If you cannot resist that craving to have that ice-cold beer in the evening, then a drug that influences the immune system in the brain may disrupt the desire, reveals a study.
The findings revealed that there was a significant reduction in alcohol drinking behaviour by mice, who were given (+)-Naltrexone, specifically at night time when the reward for drug-related behaviour is usually at its greatest.
The University Of Adelaide in South Australia researchers conducted the study on mice and switched off the impulse to drink alcohol by giving mice a drug that blocks a specific response from the immune system in the brain.
They wanted to show a link between the brain's immunity and the motivation to drink alcohol at night.
Lead author Jon Jacobsen said that alcohol is the world's most commonly-consumed drug and there is a greater need than ever to understand the biological mechanisms that drive the need to drink alcohol.
"Our body's circadian rhythms affect the 'reward' signals we receive in the brain from drug-related behaviour and the peak time for this reward typically occurs during the evening, or dark phase. We wanted to test what the role of the brain's immune system might have on that reward and whether or not we could switch it off," Jacobsen added.
The team focussed their attention on the immune receptor Toll-like receptor 4 (TLR4).
They administered the drug (+)-Naltrexone (pronounced: PLUS-NAL-TREX-OWN), which is known to block TLR4, to mice.
They concluded that blocking a specific part of the brain's immune system did in fact substantially decrease the motivation of mice to drink alcohol in the evening.
Senior author Mark Hutchinson said that these findings point to the need for further research to understand the implications for drinking behaviour in humans.
The study is part of an emerging field which highlights the importance of the brain's immune system in the desire to drink alcohol.
The research appeared in the journal - Brain, Behavior and Immunity.
Disclaimer: No Business Standard Journalist was involved in creation of this content
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