Discuss the possible role of dopamine in incentive salience? How might this lead to some of the symptoms of schizophrenia?

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Discuss the possible role of dopamine in incentive salience? How might this lead to some of the symptoms of schizophrenia?

In my essay, I will be focusing how dopamine release in the ventral stria mediates incentive salience which makes the brain direct attention to biological significant stimuli and how incentive salience is disrupted in psychiatric disorders such as schizophrenia which is responsible for some of the symptoms.

Schizophrenia is one of the most severe mental illnesses that affect individuals in their late teens and early twenties.Hallucinations, most commonly auditory ones, delusions and disorders of the form of thinking (“thought disorder”) are implicated in schizophrenia and are so called “positive” symptoms. Patients also suffer from negative symptoms such as apathy, social withdrawal and poverty of speech. The illness commonly follows a characteristic remitting relapsing course of positive symptoms.

The neurochemical basis of schizophrenia is supported by a number of models and these are useful as they provide a testable framework for studying the illness and potentially assist in the development of new treatments. The main leading model of schizophrenia is the dopamine hypothesis and is based on several lines of evidence. The main evidence is that antipsychotic drugs which are key drugs used to treat schizophrenia are antagonists at dopamine D2 receptors. The potency of these drugs has a direct correlation with their affinity for D2 dopamine receptors. Furthermore, there is evidence that rats given amphetamine enhances dopamine release and the rats demonstrate stereotyped recurrent movements which are commonly observed in catatonic schizophrenia. More recently, dopamine overactivity in the ventral striatum such as nucleus accumbens are associated in “incentive salience”. This assigns particular experiences with personal importance and this influences reward-seeking behaviour. This hypothesis in schizophrenia was developed by Shitj Kapur and he proposed that schizophrenia could be an illness of assigning inappropriate personal relevance to external as well as internal events.

When stimuli associated with drug-taking behaviour begin reinforcing themselves, incentive salience happens. Therefore if a person is not addicted to the drug and is again presented with a stimulus that is linked with a drug in the past, the craving for that drug initiates.

The incentive salience theory was based on that addiction was driven by ‘wanting’ and not by ‘liking’. If a given stimulus/event was of relevance (‘salient’), dopamine release in the ventral striatum would signal. Usually this system would be stimulated when there is a relevant appetitive or threat stimulus, so that in future the animal learns to find or avoid these same experiences (Stone et al, 2007).

The co-stimulation of other neural systems suggests the affective meaning of salience (pleasurable/fearful).Taking drugs of abuse would be described as being salient and these drugs stimulate dopamine release in ventral striatum. The stimulation of neural pathways responsible for the experience of pleasure is not relevant to drive drug dependence.

In schizophrenia the presence of abnormal salience (and personal significance) to normal internal and external events results in increased dopamine release by striatal dopaminergic neurons which causes hallucinations and delusions. Therefore in a patient suffering with schizophrenia, each and every stimulus would have its own personal significance and meaning.

Dopamine neurons such as midbrain dopamine neurons of the ventral tegmental area and substantia nigra pars compacta send projections to striatum and prefrontal cortex. These neurons are vital in the processing of rewarding stimuli which give positive reinforcing effects and induce positive hedonic reactions.

Figure 1: This figure shows the reward pathways in the brain. The nucleus accumbens have both ‘wanting’ and ‘liking’ functions. Amphetamine microinjection or 6-OHDA lesions in the accumbens alter ‘wanting’ without modulating ‘liking’.

(Cited from http://www.nida.nih.gov/pubs/teaching/Teaching3/Teaching2.html)

Dopamine encodes reward incentive salience and that it signals a reward prediction-error rule.

In response to unexpected rewarding stimuli, dopaminergic neurons demonstrate rapid and brief bursts of activity in nucleus accumbens.No activity is seen in dopaminergic neurons when an expected reward is presented (Ungless et al, 2004).

Dopaminergic neurons are only suppressed when expected reward is failed to be presented .This shows that neurons encode a reward prediction error signal. This is relevant because the reward omission event is a motivationally important non-rewarding salient event. This also shows that dopamine neurons are not all stimulated by salient stimuli but only rewarding stimuli. Tobler, Dickinson and Schultz have demonstrated this by suggesting that when a light comes on reward is initiated and when a light is with the association of tone, no reward is presented. In this example the tone predicts the reward omission (this is a stimulus which is known as a conditioned inhibitor) and hence this is non-rewarding, although it can motivate attention. A conditioned inhibitor stimulus suppresses firing of dopaminergic neurons. Therefore  the unexpected reward omission or stimulus presentation which leads to a reward omission can cause suppression of dopaminergic firing. These so called events are salient because they are of motivational relevance but not rewarding. Studies show that stimuli which induce behavioural and attentional switching suggest that dopamine neurons are stimulated(Redgrave et al,1999).The experiments demonstrate that reward omission does not induce behavioural change but a perseverance of responding. However these experiments support the idea that reward omission suppresses dopaminergic firing. But others have argued that salient stimuli can also stimulate dopaminergic neurons and these stimuli are of motivational relevance. Stimuli of the aversive kind enhance firing in a few of the putative dopaminergic neurons. Physically salient sensory stimuli for example tones and lights induce rapid phasic excitations in dopaminergic neurons and hence induce dopamine release. These dopaminergic activations could represent generalizations to stimuli that are linked to reward. As the phasic dopamine response is so quick there is insufficient detailed processing of the stimuli and this could possibly result in errors of stimulus generalization (Schultz et al, 1998).

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After many presentations of salient stimuli such as lights and tones, phasic stimulations are sustained and the stimuli is no longer needed.

Dopamine is responsible for inducing pleasure associated with reward, the impulse to seek rewards, the ability or reward-related cues to initiate and sustain interest, the anticipation of reward, the ability to distinguish whether the reward was better or worse than expected, the selection of attention to and behaviours which are directed toward the reward and the ability to learn of associations between rewards and their predictive cues (Leyton et al, 2007).

It is well known that mesotelencephalic ...

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