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Motivation and Reward describes the processes of the body that place an emphasis on certain needs, rewards are conidered to be an aspect that encourages specific behaviours that are necessary to obtain these needs[1]. Motivation is the process by which individuals adapt to change whether it be internal or external. The body is constantly attempting to achieve homeostasis, so when there is a change in the body or the environment, a negative feedback loop is created to return the body to a state of homeostasis. This may include the integration of the endocrine, behavioural, and autonomic responses[1]. Some forms of motivation are reflexively performed and have been adapted to ensure survival of the human specifies. This includes basic human needs such as eating, drinking and even sexual reproduction to ensure that one's genes are passed on. If an individual was to run out of food, he or she would instinctively be motivated to look for food in order to survive. This is an example of adaptive or reflexive motivation. A reward is a positive emotional component of positive reinforcement. It encourages a specific action or behaviour by producing a favourable outcome, so that in the future when faced with the same situation, a positive outcome can be expected to reoccur[1]. If there is an absence of present goals or motivational factors the individual must use past experience to predict the likelihood of a specific outcome.

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Figure 1: The human brain. Crucial parts involved in motivation and reward include the hypothalamus, nucleus accumbens and striatum.

Components of Reward

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Reward can be divided into three specific psychological components: (1) learning, (2) motivation and (3) affect.[2]

Learning

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Learning is a necessary component of reward. You need knowledge to be able to make predictions about reward, for anticipating how you will respond in a situation, for behaving based on external cues, and to perform internally driven actions.[2] Learning processes can be either associative or cognitive.[2]

Associative learning is a more implicit process and can occur through either Pavlovian conditioning or instrumental conditioning.[2] Animals learn to predict and respond to salient events in their environments through these two forms of conditioning.[3] Pavlovian conditioning involves conditioned responses (CRs) to a stimulus. The CRs are reflex actions that are performed based on the predictions made about the outcome.[3] For example, if the prediction is that a light signals the delivery of a reward, the conditioned response would be to move towards the light to receive the reward.[3] Instrumental conditioning involves the consequences of one's actions in obtaining a reward.[3] For example, a hungry rat can be trained to press an accessible lever to receive food.[3] The performance of an action changes as the relationship between the action and its outcome changes.[3] Subcortical (e.g. basolateral amygdala, nucleus accumbens) and cortical (e.g. prelimbic, orbitofrontal and anterior cingulate cortex) brain structures are implicated in Pavlovian and instrumental conditioning. [4]

Cognitive learning involves encoding several connections between stimuli and actions.[2] It is a more explicit process that influences goal-directed actions.[2] The neural substrates of cognitive learning are more cortical, involving such areas as the orbitofrontal and insular cortex.[2]

Motivation

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The motivational aspect of reward involves cognitive desires (wanting) as well as implicit desires ("wanting" or incentive salience).[2] Incentive salience is a distinct module of desire, different from the module of ordinary wanting.[5] Ordinary wanting is guided by explicit thoughts and memories of past experiences with a target, whereas incentive salience is a percept-bound type of "wanting" that does not need to be consciously experienced.[5] This difference may be due to the different brain mechanisms involved. Incentive salience involves mainly subcortical brain mechanisms, whereas cognitive desires involve higher cortex-based brain systems.[5]

Incentive salience converts sensory information about rewards and their cues into attractive and desired incentives.[2] Incentive salience is characterized by peaks of cue-triggered "wanting".[5] Cue-triggered wanting can be amplified in experiments by stimulating the brain's mesolimbic dopamine pathway.[5] Microinjection of an amphetamine drug into the nucleus accumbens, which causes the release of dopamine, selectively increased the peaks of "wanting" for a reward upon the presentation of a cue.[6] This procedure did not have an effect on cognitive desires.[5] Although amphetamine microinjection caused a continuous release of dopamine, the "wanting" only increased with the onset of the cue.[5] Therefore, incentive salience requires both internal mesolimbic activation and particular events in the external world.[5]

Incentive salience is generated mainly by the mesocorticolimibic dopamine system.[5] The main neurotransmitter involved is dopamine, although opioids,glutamate and GABA are also involved.[5] Increasing brain mesolimbic dopamine signals selectively increases "wanting" without increasing "liking" or cognitive desires.[5]

Affect

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The affective or emotional component of reward can be either conscious pleasure (liking) or an implicit reaction ("liking").[2] "Liking" appears to be distinct from "wanting" because many manipulations that cause "wanting" do not affect "liking".[5] Only opioid stimulation and not dopamine stimulation enhances "liking".[5] This disputes the common conception that dopamine is a pleasure neurotransmitter. "Liking" is enhanced only by hedonic hotspots but not necessarily by activation of the whole limbic structure it is a part of.[5] It also requires activation of all the hedonic hotspots in a circuit simultaneously.[5] Opioid stimulation in either the nucleus accumbens or the ventral pallidum hedonic hotspots elicited participation by the other hotspot.[7] Also, blocking the activity of one hotspot prevented enhancement in the other.[7] This evidence indicates that these two hedonic hotspots in the nucleus accumbens and ventral pallidum cooperate in a single opioid circuit to enhance the "liking" response.[7]

The Neural Structures and Mechanisms Involved

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There is evidence that the midbrain and the areas it projects to are involved in coding reward information. In a study of neural coding of reward information in humans, subjects without any neurological, psychiatric or substance abuse problems, and no gambling or medical problems were involved in a slot machine experiment.[8]. There were three phases of the trial where subjects were given a pie chart that indicated the probability of winning the said amount of money and the probability of not receiving any money. According to fMRI results, the midbrain responded briefly at the time of the cue to higher reward probability, and during the rewarded outcome to lower reward probability.[8] Also at the time of the cue, a frontal network was briefly activated for higher reward probability, which involved the left dorsolateral prefrontal cortex, the right orbitofrontal cortex and anterior cingulate cortex, the left inferior frontal gyrus, and the medial part of the superior frontal gyrus.[8] In regards to lower reward probability, during the rewarded outcome there was also a frontal network involved. This network included the left inferior frontal gyrus, medial part of the superior frontal gyrus, and left dorsolateral prefrontal cortex.[8] It could be that the expectation of reward may be coded in terms of information theory by the midbrain. Information theory says that “the more uncertain the outcome (reward or no reward), the more information the outcome contains (and information is available in the outcome only in the presence of uncertainty).”[8]

Nigrostrial and Mesolimbic Dopamine Systems

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The midbrain dopamine neurons that project to the forebrain were originally identified as a single layer[9]. However, it was suggested by researchers that because the lateral and medial portions were restricted to certain brain regions they were given separate labels instead of being considered one system. Both sections of the brain then became identified with two distinct nominal systems, a nigrostriatal system and a mesolimbic system. Research was then found that the nigrostriatal system was associated with Parkinson`s disease, and was designated as a motor function area[9]. The mesolimbic system, which has been found to be important for the habit-forming effects of drug addiction, then became associated with reward functions and motivation[9].

The nigrostriatal dopamine neurons, which originate in the substantia nigra and then move into the dorsal striatum, play a role in the performance of motor activities[10]. The mesolimbic neurons, which originate in the ventral tegmental area and project largely to the nucleus accumben and other ventral striatal regions, play a role in reinforcement or incentive motivation. The nigrostriatal pathway is a neural pathway that is one of the four major dopamine pathways within the brain[10]. It is also a part of the basal ganglia motor loops, which is involved in the production of movement. Researchers have found that lesions to the nigrostriatal system causes motivational deficits in feeding and drinking, but lesions that are restricted to the mesolimbic dopamine system do not[10].

The mesolimbic dopamine circuit, which includes the nucleus accumben, amygdala, and hippocampus, has been associated with the reinforcing effects of drugs and also with the memory and conditioned responses that have been linked to craving[11].

Hypothalamus

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There has been a plethora of evidence linking the hypothalamus to the reward motivation system. This is due to the need to reach a continuous state of homeostasis within the brain and body at all times. The hypothalamus has been considered the biological trigger for adaptive behaviours such as eating, drinking and temperature control[10]. The hypothalamus links the autonomic nervous system to the endocrine system and serves the body with a variety vital functions. It is considered to be the `control centre` of the body, as it is constantly attempting to maintain an overall balanced environment. The hypothalamus can be categorized as having three main outputs: the endocrine system, the automatic nervous system, and motivated behavioral response[12].

The theory of the involvement of the hypothalamus in motivated behaviour was proposed in 1954 by Elliot Stellar. He suggested that the amount of motivated behaviour is a direct function of the amount of activity in certain excitatory centres of the hypothalamus[12].

The theory of the involvement of the hypothalamus in motivation and reward relies heavily on the mechanics of thermoregulation[12]. Thermoregulation is a feedback loop that is initiated by an internal stimulus which then requires an external response[12]. First, the process begins with an input[10]. For example, if the body is feeling warmer than the desired internal temperature than the hypothalamus will strive to achieve homeostasis and will initiate the sweat glands to secrete water as a way to cool the body down. This is considered to be motivating behaviour to achieve homeostasis.

Striatum

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Previous neuroimaging experiments were expanded on to show that the striatum is activated in reward processing. The striatum is especially involved when primary rewards, such as food, and drugs for addicts, are available for utilization.[13] Studies on giving cocaine addicts injections of the drug show that the dorsal striatum is associated with the “rush” after being given the injections, whereas the ventral striatum is associated with feelings of craving the drug. [14]

The caudate nucleus is involved in reward feedback during learning. Activation of the caudate is altered by the information given by the reward feedback, which then leads to better choices in order to obtain continued rewards. [13] The caudate nucleus is suggested to be a vital component in updating current rewards, as well as learning. [13] It is believed that its purpose is to guide actions that will get the most out of reward expenditure. [13]

In a study by Delgado, et al. (2005), participants were asked to guess if the value of a given card was higher or lower than 5, and their response could lead to a reward or a punishment. This was shown on a computer screen, and inside the card border, the cue and feedback were displayed.[15] The participant would see a cue (a card) and then would be asked to press one button for higher than 5 or press a different button for lower than 5. The outcome was then displayed: whether they were right or wrong, and whether they got a reward or a punishment. The caudate nucleus was active during the delay between cue and action, and the delay between action and outcome.[15] There was more activity in the caudate nucleus in the early phases of learning (the first trials), which suggests it plays a fundamental role during the early learning of possible rewards.[15] However, the signal decreases as a potential reward becomes more predictable, so the caudate nucleus is not very involved in later phases of learning.[15]

Nucleus Accumbens

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The nucleus accumbens is a collection of neurons within the striatum. The nucleus accumbens is considered to play an important role in laughter, motivation, reward, pleasure, addiction, fear, and the placebo effect[16]. Each brain hemisphere has one nucleus accumbens. The nucleus accumbens is divided into two structures, the nucleus accumbens core and the nucleus accumbens shell[16]. Both are considered to have different functions and processes.

The nucleus accumbens was found in the 1950s and was considered to be part of the 'pleasure center'[17]. James Olds and Peter Milner placed electrodes into the septal area of a rat. The rat was then expected to press a level, which stimulated the septal area. It was found that the rat chose to press the lever continuously, even over eating and drinking[17]. The nucleus accumbens has been greatly studied in terms of addiction, because of this 'pleasure center' foundation. However, the nucleus accumbens also play a heavy role in reward and motivation. More recently, the nucleus accumbens has been researched in terms of the relationship in the placebo effect.

There is a widely held hypothesis of reward functions, including dopamine in the nucleus accumbens. This hypothesis originated from lesion studies done by psychology researchers. Dopamine-selective lesions of the nucleus accumbens attenuated the reward effects of certain psychoactive drugs, such as cocaine and amphetamines. However, noradrenergic and other lesions did not show the same results as aforementioned[11].

Ventral Striatum-Orbitofrontal Cortex Loop

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The ventral striatum is found to have a significant correlation with reward prediction. During reward anticipation the ventral striatum maintains its activation, which varies in the same time period with maximal reward uncertainty.[18] “This suggests that the ventral striatum reflects the expectations of reward information of the incentive value of reward while the network of prefrontal cortex regions may generate the reward prediction."[18] When looking at reward prediction in predictable and unpredictable environments, the orbitofrontal cortex was found to possibly predict an immediate reward after the behavioural response of the present state.[18] Through recent human studies it was found that there is a connection from the orbitofrontal cortex to the ventral striatum, suggesting that the orbitofrontal cortex sends predictions about immediate reward in present states to the ventral striatum, which then learns the optimal action to produce.[18] Previous evidence has found that the orbitofrontal cortex-ventral striatum loop is involved in short-term reward prediction.[19]

Dorsal Striatum-Dorsolateral Prefrontal Cortex Loop

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The dorsal striatum consists of the caudate nucleus and putamen. It is found to be significantly correlated with reward prediction and prediction error in predictable environments.[18] This study also found that the prefrontal area sends inputs to the dorsal putamen and caudate. Through this we find that the dorsoloateral prefrontal cortex sends predicted information about future states to the dorsal striatum which in turn calculates future reward prediction.[18] In a predictable environment this is how we learn the optimal action to produce. Previous findings have shown that the dorsal striatum is involved in reward prediction in the long-term.[19]

Basal Ganglia

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Patients with focal basal ganglia lesions were given different reward-based learning tasks to see if they were impaired in reward-based reversal learning.[20] Basal ganglia patients showed deficits comparative to control subjects in the attainment of stimulus-stimulus associations based on reward and non-reward.[20] In the reward-based learning task that involved the acquired equivalence of stimuli, basal ganglia lesion patients needed 17 more trials to attain the criterion than control subjects, showing they did not have a substantial carry-over effect.[20] This could be attributed to an unspecific deficit in reward-based learning, which is related to the ventral striatum and dorsal striatum and occurs only in later learning stages.[20]

Reward and Motivation in Psychiatric Disorders

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Major Depressive Disorder

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Anhedonia is a lack of interest or pleasure in normally rewarding experiences which is a defining characteristic of major depressive disorder (MDD).[21] There is evidence that MDD subjects show significantly reduced reward responsiveness compared to controls.[22] People with MDD are unable to modulate their behaviour as a function of reward as well as controls.[22] Differences in neural activation that correlate with differences in reward responsiveness have also been found between people with and without MDD. Research has shown that depressed patients have significantly less bilateral ventral striatal activation in response to positive stimuli compared to controls, which correlated with decreased interest in and performance of activities.[23] fMRI data has indicated hyporesponsivity in mesolimbic pathway during reward selection, anticipation and feedback in participants with MDD compared to controls.[21]

Attention-Deficit Hyperactivity Disorder

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Abnormalities in reward processing have been found to underlie Attention-Deficit Hyperactivity Disorder (ADHD). fMRI research has demonstrated that compared to healthy adolescent controls, adolescents with ADHD had reduced ventral striatal activation during reward anticipation.[24] Further research found that reduced ventral striatal activation occurred for both immediate and delayed rewards. [25] Delayed rewards also evoked hyperactivation in dorsal caudate nucleus and amygdala of ADHD patients.[25] An impairment of the mesoaccumbens dopamine reward pathway has also been found in ADHD.[26] Positron emission tomography studies have demonstrated that there were fewer dopamine receptors and transporters in the nucleus accumbens and midbrain in participants with ADHD compared to controls.[26]

Schizophrenia

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Abnormal reward system functioning has also been found in schizophrenia. Patients with schizophrenia have increased activity in the medial prefrontal cortex when an expected reward is omitted. [27] This hyperresponsiveness of this part of the reward system may be the cause of delusions in schizophrenics because it causes them to attribute salience to otherwise neutral stimuli.[27] Furthermore, reduced ventral striatal activation in unmedicated schizophrenics has been found when they are presented with reward-indicating cues.[28] This decreased activation in the ventral striatum was correlated with the severity of negative symptoms, such as reduced motivation and anhedonia.[28]

Bipolar Disorder

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It was found that individuals with bipolar disorder do not have the normal pattern of brain activation upon expectation of monetary rewards.[29] The normal pattern consists of activation of dopaminergic brain areas including the ventral tegmentum and nucleus accumbens when expecting high rewards compared to anticipation of no rewards.[29] Bipolar disorder participants do not experience the same activation as controls in the nucleus accumbens when differences occur in the receipt versus omission of reward.[29] In fact, they show significantly less activiation in this area. Bipolar disorder participants also fail to show accelerated response times in response to high rewards.[29] This shows that bipolar disorder individuals cannot tell the difference between rewarding or relevant, compared to non-relevant stimuli.[29] Participants completed a reward task that included correctly reacting to one of two symbols by completing a left or right button press. If they reacted correctly, they had a 60% chance of winning a set amount of money, but 40% of the time, even if they correctly reacted, they would receive no money.[29] For bipolar disorder individuals, each stimuli brought out high fMRI signals in every trial, despite the reward to be expected, indicating that all stimuli have the same amount of significance to these individuals.[29]

Reward and Motivation Systems Involved in Drug Addiction

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Incentive Motivation

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One aspect of drug addiction that is not capable of being explained using the basic theory of motivation and rewards is the aspect of drug binges or drug overdoses. It is necessary for the body to be in a constant state of homeostasis, so it is illogical that one might overindulge in something, because this would throw off the internal balance. Overindulgence occurs when homeostatic mechanisms are overridden by powerful external incentives[30]. This overriding of the homeostatic system is also present when an individual will overindulge in delicious food, even though they might not be hungry. Psychoactive drugs will repeatedly activate the motivational systems of the brain that are often activated by certain survival needs, such as hunger and thirst. These psychoactive substances will trick the brain into believing that the psychoactive drugs are biologically needed, so the same response is present as if one were to be without food for a couple of days. After repeated exposure to a specific drug, the association between the drug and the need or desire for the drug become stronger, which then invoke a larger behavioural and neurochemical response[31]. When drug substances and the stimuli that are associated with their use take on an increasing motivational and behaviour significance it is considered incentive sensitization[30]. After repeated use of the drug, the motivation to use a specific drug will become strongly activated by environmental stimuli, such as smells, people, and places[31]. This causes incentive motivation to override the bodily homeostasis system even when it is not motivated to do so. So eventually, the need for a specific psychoactive drug becomes so powerful, that the motivations associated with it are constantly being activated by both the need and desire for the drug as well as the environmental stimuli that have been associated with it. Overall, incentive motivation overrides our basic needs and goals for something that is more tempting and rewarding to us.

The Drug Addiction Cycle

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Drug addiction, which is also known as drug dependency, is a chronically and consistently relapsing disorder that is characterized by 1) compulsion to seek and administer a specific drug to the system, 2) a loss of control in being able to limit the intake of that particular drug, and 3) emergence of a negative emotional state, such as anxiety, depression, and/or dysphoria, when access to the drug is prevented or limited[30]. The drug addiction cycle involves three specific stages, 1) craving, 2) binging (loss of control) and 3) withdrawal[30]. It begins with craving, which is when your body is motivated to administer the drug, and one begins to crave the presence of the specific drug substance. Next comes binging, which is present after the specific drug has been administered to the individual, often in large doses. Incentive motivation will then begin to take over and override the state of homeostasis, and the individual will lose control and over-indulge in order to feel a sense of euphoria. The more a drug is taken by an individual, the larger the dose is needed in order to achieve this sense of elation[31]. After the second stage has been completed, the body goes into a sense of withdrawal. This is where the body attempts to achieve a sense of homeostasis again. The cycle then restarts and after a period of time the individual will begin to crave the drug once again. Most drug abuse studies have focused on the involvement of dopamine because of the ability of drugs to increase brain dopamine concentration in the limbic brain regions. The dopamine concentration is considered crucial for the drugs reinforcing effects. However, the interesting aspect of this theory is that the increase in dopamine in the brain is not sufficient enough to account for the process of drug addiction. Researchers have found that abusive drugs increase dopamine in both control and drug addicted subjects.

File:Psychoactive drugs.jpg
Figure 2: a variety of psychoactive drugs including cocaine, ecstasy and marijuana.

Neural Mechanisms Involved

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The Impaired Response Inhibition and Salience Attribution Model(I-RISA)

The I-RISA model consists of four different clusters of behaviours that are all interconnected in a positive feedback loop, and they all depend on the functioning on the prefrontal circuits via the subcortical reward pathway[31]. The four different clusters of the I-RISA model are those mentioned above in the drug addiction cycle: drug intoxication, drug craving, drug administration, and drug withdrawal[32].

Drug Intoxication

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The overall process of administering drugs has traditionally been associated with exceptionally high extracellular dopamine concentrations in the limbic system. Specifically, there have been noted higher extracellular dopamine concentrations in the nucleus accumbens[32]. However, researchers have also found evidence that there is increased dopamine concentrations in the frontal regions.

Functional Magnetic Resonance Imaging (fMRI) is used to measure the blood-oxygenation level dependent response (BOLD). Studies have shown activation of the prefrontal cortex and anterior cingulate gyrus during drug intoxication. This effect has been strongly correlated with drug reinforcement properties[32].

Drug Craving

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The process of drug craving is often associated with the learned response that links a specific drug and its environment to a pleasurable experience[30]. This is known as the process of motivation. When an individual is around a drug, or around an environment that is linked to the drug, the individual is motivated to begin craving and then administer the drug. This also includes the process of rewards, in that once the drug is administered, there is an intense and overpowering sense of euphoria[31]. The neuroanatomical subtrates for the consolidation of these memories are likely to be involved with the amygdala and the hippocampus[32]. However, the actual experiences of craving are thought to be activated in the thalamo-orbitofrontal circuit, as well as the anterior cingulate gyrus[30].

Drug Administration

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Drug administration in those individuals that are considered to be addicted to a specific drug is often compulsive[31]. Compulsive drug administration occurs when the drug experience is considered to be no longer pleasurable, but the body still functions like it needs to experience the drug. This process of loss of control and binging is associated with three different circuits, 1) dopaminergic, 2) serotonergic, and 3) glutamatergic[32]. However, just like the process of drug craving, drug administration also involves the activation of the thalamo-orbitofrontal circuit and the anterior cingulate gyrus[31].

Drug Withdrawal

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The re-occurance of drug administration followed by drug withdrawals often results in the disruption of specific behavioural circuits that culminate in dysphoria, anhedonia, anxiety and irritability[30]. This then often contributes to a relapse, in that the individual cannot live without the experience of the drug. These changes in the body are likely to involve the disruption of the frontal cortical circuits and certain neurotransmitters; including, dopamine, serotonin, and corticotropin-releasing factor[32].

Future Research

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The theory of motivation and rewards fails to explain some necessary behaviours such as mating, aggression, and exploration[33]. For each one of these examples there are obvious external triggering stimuli but no there are no identifiable deficit states. Further research on this topic is necessary in order to be able to further explain why some actions require motivation, while others do not. There is also a plethora of evidence regarding negative reinforcement in terms of aggression, yet it still exists in today's society. Research is required in order to be able to identify exactly what characteristics are adaptive, and which emotions and needs are directly shaped by society and media reinforcement.

Also, as aforementioned, the theory of motivation and rewards fails to identify why some actions are able to be overindulged, past the point of homeostasis[33]. Every individual is able to eat an extra piece of dessert even when they are full, yet there is no motivation and no positive reward. Instead, these behaviours are often explained by attractions to external stimuli that have appetizing or rewarding properties. Further research is required in order to fully explain these behaviours. Also, if these experiences are explained further, then it would be able to help those who are recovering from drug addictions because it would be able to explain why they overindulge in drugs and this then would be able to help them recover.

In terms of drug addiction, future research should target the interaction between impaired salience attribution and response inhibition. These could have possible causal or predisposing effects toward the development of a drug addiction[31]. In the I-RISA model, it is proposed that drug-addicted individuals attribute excessive salience to the drug and the drug-related cues[32]. However, insufficient salience is attributed to non-drug-related reinforcers[30]. This includes stimuli such as food or social relationships that happen to increase the probability of a subsequent behaviour.

Finally, personality traits should be taken into consideration for drug addicted individuals. For example, certain characteristics such as a tendency to avoid harm vs. approach risk can be examined to determine the probability of developing a drug addiction[30]. Certain genetic vulnerabilities may be able to lead researchers to determine whether there is a risk associated with a modified genotype[31]. With a better understanding of the interactions between genes, the environment and neural mechanisms, researchers will be able to determine more successful drug rehabilitation interventions that target specific cognitive functions. Also, by determining specific genes associated with the risk of drug-addiction, more prevention programs can be designed in order to stop drug addictions before it begins. Individuals with the determined genetic vulnerabilities will be able to receive help prior to exposure to drugs, in order to ensure that they are not at risk of developing a drug dependency.

References

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