One crucial question is “what makes some people crave alcohol in excess acutely ie a single sitting and/or chronically over time”? Scientists have long known that the answer involves the neurotransmitter dopamine in the ventral tegmental area (VTA) of the brain.
Recently Mark Brodie, Professor of Physiology and BioPhysics at the University of Illinois at Chicago published an interesting article in the journal Neuropharmacology. His research focused on the potassium channel KCNK13 which is found inside the membrane of dopaminergic neurons in the VTA.
The inhibition of this channel by ethanol causes these neurons to release more dopamine than usual. Dopamine earned its nickname due to the fact that it is a feel good chemical which the brain releases as a reward for the brain when we learn new things or during pleasurable activities such as sex and drinking thereby prolonging the pleasure.
To determine whether alcohol can influence the expression of KCNK13 Professor Brodie’s team administered ethanol (3g/kg, ip) to mice and measured the KCNK13 mRNA in the VTA at 1 H and 4 H. Significant increases in the mRNA were observed after 4 H but not after 1 H. A corresponding increase in the ability of ethanol to excite VTA neurons was also noticed after 4 H. Additionally a mouse model in which mice had their KCNK13 genetically reduced by 15-20% were produced. These mice drank 20-30% more than their normal counterparts during a 2 H session.
As the time progressed to four hours the consumption between the two groups was equal. This is explained by the fact that the KCNK13 genetically reduced mice needed to drink more in the first two hours to get the same dopaminergic reward as the normal mice but by the 4 H mark up regulation of the KCNK13 as well as other possible compensatory mechanisms “kick in” and the drinking levels off.
The question becomes “is this potassium channel a potential target for a small molecule to inhibit the effects of alcohol upon it and thereby offer a new treatment for binge drinking?”
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