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Scientists find key difference between brains of alcohol-dependent versus nondependent

Scientists found a key difference between the brains of alcohol-dependent versus nondependent rats and the research could help the development of personalised treatments for alcoholism and alcohol use disorder.

The new study, led by scientists at The Scripps Research Institute (TSRI), reveals that when given alcohol, both groups showed increased activity in a region of the brain called the central amygdala (CeA) — but this activity was due to two completely different brain signalling pathways. According to Professor Marisa Roberto, senior author of the new study, the findings could help researchers develop more personalised treatments for alcohol dependence, as they evaluate how a person’s brain responds to different therapeutics.

Marisa Roberto already discovered that that alcohol increases neuronal activity in the CeA and she and her colleagues found increased activity both nondependent, or naïve, and alcohol-dependent rats. But the new research revealed that the mechanisms underlying this increased activity differed between the two groups.

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According to an article published by TSRI’s News & Views, by giving naïve rats a dose of alcohol, the researchers engaged proteins called calcium channels and increased neuronal activity. Neurons fired as the specific calcium channels at play, called L-type voltage-gated calcium channels (LTCCs), boosted the release of a neurotransmitter called GABA. Blocking these LTCCs reduced voluntary alcohol consumption in naive rats. But in alcohol-dependent rats, the researchers found decreased abundance of LTCCs on neuronal cell membranes, disrupting their normal ability to drive a dose of alcohol’s effects on CeA activity.

Instead, increased neuronal activity was driven by a stress hormone called corticotropin-releasing factor (CRF) and its type 1 receptor (CRF1). The researchers found that blocking CeA CRF1s reduced voluntary alcohol consumption in the dependent rats.

Roberto hopes the findings lead to better ways to treat alcohol dependence. Alcohol use disorder appears to have many different root causes, but the new findings suggest doctors could analyse certain symptoms or genetic markers to determine which patients are likely to have CRF-CRF1 hyperactivation and benefit from the development of a novel drug that blocks that activity.

John Beckett

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