Over the past four years, I have have read hundreds of papers attempting to elucidate the underlying neurobiology of alcoholism. In the beginning, it was pretty mundane; I simply read papers documenting the effects of binging and chronic use on the “big five” neuromodulatory systems: glutamate, GABA, serotonin, ResearchBlogging.orgdopamine, and acetycholine. Within the past three years, however, there are numerous papers attributing alcohol’s disruptive effects on glutamatergic, GABA-ergic, dopaminergic, serotonergic, and cholinergic neurotransmission to alterations in hormone release (melatonin, ghrelin, cortisol, growth hormone, leptin, estradiol, testosterone, progesterone, aldosterone, to name a few), gene expression, and neuroanatomical functioning (reward systems, circadian systems, mating systems, visual systems, mood systems, you name it). This four-page table, recently published in an article documenting alterations of gene expression related to synaptic modeling, cell signaling, growth, and death in the nucleus accumbens of chronically-drinking rodents, is an ideal example of this complexity. In case you’re skimming this blog entry (don’t worry, I’m not offended because I do the same!), I repeat: this is ONE TABLE!!!

Yep, I know. Not to be overly pessimistic, because I am actively involved in alcohol research, but it’s studies such as these which truly reveal how fracking difficult it is to treat any type of drug addiction. I doubt that we will ever have one drug or a series of drugs that eradicates all symptoms and predispositions to alcoholism. At this point, it’s more about reducing craving and relapse and sadly, will always be.

Bell, R., Kimpel, M., McClintick, J., Strother, W., Carr, L., Liang, T., Rodd, Z., Mayfield, R., Edenberg, H., & McBride, W. (2009). Gene expression changes in the nucleus accumbens of alcohol-preferring rats following chronic ethanol consumption Pharmacology Biochemistry and Behavior, 94 (1), 131-147 DOI: 10.1016/j.pbb.2009.07.019