November 08, 2016
The cold, brutal life of a rat would probably drive any human being to drink, if not in excess, then a good bit more than they normally would. Rats, for lack of money and measurables, sadly cannot buy booze and must avail themselves of the discarded spoils of human waste.
That might be for their own good, and possibly a lesson for human beings, according to a new study from the University of Pennsylvania.
In order to better understand the roots of human disorders, neuroscience researchers at the Perelman School of Medicine examined links between the brain chemistry of stress and its impact on the risk factor for alcohol abuse.
The effects of stress on the brain, generally speaking, are to scramble the interplay of neuronal responses, deepening our susceptibility to reliance on substances that falsely normalize our perception of well-being.
“The stress response evolved to protect us, but addictive drugs use those mechanisms and trick our brains to keep us coming back for more,” said lead researcher John Dani, who chairs Penn's Department of Neuroscience. “These effects happen at the minute level of potassium, chloride, and other ions moving across the neuron outer membrane via channels and transporters."
Seated in the brain's ventral tegmental area is a set of neural circuitry identified as the heart of our biological reward system. To better understand the dynamics of stress hormones and neurons, the research team exposed rats to an acute discomfort for one hour and provided them access to sugar water laced with ethanol.
Why am I getting so much abuse all I wanted was a few drinks?! #aqabiology— Drunk Rats (@drunk_rats) May 17, 2016
After 15 hours, they checked back in on their intoxicated rodent friends, who outdrank their control peers significantly over the course of several weeks.
A superficial look at these rats' neural circuitry revealed what appeared to be an intact reward system in response to stress exposure. Closer examination showed that heavy ethanol consumption produced noticeable alterations to neurons, however, and a blunted dopamine response to alcohol. The stressed rats voluntarily drank more because their alcohol-induced dopamine response was weakened, flipping usually inhibitory neurons into an excitatory state.
“We gave the rats a chemical called CLP290 to restore the stress-altered circuitry to normal, which in turn corrected the firing of the dopamine neurons," Dani said.
Moving forward, researchers say their findings could have important implications for breaking ground on conditions such as post-traumatic stress disorder and alcoholism.
The full study can be found in the October issue of Neuron.