Psyc417 Cue And Addictive Eating

Questions

Notes

CS+ potentiated eating is seeing if an animal will learn to eat food when there is a cue and it is not hungry. In this, the CS+ induces a complex emotional or motivational state such as an appetite or crving for food target (but not a novel food).

Cue induced eating is between the amygdala, LH, mPFC.

Assymetric lesions of the basolateral amygdala and the LH eliminates cue induced eating. Contralateral lesions are lesions in what hemisphere. Bilateral regions are lesions in both.

Orexin plays a role in cue induced eating. This is shown because of bilateral lesions of the mPFC impairs cue eating and blocking orexin receptor 1 signaling in the mPFC with an antagonist impairs cue potentiated eating.

Food cue induced basolateral amygdala activation without hunger is assocaited with weight gain susceptibility. Obesisty and obesity-prompting traits such as external cue induced eating are assocaited with heightened food cue amygdala reactivity and amygdala connectivity with the ventral straitum (NAc)

There are individual differences for how animals deal with cue mediated eating. Some animals focus on the sign tracking (what the cue was), and spending a lot of time and effort with it, while other animals focus on the goal and where the food will be.

Initially, dopamine activity increases when food is delivered, but after the classical conditioning, the dopamine spikes directly after the CS is presented.

For animals that are sign trackers, after they are trained the dopamine spikes their dopamine spikes initially when the CS is presented with another smaller hump when there is reward.

For goal tracjers, there is almost no dopamine raise when there is a CS and then US, but after they are trained there is an equal response to the CS and the US.

There are multiple neural substrates that are involved in cue-induced motivation.

People categorize eating behaviors via three factors. Factor 1: Cognitive control of eating behavior (cognitive resistance) Factor 2: Disinhibition of control (loss of restraint, uncontrolled) Factor 3: Susceptibility to hunger (Feeling of hunger and emotional eating)

There are threee eating patterns, disinhibited restrained eaters (high restraint, high disinhibition), inhibited restrained eaters (high restrained/ low dishinibtion) and unrestraned (low restraint).

Disinhibitied restrained eaters are the ones with the highest chance of over eating.

Disinhibition: loss of eating control, followed by consuption of greater quantities of food.

• People with binge eating disorder have a higher disinhibition and hunger, a tendency to overeat, higher depression neuroticism, anxiety, dysfunctional eating patterns.

Equal distribution between people who stress eat, eat normallly understress and stress undereat.

Dieters are more likely to report stress-related hyperphagia and nondieters are stress-related hypophagia.

Obesity is a result of food addiction but obesity and food addiction are not the same.

There are definitions for substance dependence that can be applied to food. Some of this criteria are: Tolerance, withdrawl symptoms, taking larger amounts than intended, a lot time is spent on getting, using and recovering from the substance, important social occupational or recreational activities are given up or reduced because of substance abuse, and the substance use is continued despite knowledge about the adverse affects of the substance.

There is a correlation between obesity and food addiction but it is not very good.

It is hard to find food addiction in animals. Drug reward is a lot higher than food reward.

Food addiction does not necessarily lead to obesity, it is NOT the same as drug addiction.

Posterior pituitary glad doesn't release too much information.

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