Food reward: Difference between revisions

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==Title of Part 1==
 
'''== Motivated behaviour and food as a reinforcer ==
 
'''
The underlying pathways in motivating feeding behaviour seem to be far more complex than a simple homeostatic system, which responds to metabolic and satiety signals from the gut. One possible thought is that the brain’s reward systems react to stimuli such as sight, smell and taste, or other cues that predict food. However, neither hunger nor thirst results in unconditioned goal-directed behaviour. Chance encounters with various tastes of palatable foods are required before goal-directed behaviour can result from the interaction of the internal needs with the salience of environmental stimuli. For example an infant recognises and learn to seek out sweet tastants, but the desire for a particular food is controlled by the interaction of peptide levels (related to hunger) with the brain circuitry, coding the animal’s reinforcement history for that specific food. Subsequently, the infant will indiscriminately taste both food and non-food objects, until it has received reinforcing feedback from sufficient stimuli. In addition, the monkey’s appetite for a yellow banana requires the prior learning of the relation of the sight of the yellow skin of a banana, with the sweet taste of the white banana meat plus the consequences resulting from the ingestion of the fruit. Therefore, preference for a specific food, results only when the post-ingestional consequences of that food’ reinforce’ the tendency to eat that food. Thus, food is considered to be a strong reinforcer. Moreover, when the response of a behaviour stimulated by a reinforcer increases the rate of that specific behaviour; that is known as positive reinforcement or reward learning, and the positive events are called rewards. The reinforcing efficacy of food reward is the ability of the reward to maintain rather than to establish behaviour; consequently the stimulus learning contributes to the response learning. Dopamine is known to play an important role in both. However, evidence from various studies seem to conclude that dopamine’s contribution appears to be chiefly to cause ‘wanting’ (Dopamine signalling in the dorsal striatum/CPu) for hedonic rewards rather than ‘liking’ or learning (mesolimbic dopamine) for those rewards. The first evidence for the implication of dopamine in food reward came from studies in rats, where dopamine antagonists blocked the rewarding effects of brain stimulation (Liebman & Butcher 1974; Fouriezos & Wise 1976) and of psychomotor stimulants.  
The underlying pathways in motivating feeding behaviour seem to be far more complex than a simple homeostatic system, which responds to metabolic and satiety signals from the gut. One possible thought is that the brain’s reward systems react to stimuli such as sight, smell and taste, or other cues that predict food. However, neither hunger nor thirst results in unconditioned goal-directed behaviour. Chance encounters with various tastes of palatable foods are required before goal-directed behaviour can result from the interaction of the internal needs with the salience of environmental stimuli. For example an infant recognises and learn to seek out sweet tastants, but the desire for a particular food is controlled by the interaction of peptide levels (related to hunger) with the brain circuitry, coding the animal’s reinforcement history for that specific food. Subsequently, the infant will indiscriminately taste both food and non-food objects, until it has received reinforcing feedback from sufficient stimuli. In addition, the monkey’s appetite for a yellow banana requires the prior learning of the relation of the sight of the yellow skin of a banana, with the sweet taste of the white banana meat plus the consequences resulting from the ingestion of the fruit. Therefore, preference for a specific food, results only when the post-ingestional consequences of that food’ reinforce’ the tendency to eat that food. Thus, food is considered to be a strong reinforcer. Moreover, when the response of a behaviour stimulated by a reinforcer increases the rate of that specific behaviour; that is known as positive reinforcement or reward learning, and the positive events are called rewards. The reinforcing efficacy of food reward is the ability of the reward to maintain rather than to establish behaviour; consequently the stimulus learning contributes to the response learning. Dopamine is known to play an important role in both. However, evidence from various studies seem to conclude that dopamine’s contribution appears to be chiefly to cause ‘wanting’ (Dopamine signalling in the dorsal striatum/CPu) for hedonic rewards rather than ‘liking’ or learning (mesolimbic dopamine) for those rewards. The first evidence for the implication of dopamine in food reward came from studies in rats, where dopamine antagonists blocked the rewarding effects of brain stimulation (Liebman & Butcher 1974; Fouriezos & Wise 1976) and of psychomotor stimulants.  
===Title of Subpart 1===
===Title of Subpart 1===

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A brief overview of your interest group (be sure to put its name in bold in the first sentence) and the scope of the article goes here.[1]

The following list of sections should serve as a loose guideline for developing the body of your article. The works cited in references 2-5 are all fake; their purpose is to serve as a formatting model for your own citations.


== Motivated behaviour and food as a reinforcer ==

The underlying pathways in motivating feeding behaviour seem to be far more complex than a simple homeostatic system, which responds to metabolic and satiety signals from the gut. One possible thought is that the brain’s reward systems react to stimuli such as sight, smell and taste, or other cues that predict food. However, neither hunger nor thirst results in unconditioned goal-directed behaviour. Chance encounters with various tastes of palatable foods are required before goal-directed behaviour can result from the interaction of the internal needs with the salience of environmental stimuli. For example an infant recognises and learn to seek out sweet tastants, but the desire for a particular food is controlled by the interaction of peptide levels (related to hunger) with the brain circuitry, coding the animal’s reinforcement history for that specific food. Subsequently, the infant will indiscriminately taste both food and non-food objects, until it has received reinforcing feedback from sufficient stimuli. In addition, the monkey’s appetite for a yellow banana requires the prior learning of the relation of the sight of the yellow skin of a banana, with the sweet taste of the white banana meat plus the consequences resulting from the ingestion of the fruit. Therefore, preference for a specific food, results only when the post-ingestional consequences of that food’ reinforce’ the tendency to eat that food. Thus, food is considered to be a strong reinforcer. Moreover, when the response of a behaviour stimulated by a reinforcer increases the rate of that specific behaviour; that is known as positive reinforcement or reward learning, and the positive events are called rewards. The reinforcing efficacy of food reward is the ability of the reward to maintain rather than to establish behaviour; consequently the stimulus learning contributes to the response learning. Dopamine is known to play an important role in both. However, evidence from various studies seem to conclude that dopamine’s contribution appears to be chiefly to cause ‘wanting’ (Dopamine signalling in the dorsal striatum/CPu) for hedonic rewards rather than ‘liking’ or learning (mesolimbic dopamine) for those rewards. The first evidence for the implication of dopamine in food reward came from studies in rats, where dopamine antagonists blocked the rewarding effects of brain stimulation (Liebman & Butcher 1974; Fouriezos & Wise 1976) and of psychomotor stimulants.

Title of Subpart 1

In here you could write about various informations linked to various references for example from journals. [2] [3]


Title of Subpart 2

You can also insert diagram.

Title of Part 2

You can also cite published work accessible online. [4]

Title of Part 3

You can also cite published work from books. [5]


References

  1. See the "Writing an Encyclopedia Article" handout for more details.
  2. First Author and Second Author, "The perfect reference for Subpart 1," Fake Journal of Neuroendocrinology 36:2 (2015) pp. 36-52.
  3. First Author and Second Author, "Another perfect reference for Subpart 1," Fake Journal of Neuroendocrinology 25:2 (2009) pp. 62-99.
  4. "Part 2," Appetite and obesity. 2006. Retrieved July 21, 2009 from http://www.appetiteandobesity.org/part2.html
  5. Authors names, "The perfect review for part 3," Publishers City (2009)