Study Finds New Key Link Between Alcoholism and Brain Function
Investigators at The Scripps Research Institute have identified a key difference in function between the alcohol-dependent brain and the non-alcohol dependent brain. That is, when rats received alcohol, activity increased in a region of the brain called the central amygdala – but this was accomplished via two different signaling pathways.
In a previous study, researchers found that alcohol increases activity in the central amygdala in both groups, but they were unaware of the two different mechanisms involved in this increased activity.
Moreover, when “naive” rats, or those rats who were not alcohol-dependent, were given a dose of alcohol, calcium channels were engaged, increased neuronal activity. This, in turn, boosts GABA, a neurotransmitter that has a calming effect on the central nervous system. Blocking these channels, conversely, was found to decrease voluntary alcohol use in naive rats.
In rats dependent upon alcohol, however, calcium channels on cell membranes were decreased, a state that impaired their ability to effect central amygdala activity. Rather, increased activity was driven by a stress hormone and its receptor. Researchers then discovered that blocking this receptor led to reduced alcohol consumption in dependent rats.
TSRI Professor Marisa Roberto, senior author of the new study:
“There is a switch in the molecular mechanisms underlying the response to alcohol as the individual transitions to the alcohol-dependent state.”
Roberto also said that examination of these two groups offers new insight into the association between alcoholism and brain function and could have implications for more personalized treatment for alcohol dependence in the future.
The findings were published recently in The Journal of Neuroscience.
~ G. Nathalee Serrels, M.A., Psychology
Florence P. Varodayan, Giordano de Guglielmo, Marian L. Logrip, Olivier George, Marisa Roberto. Alcohol dependence disrupts amygdalar L-type voltage-gated calcium channel mechanisms. The Journal of Neuroscience, 2017; 3721-16 DOI: 10.1523/JNEUROSCI.3721-16.2017