Addiction and the reward circuit essay

Understanding Addiction How Addiction Hijacks the Brain Addiction involves craving for something intensely, loss of control over its use, and continuing involvement with it despite adverse consequences. Addiction changes the brain, first by subverting the way it registers pleasure and then by corrupting other normal drives such as learning and motivation.

Addiction and the reward circuit essay

The brain structures that compose the reward system are located primarily within the cortico-basal ganglia-thalamo-cortical loop ; [11] the basal ganglia portion of the loop drives activity within the reward system. The reward system includes the ventral tegmental areaventral striatum i.

These LHb projections are activated both by aversive stimuli and by the absence of an expected reward, and excitation of the LHb can induce aversion. The inhibition or hyperpolarization hypothesis proposes that the nucleus accumbens exerts tonic inhibitory effects on downstream structures such as the ventral pallidum, hypothalamus or ventral tegmental area, and that in inhibiting MSNs in the nucleus accumbens NAccthese structures are excited, "releasing" reward related behavior.

While GABA receptor agonists are capable of eliciting both "liking" and "wanting" reactions in the nucleus accumbens, glutaminergic inputs from the basolateral amygdalaventral hippocampus, and medial prefrontal cortex can drive incentive salience. Furthermore, while most studies find that NAcc neurons reduce firing in response to reward, a number of studies find the opposite response.

This had lead to the proposal of the disinhibition or depolarization hypothesis, that proposes that excitation or NAcc neurons, or at least certain subsets, drives reward related behavior. Regions include the lateral hypothalamus and medial forebrain bundles, which are especially effective.

Stimulation there activates fibers that form the ascending pathways; the ascending pathways include the mesolimbic dopamine pathwaywhich projects from the ventral tegmental area to the nucleus accumbens.

There are several explanations as to why the mesolimbic dopamine pathway is central to circuits mediating reward. First, there is a marked increase in dopamine release from the mesolimbic pathway when animals engage in intracranial self-stimulation. Pleasure centers [ edit ] Pleasure is a component of reward, but not all rewards are pleasurable e.

The posterior ventral pallidum also contains a hedonic hotspot, while the anterior ventral pallidum contains a hedonic coldspot. Microinjections of opioidsendocannabinoidsand orexin are capable of enhancing liking in these hotspots. Furthermore, inhibition of one hotspot results in the blunting of the effects of activating another hotspot.

Incentive salience Tuning of appetitive and defensive reactions in the nucleus accumbens shell. Above AMPA blockade requires D1 function in order to produce motivated behaviors, regardless of valence, and D2 function to produce defensive behaviors. GABA agonism, on the other hand, does not requires dopamine receptor function.

Addiction and the Reward Circuit

Below The expansion of the anatomical regions that produce defensive behaviors under stress, and appetitive behaviors in the home environment produced by AMPA antagonism. This flexibility is less evident with GABA agonism.

Addiction and the reward circuit essay

In the NAcc, such a dichotomy is not as clear cut, and activation of both D1 and D2 MSNs is sufficient to enhance motivation, [37] [38] likely via disinhibiting the VTA through inhibiting the ventral pallidum. To explain increasing contact with a certain stimulus such as chocolate, there are two independent factors at work — our desire to have the chocolate wanting and the pleasure effect of the chocolate liking.

According to Robinson and Berridge, wanting and liking are two aspects of the same process, so rewards are usually wanted and liked to the same degree.

However, wanting and liking also change independently under certain circumstances. For example, rats that do not eat after receiving dopamine experiencing a loss of desire for food act as though they still like food.

In another example, activated self-stimulation electrodes in the lateral hypothalamus of rats increase appetite, but also cause more adverse reactions to tastes such as sugar and salt; apparently, the stimulation increases wanting but not liking.

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Such results demonstrate that our reward system includes independent processes of wanting and liking. The wanting component is thought to be controlled by dopaminergic pathwayswhereas the liking component is thought to be controlled by opiate-benzodiazepine systems.

The same animals do not work to obtain the opiates if the dopaminergic neurons of the mesolimbic pathway are inactivated. In this perspective, animals, like humans, engage in behaviors that increase dopamine release.

Kent Berridgea researcher in affective neurosciencefound that sweet liked and bitter disliked tastes produced distinct orofacial expressionsand these expressions were similarly displayed by human newborns, orangutans, and rats. This was evidence that pleasure specifically, liking has objective features and was essentially the same across various animal species.

Most neuroscience studies have shown that the more dopamine released by the reward, the more effective the reward is.

This is called the hedonic impact, which can be changed by the effort for the reward and the reward itself. Berridge discovered that blocking dopamine systems did not seem to change the positive reaction to something sweet as measured by facial expression.

In other words, the hedonic impact did not change based on the amount of sugar. This discounted the conventional assumption that dopamine mediates pleasure. Even with more-intense dopamine alterations, the data seemed to remain constant.

It explains the compulsive use of drugs by drug addicts even when the drug no longer produces euphoria, and the cravings experienced even after the individual has finished going through withdrawal. Some addicts respond to certain stimuli involving neural changes caused by drugs.Drug Addiction, Disease or Choice Essay; Drug Addiction, Disease or Choice Essay.

Words May 5th, 9 Pages. Tia Little the overwhelming surges in dopamine by producing less dopamine or by reducing the number of dopamine receptors in the reward circuit. The result is a lessening of dopamine’s impact on the reward circuit, which.

To clarify, this occurs only when an individual is addicted to exercise. Both addictions to exercise and addictions to drugs access the brain’s limbic system, which contains an essential “reward circuit”.

This reward circuit is what teaches us to associate functions essential to life, such as eating, with a pleasurable feeling. The VTA and nucleus accumbens are involved in the reward circuit of all drugs. The natural function of the reward circuit is to provide a reward and associated pleasurable feelings in response to life sustaining functions, such as eating, to encourage repetition of that function.

- Addiction and the Reward Circuit Most people are affected directly or indirectly by drug addiction. Many stereotypes including race and socio-economic class are associated with drug addiction. Despite longstanding stereotypes there is more and more evidence being discovered pointing to an explanation from within the brain of the addict.

Thus, “addiction” can be partially explained by the action of drugs of abuse on this common reward pathway, in which drug use stimulates further use and drug seeking behavior (1,2,3,4).

In the following paragraphs, the basic anatomy of the reward pathway and brain structures that interact with this pathway will be discussed. 1: The reward pathway and addiction Introduce the concept of reward.

Humans, as well as other organisms engage in behaviors that are rewarding; the pleasurable feelings provide positive reinforcement so that the behavior is repeated.

Understanding Addiction: How Addiction Hijacks the Brain