP



(aka: long-term memory)

Recall events that happened years ago


STM



(aka: short-term memory)

Temorarily remember new information

Episodic memory

Memory for autobiographical events that occurred at a particular time and place

What distinguishes the hippocampus?

That is accomplishes this feat in a rapid manner, incidentally in the absence of explicit reinforcement.

What happens if a shock is given immediately after the rat is placed in the chamber?

It is unable to presumably form a conjunctive representation of the context, it fails to associate the context with a shock.


How can this immediate shock deficit be eliminated?

Simply exposing the rats to the context got 2-3 minutes the day before.


What happens if you lesion the hippocampus?

It eliminates the capacity (context conditioning).


It does so without affecting the capacity to learn that a discrete cue (e.g. a tone) predicts shock.


The rat will notice that an objet has been changed (object memory) but not whether its location has been changed (spatial memory).

What does context conditioning depend on?

The derivation of a conjunctive representation and out-put from the hippocampus.

LTP



(aka: long-term potentiation)

A lasting increase in neural excitability observed in a (postsynaptic) neuron that has been strongly depolarized. The induction of LTP has been linked to the activation of the NMDA receptor.

What happens when a high frequency is observed?

LTP is typically observed


What happens when a low frequency stimulus is given?

An opponent-like phenomenon is induced, long-term depression (LTD) that weakens the synaptic connections.

What happens in the absence of LTD?

Input to the hippocampus could saturate plasticity, which would prevent further learning.

How could a strong input increase the strength of a chemical synapse and induce LTP?

By enchancing either the amount of transmitter released or the responsiveness of the postsynaptic cell.

What does the presynaptic cell release?

A neurotransmitter (glutamate) that can engage two types of receptors (AMPA and NMDA) on the postsynaptic cell

Stimulus Discrimination

Differential responding to two stimuli; treating each stimulus as different from the other; an organism is said to exhibit this if it responds differently to two or more stimuli.

Stimulus Generalization

Opposite of differential repsonding, or stimulus discrimination if organism responds in a similar fashion to two or more stimuli.

Stimulus Generalization Gradient

As a function of how similar each test stimulus was to the original training stimulus; they provide precise information about how sensitive the organism's behavior is to systematic variation in a stimulus.

Overshadowing

Illustrates competition among stimuli for access to the process of learning; how strongly organisms learn about one stimulus depends on how easily other cues in the situations can become conditioned.

Stimulus- element approach

Simultaneous presentation of a light and tone as consisting of seperate visual and auditory cues; a way of thinking about a compounds stimulus.

Configural- cue approach

Organisms treat a compounds stimulus as an integral whole that is not divided into parts or elements; alternative to stimulus-element approach; example: the sound of a symphony orchestra, originates from sounds of individual instruments, but very different from individual instruments by themselves.

Stimulus discrimination training

Stimulus control can be dramatically altered by learning experiences; conducted using either classical or instrumental conditioning procedures

Stimulus discrimination procedure

Establishes control by the stimuli that signal when reinforcement is and is not avaliable

Discriminative stimuli

Once the S+ and S- have gained control over the individual's behavior

Multiple schedule of reinforcement

a different schedule or reinforcement is in effect during different stimuli; example: an FR schedule may be in effect when a light is turned on, and VI schedule of reinforcement may be in effect when a tone is presented

Positive patterning

Whenever each of two stimuli occur individually, they are not reinforced (A- and B- trials); but reinforcement occurs when the two stimuli are presented simultaneously (AB-)


Negative patterning

The role of the reinforced and non-reinforced is reversed than positive; reinforcement is avaliavle when the cues are presented individually (C+ and D+) and not when they appear simultaneously (CD-)

Intradimensional discrimination

A training procedure in which the S+ and S- different only in terms of the one stimulus feature; related to issue of expert performace

Peak- shift effect

A displacement of the highest rate of responding in a stimulus generalization gradient away from the S+ and a direction oppositre the S-

Excitatory generalization gradient

A gradient of responding that is observed when organisms are tested with the S+ from a discrimination procedure and with stimuli that increasingly differ from the S+. Typically the highest level of responding occures to the S+; progressively less responding occurs to stimuli increasingly differ from the S+; the gradient has an inverted U-shape.


Stimulus equivalance

Generalized responding among a set of stimuli; encouraged by equivalence training

Conditional relation

A relation in which the significance of one stimulus or event depends on the status of another stimulus


NMDA receptor

A specialized receptor that functions as a gated channel. Engaging the receptor requires both a strong depolarization (to displace the Mg++ ion blocking the channel) and the binding of the neurotransmitter glutamate


Occasion setting/ Facilitation

A procedure in which one cue disignates when another cue will be reinforced

What does engaging the AMPA receptor allow to enter the cell?

Allows to Na+ to enter the cell and initiates the chemical process to produce an action potential.


What happens at rest?

The NMDA channel is blocked by the ion magnesium (Mg++)


What needs to happen for NMDA receptors to work?

The Mg++ must be displaced, which requires a strong depolarization of the postsynapic cell. This can be produced by strongly engaging the AMPA receptors at the same synapse or from a depolarization provided at another synapse on the same cell.

What disrupts spatial learning within the Morris water maze?

NMDA antagonist MK-801

Premack

Simple, empirical approach to reinforcement; try to relate reinforcement to biological needs

Premack Theory

"Given two responses arranged in an operant conditioning procedue, the more probable response will reinforce the less likely behavior but the less probable response will not reinforce the more likely behavior"

Response Deprivation Theory



(Timberlake & Allison)

Thought that all that matters is that the schedule deprive the organism of the consequent response


Took Premack's second idea and made it their complete theory


Don't have to worry about how you go measure behavior

Problem's with Premack's approach

Difficult to measure some behaviors


Difficult to quantify relative probability


Sometimes a more likely R does not reinforce a less likely R

Oribitofrontal cortex

Allows you to put a brake on the implusive side


Responsible for waiting it out

What does CS allow to enter?

CS allows Ca++ to enter, which fosters the conversion of ATP to cAMP by adenylate cyclase


(adenylate cyclase works better in the presence of calcium)


If calcium is higher in the cell it will make more cAMP--> Greater sensitization

How can you get greater sensitization?

More calcium--> adenylate cyclase makes more cAMP--> more protien kinase is activated--> more potassiun channels close--> GREATER SENSITIZATION

What gets calcium into sensory neurons?

Touch it. If you touch it RIGHT BEFORE shock there will be more calcium in the cell WHILE shock process what happens, so adenylate cyclase finds more calcium to make more PKA which generates larger sensitization.

Lesion



electrolytic & neurochemical (spares fibers of passage)


Inference of function through dysfunction


Demonstrates the necessity of particular neural region

Activation



electrical and neurochemical

Mimicry/ substitution


Demonstrates that particular neural region is sufficent

Record activity



cellular and regional

Correlations aren't always perfect


Find out by proving it wrong

Neural system pathways

US pathway (from trigeminal)


CS pathway (frim auditory)


Convergence (interpositus)


Inhibition of inferior olive and blockinh

Amygdala and Emotion

Most sensory information goes through the thalamus

Neural systems



mort detailed

CS pathways- PAG causes freezing response


Convergence within the basolateral amygdala


Basolateral amygdala (BLA)


Shock input goes into BLA; it gets info about pain


CS also have input to thalamus


Amygdala gets what 2 kinds of info about the CS?

Simple (thalamus) conditional stimulus from the sensroy thalamus


Context (hippocampus) fear-conditioning from the hippocampus

If you lesion the PAG what happens?

You will eliminate freezing

What is the distinction between explicit and implicit?

Explicit (mediated/ declarative) appear to require the hippocampis


Implicit (unmediated) no cognition is involved; don't seem to require a conscious process


-Ex: sports

Delayed conditioning

Where the CS stayed on until US occured; in these conditions hippocampus and forebrain is NOT needed

Trace conditioning

Hippocampus is needed; pause between CS and US occuring; requires conscious process


Context conditioning

This conditioning requires hippocampus


Hippocampal lesions disrupt context conditioing but not learning about an embedded cue


Initially, it requires hippocampus, but over a few weeks the memory is consolidated and laid down in cortical tissue


Hippocampal lesions a month after training do not affect context conditioning


After this, you can remove hippocampus and it doesn't matter


Antagonists



(APV: AP5 and MK-801)

The antagonists sit on the channel to prevent it from working. If you give the drug before learning occurs it will block learning. If you let them learn drug free then give the drug before the test it will not affect anything.


Affect induction, not expression: blocks new learning but not retention retrieving.

Impact of MK-801 on spatial learning

MK-801 block learning

Impact of AP5 on fear conditioning

The hippocampus is needed. If given the drug AP5 before an experiment, the rats don't remember to freeze the next day. It blocks learning. If the AP5 is given on day 2, it has no effect, they freeze on day too.

Genetic manipualtions

Gene targeting: knockout and transgenic- knowing out is targeting a specific gene and make a bad copy of it and inserting a gene that the mouse never had


Knockout

Genetic manipulation where you take out a gene. No longer has a specific gene.

Transgenic

Insert a new gene that was never there.


Impact of knocking out CaMKII (alpha subunit) or CREB (silva)

Disrupts hippocampal LTP and spatial learning: this mouse fails at learning and conditioning.

A conditional knockout for CaMKII

Mutation was only expressed when DOX was removed from the diet. The presenxe of DOX tuens off the tTAm which makes mice dumn, so mouse becomes normal.

Doogie

Created mice that made the NR2B subunit of the NMDA receptor into adulthood.


Tsein tested Doogie in water maze:


Exhibited enhanced LTP and learning

Preparedness

Biological connections that are predetermined


Adding extra (free) reinforcers degrades performance: learned helplessness


Instrumental learnning within the spinal cord

Doral Raphe Nucleus is tied to learned helplessness, vmPFC is essential to block the effects of shock