Lecture 3 - Pleasure and reward Flashcards
What are the 3 theoretical components of the brain reward system?
- Learning what is rewarding
- Motivation (wanting)
- Pleasure (liking/reward)
What neurones produce dopamine, and where do they terminate?
- VTA neurones (ventral tagmental area)
- Terminate in the Nucleus accumbens
The midbrain pathways of interest for the dopamine systems originate in A9 neurones – the _______ pathway and
A10 (VTA) ________ and ________ pathways.
The midbrain pathways of interest originate in A9 neurones – the nigro-striatal pathway and
A10 (VTA) mesolimbic and mesocortical pathways.
The A9 nigro-striatal pathway is involved with _______.
The A10 mesocortical pathway is related to _________.
The _______ path to the nucleus accumbens is the “reward path”.
The A9 nigro-striatal pathway is involved with motor control.
The A10 mesocortical pathway is related to perception and motivation.
The VTA path to the nucleus accumbens is the “reward path”.
Where are opiates released in response to pleasure or pain?
- Nucleus Accumbens (NAc)
- Orbito-Frontal Cortex (OFC)
- Ventral Pallidum (VP)
- Amygdala
- What is released in the NAc in response to reward wanting?
- What is released in the NAc in response of reward achievement?
- Reward wanting = Dopamine
- Reward achievement = Opioid
What is anhedonic state and how does it occur?
- absence of being able to achieve pleasure
- Raised tonic/baseline of dopamine - reduces phasic signal bursts, reducing anticipation of reward.
Why may a raised baseline and therefore reduced ability for phasic signal bursts have evolved for survival reasons?
It may have evolved to ensure rest and low activity during recovery from injury. (You don’t have to motivation to do stuff therefore you recuperate better)
What happens to dopamine neurones:
a) in response to an unexpected reward
b) in response to a predicted reward
c) if a reward was predicted but not recieved
a) Increase phasic firing
b) Do not respond
c) Firing is depressed
Why (on a dopamine level) do drug addicts need increased doses of the drug in order to be satisfied?
Because predictor vs reward is learnt behaviour. If the result is as good as what was predicted, the dopamine reward signal would not fire - so it always needs to be better than predicted.
What is the behavioural evidence in the motivation-decision model that indicates that the brans pleasure and pain systems mutually inhibit one another?
Pain can be decreased by pleasant experiences such as food, sex, pleasant odours, images and music.
Pleasure (the hedonic experience) is reduced by pain (e.g. appetite reduced by pain).
- Raised tonic/baseline of dopamine - increases/reduces phasic signal bursts, reducing/increasing anticipation of reward.
- Raised tonic/baseline of dopamine - reduces phasic signal bursts, reducing anticipation of reward.
Where are opioids released in response to pleasure/pain? (3)
Nucleus Accumbens (NAc) Ventral Pallidum (VP) Amygdala.
What dopamine pathway is associated with schizophrenia?
A10 mesocortical pathway
What is the action of cocaine at the nucleus accumbens?
The opiates bind to opiate receptors that are concentrated in areas within the reward system.
Three neurons participate in opiate action: the dopamine terminal, another terminal containing a different neurotransmitter (probably GABA for those that would like to know), and the post-synaptic cell containing dopamine receptors. Show that opiates bind to opiate receptors on the neighbouring terminal and this sends a signal to the dopamine terminal to release more dopamine. One theory is that opiate receptor activation decreases GABA release, which normally inhibits dopamine release, so dopamine release is increased.
