Alcohol dependence ‘driven by brain changes’

Alcohol dependency appears to be driven by changes in the brain that may, when fully understood, lead to more personalised treatments for alcoholism.

A study on rats at the Scripps institute found that both alcohol-dependent and non-dependent rats showed increased activity in the central amygdala (CeA) region of the brain, but with different brain signalling pathways being used in each case.

Among the non-dependent rats, alcohol doses engaged calcium channels called L-type voltage-gated calcium channels (LTCCs), which increased the release of GABA neurotransmitters. Blocking these LTCCs lowered alcohol consumption in these rats, the study, published in The Journal of Neuroscience, found.

However, for the dependent rats, fewer LTCCs were present on neural cell membranes, meaning they did less to influence the effects of alcohol on CeA activity. Instead, the stress hormone corticotropin-releasing factor (CRF) and its type 1 receptor (CRF1) had the main impact.
Professor Marisa Roberto, who led the study, said these differences could lead to the development of more personalised treatments for alcohol-dependent patients.

She said: "There is a switch in the molecular mechanisms underlying the CeA's response to alcohol (from LTCC- to CRF1-driven) as the individual transitions to the alcohol-dependent state."

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