Abstract
In the early sixties we knew relatively very little about the workings of the brain especially the interrelatedness of the brain reward circuitry and the Pre-frontal cortices. Understanding the importance of the main neurotransmitters such as serotonin, GABA, dopamine and acetylcholine were unknown for the most part and endorphins was not even a part of our scientific acumen. The 1956 doctrine of Jellinek and the disease concept of alcoholism was new and not generally accepted [1]. At that time most scientists working in the field of addiction agreed that alcoholism is the result -at least in part -of deficiencies or imbalances in brain chemistry-perhaps genetic in origin. However so little was known that nothing specific was espoused by the then newly called neuroscientists.
Highlights
In the early sixties we knew relatively very little about the workings of the brain especially the interrelatedness of the brain reward circuitry and the Pre-frontal cortices
This work was extended to another substance known to reduce both dopamine and norepinephrine call alpha-methyl- para – tyrosine) alpha-mPT) shown to induce aversion to ethanol. These experiments were the beginning of understanding neurotransmitter imbalances and subsequent alcohol intake in humans [12]; including the dopamine antagonistic therapy for alcohol and opiate addiction favored by FDA approved drugs
Willuhn et al [40] found that phasic dopamine decreased in the Ventral Medium Striatum (VMS) as the rate of cocaine intake increased, with the decrement in dopamine in the VMS significantly correlated with the rate of escalation
Summary
In the early sixties we knew relatively very little about the workings of the brain especially the interrelatedness of the brain reward circuitry and the Pre-frontal cortices. This work was extended to another substance known to reduce both dopamine and norepinephrine call alpha-methyl- para – tyrosine) alpha-mPT) shown to induce aversion to ethanol These experiments were the beginning of understanding neurotransmitter imbalances and subsequent alcohol intake in humans [12]; including the dopamine antagonistic therapy for alcohol and opiate addiction favored by FDA approved drugs. The promotion of long term dopaminergic activation by lower potency dopaminergic repletion therapy will lead to a common, safe and effective modality to treat RDS behaviors including Substance Use Disorders (SUD), Attention Deficit Hyperactivity Disorder (ADHD), obesity and other reward deficient aberrant behaviors This concept is further supported by the more comprehensive understanding of the role of dopamine in the NAc as a “wanting” messenger in the mesolimbic DA system [38]. Utilizing novel methods [54,55] to detect dopamine across the entire brain to assist in determining functional connectivity seems prudent and will result in further understanding of how our dopaminergic pathway predicts future substance and non-substance aberrant seeking behavior [56]
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