A new study conducted at the Waggoner Center for Alcohol and Addiction Research at The University of Texas at Austin appears to indicate that alcohol actually helps your memory, at least at the synapse level; that “alcohol primes certain areas of our brain to learn and remember better.” The new study, published in the April 6 edition of the Journal of Neuroscience, is a mouthful, entitled Previous Ethanol Experience Enhances Synaptic Plasticity of NMDA Receptors in the Ventral Tegmental Area. And the Abstract isn’t much clearer:

Alcohol addiction (alcoholism) is one of the most prevalent substance abuse disorders worldwide. Addiction is thought to arise, in part, from a maladaptive learning process in which enduring memories of drug experiences are formed. However, alcohol (ethanol) generally interferes with synaptic plasticity mechanisms in the CNS and thus impairs various types of learning and memory. Therefore, it is unclear how powerful memories associated with alcohol experience are formed during the development of alcoholism. Here, using brain slice electrophysiology in mice, we show that repeated in vivo ethanol exposure (2 g/kg, i.p., three times daily for 7 d) causes increased susceptibility to the induction of long-term potentiation (LTP) of NMDA receptor (NMDAR)-mediated transmission in mesolimbic dopamine neurons, a form of synaptic plasticity that may drive the learning of stimuli associated with rewards, including drugs of abuse. Enhancement of NMDAR plasticity results from an increase in the potency of inositol 1,4,5-trisphosphate (IP3) in producing facilitation of action potential-evoked Ca2+ signals, which is critical for LTP induction. This increase in IP3 effect, which lasts for a week but not a month after ethanol withdrawal, occurs through a protein kinase A (PKA)-dependent mechanism. Corticotropin-releasing factor, a stress-related neuropeptide implicated in alcoholism and other addictions, further amplifies the PKA-mediated increase in IP3 effect in ethanol-treated mice. Finally, we found that ethanol-treated mice display enhanced place conditioning induced by the psychostimulant cocaine. These data suggest that repeated ethanol experience may promote the formation of drug-associated memories by enhancing synaptic plasticity of NMDARs in dopamine neurons.

Professor Hitoshi Morikawa, who wrote the paper, is slightly less jargon-laden and impenetrable on the University’s website, where he more generally lays out the goals of his research:

This lab specifically focuses on the dopaminergic neurons in the ventral midbrain. They are activated by the perception and expectation of rewards. Therefore, the dopaminergic projections from the midbrain to the limbic structures constitute an endogenous reward circuit. Behaviors that lead to the enhancement of dopamine release in this brain reward circuit tend to be repeated (reinforced). Addictive drugs induce stronger stimulation of dopaminergic transmission than almost any natural reinforcers (food, sex, etc). Thus, drugs are repeatedly used (abused) in vulnerable individuals, which will lead to plastic changes in the reward circuit.

The amount and temporal profile of dopamine release is controlled by the firing pattern of dopamine neurons, which is determined by the interaction of their intrinsic membrane properties and the afferent inputs they receive from other neurons. Accordingly, we make detailed analyses of the influence of addictive drugs on membrane ionic conductances and neurotransmitter inputs of dopamine neurons, and investigate the resulting alteration in the firing pattern. We use brain slices because they retain intact synaptic connections that are necessary for these studies. Brain slices are obtained from drug-naïve animals and animals that are chronically treated with drugs to elucidate the plastic changes induced by repeated exposure to drugs in vivo. Technically, we perform patch clamp electrophysiological recordings combined with confocal fluorescent imaging of intracellular ions. These methods will allow us to delineate the cellular events that determine the excitability of neurons with a preciseness that could not be attained by other conventional techniques. Therefore, this lab offers an ideal system to link the behavior of certain types of central neurons to that of a whole organism.

But a science news website, Physog.com has the most understandable account of the study, and what it means.

Essentially, and somewhat confusingly, the study shows that while common view that too much alcohol can be bad for memory retention and learning, that how your brain reacts to it is more complicated than that.

“Usually, when we talk about learning and memory, we’re talking about conscious memory,” says Morikawa, whose results were published last month in The Journal of Neuroscience. “Alcohol diminishes our ability to hold on to pieces of information like your colleague’s name, or the definition of a word, or where you parked your car this morning. But our subconscious is learning and remembering too, and alcohol may actually increase our capacity to learn, or ‘conditionability,’ at that level.”

So while short terms losses may occur, long term gains in subconscious memory may also be taking place. “Morikawa’s study found that repeated ethanol exposure enhances synaptic plasticity in a key area in the brain, [and] is further evidence toward an emerging consensus in the neuroscience community that drug and alcohol addiction is fundamentally a learning and memory disorder.”

When we drink alcohol (or shoot up heroin, or snort cocaine, or take methamphetamines), our subconscious is learning to consume more. But it doesn’t stop there. We become more receptive to forming subsconscious memories and habits with respect to food, music, even people and social situations.

In an important sense, says Morikawa, alcoholics aren’t addicted to the experience of pleasure or relief they get from drinking alcohol. They’re addicted to the constellation of environmental, behavioral and physiological cues that are reinforced when alcohol triggers the release of dopamine in the brain.

“People commonly think of dopamine as a happy transmitter, or a pleasure transmitter, but more accurately it’s a learning transmitter,” says Morikawa. “It strengthens those synapses that are active when dopamine is released.”

Alcohol, in this model, is the enabler. It hijacks the dopaminergic system, and it tells our brain that what we’re doing at that moment is rewarding (and thus worth repeating).

Among the things we learn is that drinking alcohol is rewarding. We also learn that going to the bar, chatting with friends, eating certain foods and listening to certain kinds of music are rewarding. The more often we do these things while drinking, and the more dopamine that gets released, the more “potentiated” the various synapses become and the more we crave the set of experiences and associations that orbit around the alcohol use.

Between that, and new research from the University of Michigan that may have identified a gene — the GABRA2 — that increases the risk of alcoholism in certain individuals, it seems clear that there are environmental and genetic factors that make some people more susceptible to becoming unable to drink responsibly, along with the obvious psychological factors, too. But what that also suggests is that alcoholism is more like a food allergy insofar as it does not effect everyone in the same way, and in fact the vast majority of people who do consume alcohol are able to do so responsibly and in moderation, which also allows them to take advantage of the many health benefits of drinking in moderation. Contrary to neo-prohibitionist propaganda, not everyone becomes an alcoholic with the first sip they take. Most, in fact, not only don’t, but never do, yet the anti-alcohol contingency tends to treat alcohol as a toxic substance that is dangerous to everyone equally or that everyone has the potential to become an alcoholic. I just don’t think that’s true. And the science seems to bearing that out. And because of all the beer I’ve consumed, I can remember all that, too. Thank you, beer.