The impulse to minimize pain while maximizing rewards is an essential part of the human brain. Humans are driven to seek actions that may have the appearance of rewards with limited negative results to fulfil this drive. The data from feedback signals from our brain is used to determine our choices. This feedback network of the brain based on rewards and negative outcomes is known as the reward pathway. The regions of the brain that constitute the reward network include the limbic system. The limbic system is responsible for memory and learning. It also plays a significant role in the generation, control and behavioral responses of emotions. The expression of behavioral responses such as fight or flight is influenced by the prefrontal cortical and amygdala regions of the limbic system. Also, the limbic system is connected to the nervous system through the hypothalamus. The hypothalamic-pituitary-adrenal axis (HPAA), the main stress response system, is responsible for neuroendocrine adaptation.
Other regions of the brain, the accumbens nucleus, caudate, thalamus bilateral anterior cortex and orbitofrontal cortex, also influence reward, emotions, fear and pleasure (Liu et al., 2011). The core subregion of the accumbens nucleus involves learning and memory processes by getting signals from the amygdala and hippocampus. The shell subregion of the accumbens nucleus links motivation to rewards and their predictive stimuli (Liu et al., 2011). This function is critical in the initial learning stages of reward-seeking behavior, but once it becomes ingrained, the caudate and putamen brain structures support the learned habits. Dopamine from the neurons in the ventral tegmental area significantly influences binding rewards to adaptive responses. It has been determined that rewards cause dopamine release in the accumbens nucleus. When this action is prevented by blocking dopamine receptors, rewards fail to motivate habits and behaviors associated with them.
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Reward network also involves other neuropsychological aspects such as sensation from pleasure, incentive or motivation component and learning aspect of rewards. It has been noted that distinct rewarding stimuli differ in magnitude and nature, influencing the reward network's neuropsychological components. Other neurotransmitters key in the reward pathway besides dopamine is a serotonin and aminobutyric acid (GABA) Glutamate. Serotonin is involved in regulating dopamine levels and is used to determine the level of motivation an individual has to seek a reward (Breedlove & Watson, 2020). On the other hand, GABA is an important neurotransmitter in inhibiting dopaminergic neurons, especially in the reward mechanism involving addictive drugs and substances. Most drugs of abuse work by hyperpolarizing neurons, thus disinhibiting the firing of dopamine neurons in the reward pathway.
From an evolutionary perspective, the two most important regions of the reward pathway, the accumbens nucleus and ventral tegmental area, are vital in detecting reward stimuli (Breedlove & Watson, 2020). Social interactions, sexual intercourse and food are natural rewards that determine an individual's response. The reward pathway informs the individual to repeat an action that led to the reward. It also stores the experience of the reward in memory for predicting future behaviors. The reward pathway's main purpose is to drive behaviors that ensure an individual's survival and species.
Beyond the reward pathway's evolutionary survival purpose in motivating the drive for a natural reward, the reward pathway also influences drugs and substance addiction. Different addictive drugs and substances affect the neurochemical and neuropsychological response in different brain regions (Schultz, 2000). However, a common response to drugs and substances is the increase in dopamine release. As the substance of choice in this article, alcohol stimulates neurons in the ventral tegmental area (VTA) and some response in the accumbens nucleus. Dopamine and other neurotransmitters such as serotonin mainly influence alcohol dependency. Dopamine influences the positive reinforcement of alcohol by activating the dopaminergic reward network. Research has demonstrated a dose-response link between alcohol and the release of dopamine in the VTA. Alcohol effect on the GABA neurons and receptors in the accumbent nucleus is directly responsible for the ethanol-induced release of dopamine.
Serotonin deficiency has also been shown to affect alcohol consumption and its impulsivity but not as much as the dopamine effect. Therefore, alcohol dependence is characterized by an unexpected change in the reward pathway, mainly fewer dopamine receptors. Further research also highlights that different subregions of VTA respond with varying abilities in modulating ethanol-induced dopamine release. Acute alcohol consumption increases ventral striatum dopamine release in humans as well as rodents. While hypothetically, chronic alcohol exposure develops dopamine deficiency creating a cycle of craving and relapse in consumption.
Recent studies have also illustrated that chronic alcohol exposure also leads to decreased dopamine levels in prefrontal cortical and not only the brain's ventral striatum regions. This factor implies that long-term alcohol consumption significantly alters key neuropsychological functions such as decision-making and working memory. This implication has been attributed to play a role in relapsing individuals dependent on alcohol since reduced executive functions may hinder the ability to practice treatment approaches (Volkow & Boyle, 2018). In general, it is demonstrated that dopamine is vital in rewarding and motivating alcohol dependency. Approaches to using pharmacotherapies as treatment options for alcohol dependency consider this factor. Other factors such as dopamine D4 have been associated with novelty pursuit personality, a common habit among individuals with alcohol dependency.
All these factors make the dopamine system a potential treatment target for alcohol dependency. The effectiveness of treatment interventions and their consistency in practice should guide the treatment option's utilization (Glasner-Edwards & Rawson, 2010) . Preclinical and clinical studies on dopamine D2 antagonists are central in treating alcohol dependency and psychiatric disorders largely due to their action in counteracting increased dopamine activity. The dopamine receptor antagonist also affects other receptors such as alpha1 and dopamine D1 receptors. These factors were considered in formulating the hypothesis that dopamine D2 receptors antagonists could effectively block the rewarding effect of alcohol in the brain, making them a potential treatment target for alcohol dependency. Studies on rodents have supported the hypothesis on the attenuation effect of dopamine D2 on alcohol mediated habits. In a clinical study on 16 participants with alcohol dependency, Dopamine D2 receptor antagonists have been determined to be effective in decreasing novelty seeking, impulses and craving for alcohol. However, D2 antagonist flupenthixol has also been seen to increase relapse rates in individuals. These traditional dopamine D2 antagonists have also produced severe side effects such as sedation and neuroleptic malignant symptoms in patients.
The second generation of dopamine D2 receptor antagonists have better-promising results since they target a larger scope of dopamine receptors and other neurotransmitters receptor systems. They also present fewer and less severe side effects as compared to their traditional predecessors. The new generation D2 receptor antagonists have also proven effective in acute alcohol detoxification to stop hallucination and agitation (Singh & Goel, 2016). D2 receptor antagonist tiapride has been used in a clinical study that demonstrated an extended period of abstinence and low alcohol consumption. A similar D2 receptor antagonist drug, quetiapine, has also shown low consumption levels and decreased cravings in alcohol-dependent individuals. Atypical dopamine D2 receptor antagonists are a much better approach to treating both alcohol dependency and psychiatric disorders.
This article illustrates the brain's reward pathways and their effect in influencing natural rewards and substance abuse. The dopamine activity between the ventral tegmental area and the accumbens nucleus circuit is significant in the reward pathway. Alcohol reinforcement is mainly induced by increased dopamine release, but other neurotransmitters in the mesolimbic pathway contribute to alcohol effects. The evidence of dopamine effects on alcohol has led to the development of treatment approaches that target dopamine. Traditional dopamine D2 receptor antagonist has been evaluated and demonstrated to reduce craving and consumption of alcohol. However, they have had numerous and severe side effects causing their limited use. Second generation dopamine agents have had some success in the treatment of alcohol dependency with little side effects. More investigation on this could be a breakthrough in the treatment of alcohol abuse and dependency.
References
Breedlove, S. M., & Watson, N. V. (2020). Chapter 4, "The Chemistry of Behavior". In Behavioral neuroscience (9th ed.). essay, Sinauer Associates.
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Liu, X., Hairston, J., Schrier, M., & Fan, J. (2011). Common and distinct networks underlying reward valence and processing stages: A meta-analysis of functional neuroimaging studies. Neuroscience & Biobehavioral Reviews , 35 (5), 1219–1236. https://doi.org/10.1016/j.neubiorev.2010.12.012
Schultz, W. (2000). Multiple reward signals in the brain. Nature Reviews Neuroscience , 1 (3), 199–207. https://doi.org/10.1038/35044563
Singh, T., & Goel, R. K. (2016). Evidence in support of using a neurochemistry approach to identify therapy for both epilepsy and associated depression. Epilepsy & Behavior , 61 , 248–257. https://doi.org/10.1016/j.yebeh.2016.05.005
Volkow, N. D., & Boyle, M. (2018). Neuroscience of Addiction: Relevance to Prevention and Treatment. American Journal of Psychiatry , 175 (8), 729–740. https://doi.org/10.1176/appi.ajp.2018.17101174
