Psyc417 Reward Dopamine And Feeding
Last updated: 1/9/2025
Questions
Notes
Natural rewards are rewards that are produced by sensory stimuli (fresh-air, cat). Non-natural reward are rewardsa produced by drug or brain stimulation. Rewards are anything that makes you "feel good" (it would support operant learning)
Negative reinforcement is when you increase behavior by taking away an adversive stimulius while punishment is a negative stimulus to decrease behavior.
Intra-cranial self-stimulation (ICSS) is when a wire stimulates your brain center that makes you feel reward.
ICSS can occur in rat pups are young as 3 days old.
The main pathways that connect the ICSS area incluee the medial forebrain bundle (MFB) and the fornix (neighboring the lateral hypothalamus).
When noradrenergic system system is inhibitied then they are less motivated to do tasks for operant conditioning. This is the same for the dopaminergic system.
Dopamine
Dopaminergic is important for reward seeking. Noradrenergic system is important for staying awake and aroused.
Noradrenegenic system starts at the locus coeruleus and projects to almost everywhere in the brain. The dopamergeric system has 3 parts:
- The nigrostriatal tract starts from the substantia nigra which goes to the striatum.
- Mesolimbic pathway: ventral tegemenal area (VTA) which projects to the limbic forebrain, the nucleus accumbens (NAc),
- The mesocortical pathway starts at the ventral tegemental area which projects to the cerebral cortex (notablly the preforntal cortex (PFC)).
Based on what enzymes the neurons have you can guess what chemical receptors it has. For example, if it has the Dopamine Beta-Hydroxylase enzyme then it will express norepinepherine. Phenylalanine -> L tyrosine -> L-dopa -> Dopamine -> Norepinepherine -> Epinepherine Dopmaine transporter reuptakes synaptic dopamine.
The anhedonia hypothesis is a hypothesis that dopamine is important for objectively measured reward function. Also that dopamine is important for emotional health. To Test this hypothesis they used pimozide (antagonist for D2-like receptors), an antipsychotic drug, to test the hypothesis. Blocking the dopamin system with pimozide gives the same results as not giving any reward at all (making the target behavior go extinct).
Palatable foods increase dopamine in the nucleus accumbens and aversive tastants produce the opposite effect. Any conditioned taste aversion behavior causes a decrease in dopamine when it is eaten.
When killing dopamine neurons animals have no motivation and they just starve themselves.
Leptin receptor knockdown on on midbrain dopamine neurons increases palatable food intake and preference.
Feeding behavior can be manipulated through manipulating the dopaminergic system.
For obese patients, they most likely have a reward deficiency. This was tested by a test to see what the threshold is to simulate the lateral hypothalamus for the animal to start ICSS. In my own words, this shows what the dopamine threshold is to feel the same type of pleasure. The experiment showed that animals that have the cafeteria diet (high fat high sugar) vs. standard chow diet require a stronger stimulus to have the same reward. This is CRAZY results!
There is a inverse relationship with body-weight and D2R amount. THIS IS CRAZY. Gaining weight causes you to have reduced expression of D2 receptor. Losing weight sensitizes you to dopamine!!! This theory applies also to drug dependence, they have lower level of D2 receptor.
Giving a normal body weight individual a drug (ritalin) that increases dopamine signaling causes people to eat less snacks and have a lower appetite.
Giving obese males taking ritalin increases their appetite while giving it to obese females decreases their apetite.
Two other drugs to block dopamine signaling is Haloperidol is a D2 antagonist, and might be a D2 inverse agonist. Inverse agonist decreases the signaling of the receptor too. Olanzapine is a D1 and D2 antagonist. Olanzapine causes people to gain a LOT of weight.
Amphetamine or GBR (DA reuptake inhibitor) reduces meal size, total feeding time, and food intake. Amphetamine increases dopamine levels in the synaptic cleft and certain lower doses of amphetamine increases meal frequency.
There are designer receptors that exclusively are activated by designer drugs (one eaxample is CNO).
When chemogenetic activation of dopamine neurons in the VTA reduces meal size and food intake but increases meal frequency. For chemogenetic activation of domapine meurons on the substantia nigra has no effects.. To figure out which dopaminergic pathway is responsible for this, they injected the virus to the NAc and PFC and found that the NAc pathway is reponsible for decreasing food intake and increasing meal frequency.
Why is this happening? It appears that the dopaminergic pathway that impacts food intake causes the animals to run around a lot more, they have increased activity. The animals become hyperactive.