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Neurophysiology Of Reward And Addiction Flashcards

1
Q

What does reward drive?

A

incentive based learning, appropriate response to stimuli, and development of goal directed behavior

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2
Q

What NTR plays a key role in processes modulating reward seeking behaviors?

A

Dopamine

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3
Q

How does dopamine arrive at the hypothalamus?

A

a. Medial forebrain bundles carries dopaminergic fibers from vetnral tegmental area (VTA) of midbrain to Nucleus Accumbens
b. All structures —> hypothalamus

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4
Q

Where else do VTA projections go and influence?

What will this cause?

A

hippocampus, amygdala, and prefrontal cortex

Prefrontal cortex —> feedback to VTA (directly or thru nucleus accumbens)

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5
Q

What initiatives the Neuroendocrine and visceral response to reward?

A

Hypothalamus

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6
Q

What is motivation in human behavior?

A

◦ Process that mediates goal-directed responses or goal-seeking behavior to changes in external or internal environment

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7
Q

What is reinforcement in human behavior?

A

consequence of learned behaviors that alters probability that a behavior will or will not be repeated under similar conditions each time

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8
Q

What is Saliency?

A

◦ Impt. Thing in surrounding environment worth paying attention to

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9
Q

What is a reward for human behavior?

A

◦ Objects, stimuli, or activities that have positive value

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10
Q

What is aversion in human behavior ?

A

◦ Negative reinforcement of behavior - teaches individual to avoid future encounters

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11
Q

What is pleasure in human behavior?

What is the physiologic purpose of it?

A

◦ Positive sensation; referred to as euphoria or hedonia

◦ Physiologic purpose:
‣ Promote behaviors consistent w/ survival of self and the species

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12
Q

What is a Reward Prediction error?

A

Measure of how much the expected value of a reward differs from the actual reward being received.

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13
Q

What is a positive reward prediction error result from?

A

When an unanticipated reward is received

if one predicts a minimal reward, yet experiences a larger reward

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14
Q

When would a negative reward prediction error occur?

What is this associated with?

A

when a reward is expected, yet a minimal reward is received

Depressive response

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15
Q

When would the Reward Prediction Error not be activated?

A

If a reward is anticipated and an equally stimulating reward is received, (aka, a fully predicted reward is received)

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16
Q

What type of RPE will drug use initially cause?

A

Positive RPE

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17
Q

What happens with Repeated Drug use in terms of RPEs?

A

the repetition of these reward prediction error signals the reinforcement of continued drug-released consumption (or exposure to drug-related cues, behaviors, and environments).

These unnatural exposures set up the brain for a reward prediction error that learns over time to formulate better predictions of the future.

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18
Q

What encodes for the difference between reward received and predicted (aka the RPE)?

A

Dopamine

involved in the prediction of reward, assignment of salience, and behavioral learning that occurs.

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19
Q

What does the extracellular dopamine released in the Limbic systems and other reward centers by drugs of abuse do?

A

motivates further procurement of more drug

(regardless of whether or not the effects of the drug are consciously perceived to be pleasurable

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20
Q

When do natural re-enforcers of reward cease dopamine signaling?

Compared to Drugs of Abuse?

A

once the activity/event concludes.

drugs of abuse continue to increase dopamine signaling unnaturally after event is done.
exacerbates the reward prediction error compared to a natural RPE.

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21
Q

What will natural rewards produce?

A

Error correcting Dopamine-RPE signals

Will act until predictions match actual events

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22
Q

When given a choice between event leading to drug and event leading to natural reward what will an individual exposed to a Drug of Abuse do?

A

Develop bias toward drug that will strengthen with each drug use

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23
Q

How do Drugs of Abuse reinforce their use?

A

increase Extracellular dopamine concentration in Limbic regions (incl. Nucleus Accumbens)
◦ Increase it for longer and larger (5-10 fold) than natural rewards (food or sex)

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24
Q

Which drugs of abuse increase dopamine directly? How?

A

Cocaine, amphetamine, methamphetamine, and ecstasy

Inhibit DA reuptake
Promote DA release

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25
Q

What drugs of abuse indirectly modulate dopamine levels?

How?

A

Nicotine
Alcohol
Opiates
Marijuana

Via other neuron receptors

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26
Q

What predictions are Dopamine involved in?

A

Reward and Salience

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27
Q

What is salience?

A

stimuli or environmental changes that are arousing or elicit an attentional behavioral switch

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28
Q

How does dopamine facilitate seeking behavior thru Conditioned learning?

A

drugs —> increase DA —> motivate further procurement of more drugs (bc of salience, i.e. arousal)

will drive you to situation where sensory stimuli (assoc. w/ drug or w/ drug taking) can lead to increase dopamine and elicit desire for drug
= environment where you had drug or stimuli where you had drug, will increase Dopamine and lead to desire for drug

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29
Q

Why will a person relapse when placed in an environment similar to where they had previously taken a drug?

A

environment where you had drug or stimuli where you had drug,
will increase Dopamine
&
lead to desire for drugs = relapse

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30
Q

What does the Mesolimbic system network contain?

A

Nucleus Accumbnes (NA)
Ventral Tegmental Area (VTA)
Limbic system
Pre-frontal cortex (PFC)

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31
Q

What NTR does the mesolimbic system primarily use?

A

Dopamine

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32
Q

What other systems also use DA?

A

Nigrostriatal system
Mesocortical system
Tuberoinfindibular system

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33
Q

What other NTRs are used by the Mesolimbic system besides DA?

A 
‣ GABA
		‣ Opioids
		‣ Excitatory amino acids (EAA: glutamate) 
		‣ Dynorphins
		‣ Orexin
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34
Q

What is the basic circuit of the Mesolimbic system?

Resutls in?

A

Nucleus accumbens —> Pre frontal cortex

= absents of pleasure

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35
Q

How does the Nucleus Accumbens supresses the sensation of pleasure

A

NA always active via trickle of EAAs from hippocampus, amygdala or PFC

NA neurons = GABAeric —> PFC, inhibit it

Keeps brain in reward neutral state = no pleasure

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36
Q

What kind of neurons are Nucleus Accumbens?

What is their target?

A

GABA-ergic

PFC

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37
Q

When an action elicits a reward, what region of the Mesolimbic system becomes active?

A

Ventral tegmental Area

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38
Q

When a reward activates the VTA, what happens?

A

VTA inhibits NA which then can no longer inhibit PFC

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39
Q

How does the VTA inhibit NA?

A

VTA —> DA to NA
DA inhibits NA neurons
NA activity decreases = no GABA to PFC

Pleasure can be sensed

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40
Q

What is the “Reward circuit”? Allows for what?

A

VTA —> NA

Allows for presence of pleasure

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41
Q

What is the Reward Feedback circuit?

A

Projections from NA back to VTA

NA will release GABA, inhibit VTA

NA also releases Dynorphin, causes dysphoria

Suppresses DA release from VTA = halts reward process

42
Q

What is Dynorphin?

What will it bind?

What will it cause?

A

An opioid released by NA at VTA

Binds Kappa Receptor in VTA

Causes dysphoria

43
Q

What does the dopamine hypothesis of reward postulate?

A

that the actions of drugs of abuse are rewarding as a consequence of activation of dopamine in the mesolimbic dopamine system

DA from DRUGS —> NA —> PFC can be activated
====pleasure

44
Q

What is Does the Dopamine Independent reward pathway use?

Receptors?
Result?

A

Uses endogenous opioids

Activates mu receptors

Profound sense of pleasure

45
Q

What are endogenous opioids?

Where do they increase signaling?

A

Exercise, ethanol, other activities

Increase signaling at all levels of reward network (VTA, NA, and PFC)

46
Q

What will activation of Mu receptors by endogenous opioids cause?

A

Activation of DA neurons

Activation of local interneurons in NA, inhibiting local GABA neurons

Activation of PFC itself

47
Q

How are dopamine neurons activated in the VTA?

A

Thru inhibition of local VTA interneurons that normally suppress DA activity

48
Q

What is the purpose of Normal Reward Stimuli?

A

Reinforce behaviors consistent with health, longevity, and otherwise don’t seem to have an immediate benefit

49
Q

What is the reward gained by normal reward stimuli/

A

Sense of pleasure that is derived

50
Q

What is the reward gained due to Drugs of abuse?

A

Enhanced euphoria and exaggerated reward to an otherwise mild stimulus

51
Q

How does chronic drug exposure alter the morphology of neurons in DA regulated circuits?

A

alter expression of transcription factors (nuclear proteins that bind to regulatory regions of genes, regulating transcription into mRNA)

&

alter wide variety of proteins

52
Q

What NTRs can be altered due to Chronic drug exposure?

A

dopamine, glutamate, GABA, opioids, serotonin, and various Neuropeptide

53
Q

Where do we see abnormal NTR levels in the mesocortical region of the brain?

A

Orbitofrontal center

Cingulate gyrus

54
Q

What is the Orbitofrontal cortex involved in?

A

Compulsive behavior

55
Q

What is teh cingulate gyrus involved in?

A

Regulation of disinhibition

56
Q

What is the role of the hippocampus?

A

creates lasting memories associating good feeling w/ circumstance and environment they occurred in

57
Q

How do Memories facilitate addiction?

A

Memories are conditioned associated that use same circuits that mediates craving (amygdala)

So when abuser sees person/thing they are driven to make poor decision or seek our more drugs in spite of obstacles because they are CONDITIONED

58
Q

What are the mechanisms for learning and memory?

A

‣ Persistent increase in synaptic strength following high-frequency stimulation of chemical synapse

‣ Requires repeated strong stimulation

  • Increased phosphorylation of AMPA receptors and more AMPA receptors on post-synaptic membrane
  • Will lead to activation of Ca-Calmodulin CREB mechanism
59
Q

What is CREB?

A

◦ cAMP Response-Element Binding Protein targeting CRE (cAMP response elements)

60
Q

What is the target of CREB within the NA?

A

Dynorphin DNA

Previously shut down pleasure

61
Q

What is the target of CREB in locus ceruleus?

A

Target genes in locus ceruleus —> increase NE output —> Physical dependency

62
Q

What are the two targets of CREB in reward pathways/

A

NA

Locus ceruleus

63
Q

What is the purpose of CREB in the Locus ceruleus?

A

Mediate physical dependency

64
Q

What is the acting limit of CREB?

A

Short acting

Will return to normal when you stop using drug

65
Q

What upregulates FosB and AP-1?

A

Stress and drugs of abuse

66
Q

What will upregulation of FosB and AP-1 cause?

A

Upregulated expression of

‣ EAA REceptor expression (AMPA/NMDA)
‣ Elements of cell signal transduction pathways
‣ Factors promoting drug, seeking, motivation, locomotion

67
Q

What is the acting period for TF’s FosB and AP-1?

A

Mos. Or years

68
Q

What is AP-1?

A

Dimer formed by Fos/Jun interactions

69
Q

What can large increases in Dopamin induce?

A

Conditioned learning

70
Q

What will the conditioned learning induced from large DA increase from drugs cause?

A

Large,fast, short lived increase of DA in VTA to NA that reflect EXPECTATION of reward

71
Q

How does this learned conditioning in drug users differ from natural reinforcers?

A

Natural reinforcers: DA firing stop when event stops

Drug conditioned learning = continued increase in DA release

72
Q

What are the conditioned responses induced by Drugs?

A

◦ Provide powerful cues to drug taking in social situation

◦ Drug associated cues: person who they took drug with, or drug paraphernalia

‣ Elicit drug urges and physiologic responses (sympathetics activation)

‣ Activates reward circuits in addicted human subjects

73
Q

What does fear conditioning in terms of drug withdrawal cause?

Leads to?

A

Fear drug withdrawal symptoms

Learn that drug can resist these effects

Leads to any source of stress or frustration becoming cue for drug use

74
Q

What is fear conditioning?

A

‣ Learned behavior assoc. with something unpleasant or aversive

75
Q

How does DA alter conditions thru which fear occurs?

A

Thru the association itself and the expression of memory

Due to DA receptors and signaling cascades in different regions of brain

76
Q

In a non-addicted brain, what will the arousal to a substance be?

How do conditioned cues affect it?

A

Salience and substance cues = low
(Brain inhibits it)

Little to no influence on salience of drug subst.

77
Q

In a non-addicted brain, will salience to natural rewards or to drugs be higher?

A

Natural rewards

78
Q

In an Addicted brain, how does the addictive substance influence salience and cues?

What will an addicted brain do to the PFC?

A

Cues and saliency toward substance = HIGH

Will override PFC’s control of behavior

79
Q

In an addicted brain, what has more saliency: natural rewards or substance?

A

Substance of abuse

80
Q

What is the role of amygdala?

A

Retrieval of fear memories

81
Q

What does the VTA signal?

A

Signals prediction error b/w expected outcome and actual reward experience thru DA

82
Q

What does the NA assign and mediate?

A

Assigns arousal to certain stimulus

Mediates decision to seek or avoid situation

83
Q

What does acute stress cause?

A

Corticotrophin releasing factor

Will increase DA release in NA for a short term

84
Q

What does the short increase in DA cause during acute stress?

A

Causes reward experienced during times of acute stress to have more significance

(e.g. I eat chocolate ice cream when I’m stressed and it helps me feel better compared to eating chocolate ice cream when I am happy and calm)

85
Q

What does prolonged, chronic, severe stress do to the reward system?

A

Erodes the reward-process

86
Q

Why does chronic stress present differently than acute?

A

CRF —> CRF1 and F2 subtypes receptors in NA —> DA release —> associates DA with aversive things

Messes up reward-process pathway

87
Q

What does the hippocampus provide?

A

place and direction-contextual info about environment where stimuli is expereinced

88
Q

What is the role of Substantia Nigra and DOrsal Striatum with reward-pathway?

A

‣ facillitates motor response assoc. w/ navigating environment toward desirable cue

• W/ goal of engaging in activity that elicits reward

89
Q

How can you treat withdrawal symptoms?

A

Act on Noradrenergic neurons in the locus ceruleus w/ a receptor agonist

90
Q

What is physical dependence on a drug due to?

A

Excess NE output from locus ceruleus (involves CREB dependent upregulation of target genes in locus ceruleus)

91
Q

What does salience do?

A

Heightens perception and focuses attention toward particular sights, sounds, and smells associated w/ rewards

92
Q

What triggers salience?

How does one experience salience?

A

Encounters w/ reward-related cues

Surges of motivation

93
Q

What is ANhedonia?

A

Lack of interest in something

No longer liking something that was previously lived

94
Q

What 3 things does reward involve?

A

1) hedonic “Liking” effect of pleasure
2) motivation to obtain reward bc of its value
3) associated learning

95
Q

What is the NTR from the PFC(!) to the Nucelus Accumbens?

A

EAAs

Glutamate!

96
Q

How can you treat withdrawal symptoms?

A

Act on Noradrenergic neurons in the locus ceruleus w/ a receptor agonist

97
Q

What is physical dependence on a drug due to?

A

Excess NE output from locus ceruleus (involves CREB dependent upregulation of target genes in locus ceruleus)

98
Q

What does salience do?

A

Heightens perception and focuses attention toward particular sights, sounds, and smells associated w/ rewards

99
Q

What triggers salience?

How does one experience salience?

A

Encounters w/ reward-related cues

Surges of motivation

100
Q

What is ANhedonia?

A

Lack of interest in something

No longer liking something that was previously lived

101
Q

What 3 things does reward involve?

A

1) hedonic “Liking” effect of pleasure
2) motivation to obtain reward bc of its value
3) associated learning

102
Q

What is the NTR from the PFC(!) to the Nucelus Accumbens?

A

EAAs

Glutamate!

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