Breaking the “Break” With over-drinking linked to Neurobiological Imbalance
We’ve all seen these people. Maybe at one point in time we’ve actually been these people: messy, falling-down drunk, slurring and incoherent, precariously close to catastrophe … and asking the bartender for another shot.
For the majority of us who imbibe, there is a certain point at which we stop pounding the drinks, and many reasons we do so. Maybe we sense that we’re close to our limit, or we notice we don’t feel as well — physically and emotionally — as we did a couple of glasses ago. And sometimes the sedative effects of the alcohol just take over. But for a certain subset of people, nothing — not the risk of losing control or the threat of nausea and dizziness — is enough to put the brakes on their drinking.
UC Santa Barbara neuroscientist Karen Szumlinski, who investigates binge drinking and the repeated stress of overdrinking on the brain, suggests a neurobiological mechanism might underpin this behavior. She and her team have uncovered a mechanism in a small brain structure called the bed nucleus of the stria terminalis (BNST) that helps sense alcohol’s negative effects and modulates the urge to drink. When it doesn’t function properly, however, we lose the ability to perceive when we’ve had enough — or, perhaps, one too many — and we continue to drink.
“If a little bit of intoxication is making you nervous, the BNST is doing its job,” said Szumlinski, a co-author of a paper that appears in The Journal of Neuroscience.
The urge for us to do virtually anything comes from signals that loop in and around our brains in areas that govern our perceptions, emotions and desires. These in turn connect to our motor functions and create behaviors. This process involves a complex set of signaling pathways, involving many neurotransmitters, as well as their associated proteins and receptors. Those examined in this study are specific to an area of the brain highly implicated in the interface between anxiety and motivation — the BNST, which is connected to, among other things, both the amygdala (which modulates fear and anxiety), and the nucleus accumbens (reward, aversion, motivation).
In previous studies, the researchers found that binge drinking elevates several aspects of signaling through the excitatory neurotransmitter glutamate in both the amygdala and the nucleus accumbens. Using a variety of experimental approaches, they also showed that this increased glutamate signaling drove excessive drinking. Along with the BNST, these regions form a subcircuit in the brain known as the extended amygdala.
“So in the amygdala the increased glutamate signaling is going to possibly generate negative emotions, and maybe you start feeling depressed or anxious, and then that will translate to a higher motivation to drink coming out of the nucleus accumbens,” Szumlinski said. Alcoholism — addiction in general — is a shifting target that moves between the motivation toward the “feel-good” effects of the drug and motivation to avoid the unpleasant withdrawal symptoms or to simply feel normal again after the dependency has been established.