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Neuroendocrine Exam 3 > Reward and Addiction > Flashcards

Reward and Addiction Flashcards

1
Q

Motivation

A

Use goal oriented responses and behavior to change external or internal environments
Reinforcement can be used to cause similar behaviors to occur

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2
Q

Salience

A

Something important that is worth paying attention to in the environment
“Wanting”
You notice a feature that indicate that good rewarding things can come from it

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3
Q

Reward

A

Involves

  1. Hedonic effect of pleasure
  2. Motivation to obtain reward because of its value(Salience)
  3. Associated learning
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4
Q

Aversion

A

Negative reinforcement of behavior to avoid future encounters

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5
Q

Pleasure/ Hedonia

A

Positive sensation, euphoria or hedonia “Liking”

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6
Q

Reward Production Error (RPE)

A

Dopamine neurons encode the discrepancy between reward prediction and what you actually get ——> brain regions for reward learning

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7
Q

Positive Prediction Reward Error

A
  1. Unpredicted reward is elicited (massive brain stimulation)
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8
Q

No RPE

A

Fully predicted reward is eliciting no reward(no RPE) so you get the reward you expected

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9
Q

Negative Prediction Error

A

Don’t get reward you expect —-> depression in stimulation

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10
Q

Drugs vs natural rewards

A 
Drugs: have a continuous negative RPE which increases stimulation of brain and is therefore preferred 
Natural Rewards(caring for young, food, exercise, mating): they are error-correcting DA-RPE, so you get the reward you expect (you learn to predict the outcome)
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11
Q

Drug abuse increases what NT and where

A

Dopamine in ECM of the Nucleus Accumbens

Cause 5-10 times higher Dopamine then natural reinforcement like sex and food

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12
Q

Drugs increasing Dopamine directly

A

Cocaine, Amphetamine, Methamphetamine, and ecstasy ——I dopamine reuptake
——> dopamine release

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13
Q

Drugs indirectly increase Dopamine

A

drugs bind to neurons that regulate other neurons to release more dopamine
Nicotine, Alcohol, opiates, marijuana

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14
Q

how environment and stimuli elicits behavior change (SALIENCE)
How this works in drugs and the reason people relapse

A

Drugs release 5-10 times more dopamine = more motivation to find the drug or stimuli then natural reward= you have motivation even if you can’t consciously feel the pleasure (since dopamine still increases)
+
Salience and Dopamine increases with even the sight, sound…. of anything associated with the drug in the environment = elicit desire for the drug

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15
Q

Mesolithic System uses what NT

What 4 parts to it

A

Uses DOPAMINE

  1. NA-> GABA
  2. Ventral Tegmental area -> Opioids
  3. Limbic System -> Dynorphin
  4. PFC-> EAA
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16
Q

NA (Nucleus Accumbens) Function

The Basic Circuit

A

To suppress sensation of pleasure and reward
Is default activated continuously by some EAA(GLUTAMATE) from hippocampus, amygdala, or PFC
Stimulated NA neurons release GABA at the PFC which keeps the brain in a reward neutral state (no pleasure)

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17
Q

The reward circuit

A 
The VTA is activated 
VTA Neurons release Dopamine on NA
NA neurons are inhibited 
NA doesn’t release GABA on the PFC
Sensation and pleasure is felt
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18
Q

What activated the VTA

A

Due to engaging behavior which results in reward innately
Or due to a drug in innately
EEA GLUTAMATE from the PFC
ACH from the Tegmental Nuclei like Dorsal Tegmental Area
OREXIN from the hypothalamus when eating food

19
Q

The reward feed back to shut it off

A

Neurons from the NA go to the VTA releasing GABA ——I VTA
And releasing Dynorphin (opioid) ——I(binds kappa-opioid R) VTA

= inhibit dopamine release

20
Q

Dopamine hypothesis of reward

A

Inactivation of NA by the VTA

21
Q

Dopamine-Independent Reward Pathway

A

Exercise, alcohol, and other activities increase opioid at all levels= VTA, NA, PFC: (BIND TO mu- receptors)

  1. VTA = bind/activate VTA dopaminergic inhibiting interneurons to allow VTA to release Dopamine
  2. NA = bind/activate to NA GABA releasing interneurons to inhibit NA form releasing GABA
  3. PFC= activate it directly

Uses endogenous opioids, a lot of pleasure

22
Q

Reward from drug

A

Causes dopamine signal to the NA that is not proportional to a stimuli
REWARD= enhanced euphoria and exaggerated reward to a mild stimulus
Not learned behavior

23
Q

Reward from natural thing like exercise

A

Dopamine release from VTA to inhibit NA due to a specific stimulus like running
To promote healthy living that may not have immediate benefits
REWARD= sense of pleasure
Learned behavior

24
Q

Chronic Drug use alters neurons at a cellular level

A

Changes expression of TF and proteins involved in neurotransmission to regulate dopamine release

25
Q

Chronic Drug use alters neurons at a neurotransmitter level

A

Adapting to the stimulus from Dopamine, GABA, ,opioids, serotonin, and others

26
Q

Hippocampus in reward to a drug

A

Conditioned associations

Lasting memory associating reward with circumstance and environment

27
Q

Amygdala in reward form drug

A

Causes cravings

28
Q

Orbitofrontal cortex in reward from drug

A

Person sees, hears, smells, associated things to drug they are driven to make bad decisions to get the drug despite obstacles

29
Q

Learning and memory mechanisms

A

Continuous increase in synaptic strength following a high frequency stimulation of a chemical response

30
Q

How is synaptic strength increased form memory and learning

A
  1. Short-term memory = phosphorylation of AMPA receptors in the post-synaptic membrane
  2. Long-term memory(days -years) = activated Ca+2-Calmodulin-CREB mechanism
  3. Life long memory= activate delta-FosB and AP-1 cascade
  4. Dynorphin can also cause memory
31
Q

How does CREB work and where is it used to make memory

IN NA

A

In the NA
(Days-weeks) memory of reward stimulation
1.Ca+2 binds to Calmodulin
2. increase in cAMP—-> activate PKA
3. PKA activates CREB
4. CREB is a TF that goes to DNA to transcribe a lot of Dynorphin

32
Q

How does CREB work and where is it used to make memory

In the Locus Ceruleus

A

For physical dependency
Due to excessive NorE causing CREB pathway
1.Ca+2 binds to Calmodulin
2. increase in cAMP—-> activate PKA
3. PKA activates CREB
4. CREB is a TF that goes to DNA to transcribe a lot of proteins for learning and memory in the Locus Ceruleus

33
Q

delta-FosB and AP-1 are activated by what and cause what in their pathway

A

Life long learning
Drugs abuse, chronic stress….
Activates the delta-Fos-B and AP-1 cascade
They go to the DNA to transcribe structural proteins, EAA receptors, factors that increase motivation for seeking drug

34
Q

Basic pathway of drug and its effects

A
  1. Drug binds to Ligand, voltage, or GPCR receptor
  2. 2nd messengers made which increase Ca+ or other messengers and cause cascade
  3. TF made
  4. Expression changes: BDNF (neural growth), Cytoskeleton, synapse and growth, NT synthesis, NT receptors
35
Q

Dopamine release from the VTA with conditioning (learning)

A

Short, fast, large released
To expect reward

Stop firing after event concludes
Except drugs keep DA release

36
Q

Fear conditioning

A

You feel the withdrawal effects after drug effects go away causing fear of withdrawal causing drug consumption

37
Q

Role of dopamine in addiction

A

Causes change in memory and emotion to a stimuli
Attached a euphoric feeling to previously feared stimuli and attaches an excepted reward feeling to a stimuli

LEARNED CONDITIONING

38
Q

Stress in the NA

A

NA assigns salience to certain stimuli and make us seek that or avoid that
ACUTE STRESS= Corticotrophin releasing factor (CRF) causes DOPAMINE to get released in the NA (short-term)
SEVERE, CHRONIC STRESS= CRF causes DOPAMINE increase causing aversive results now, not pleasurable

They act on different CRF receptors causing different results from dopamine

39
Q

VTA in reward

A

Signals the prediction error

40
Q

Hippocampus in reward

A

Provides place and direction information about the stimuli you experienced

41
Q

Substantia Nigra and Dorsal Striatum in reward

A

Motor response to navigate environment toward the desire with goal to get the reward

42
Q

Amygdala in reward

A

Retrieves memories of fear and fear conditioning

43
Q

Non- addicted brain

A
  1. Saliency to something cues are low (brain inhibits drive to seek substances=all areas)
  2. Learned/conditioned cues have little or no influence on the saliency of the drug
  3. Saliency of natural rewards&raquo_space;> saliency of drugs
44
Q

Addicted brain

A
  1. The saliency of stimuli or substance is increased and HIGH
  2. The PFC can’t control behavior or inhibit drive to seek the substance
  3. Learned/conditioned cues increase saliency of substance -> increasing seeking it more
  4. Saliency of drug&raquo_space;> natural rewards that don’t influence behavior anymore

Neuroendocrine Exam 3 (18 decks)

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