Researchers pinpoint neurons that tell the brain when to stop drinking According to new research in the journal Biological Psychiatry, it may be possible to influence alcohol drinking behaviour by activating particular neurons. The investigators say that their findings provide an insight into another mechanism underlying the complicated disease of alcoholism.
The group’s prior research showed that alcohol consumption alters the physical structure and function of neurons, called medium spiny neurons, in the dorsomedial striatum and the activation of one type of neuron, called D1, determines whether one drink leads to two. The latest research has identified the neurons that tell drinkers to stop.
These neurons can be thought of like a tree, with many branches, and many small protrusions, or spines, coming off of them. Each neuron has one of two types of dopamine receptors--D1 or D2--and so can be thought of as either D1 or D2 neurons. D1 neurons are informally called part of a “go” pathway in the brain, while D2 neurons are in the “no-go” pathway. In other words, when D2 neurons are activated, they discourage action-telling you to wait, to stop, to do nothing.
Jun Wang, MD, PhD, the corresponding author on the paper and assistant professor in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M College of Medicine said, “When they are activated, they (D2 neurons) inhibit drinking behaviour, and therefore activating them is important for preventing problem drinking behaviour.”
Research has found that even in individuals without alcoholism, D2 neurons tend to become deactivated when we drink too much. This deactivation means there is nothing telling us to stop drinking, so we drink more, in a self-perpetuating cycle. The researchers found that in animal models, repeated cycles of excessive alcohol intake, followed by abstaining from alcohol, actually changed the strength of these neuronal connections, making D2 signals less powerful--which results in essentially training the individual to seek alcohol. “Think of the binge drinking behaviour of so many young adults,” Wang said. “Essentially they are probably doing the same thing that we’ve shown leads to inhibition of these so-called ‘good’ neurons and contributes to greater alcohol consumption.” “Our current and previous research are essentially two sides of the same coin,” Wang said. “D1 and D2 medium spiny neurons have essentially opposing roles in alcohol consumption.” By manipulating the activity of these neurons, the researchers were actually able to change the alcohol-drinking behaviour of the animal models who had been “trained” to seek alcohol. By activating D2 neurons, they were able to decrease alcohol consumption, and the more the D2 neurons were activated, the greater the effect is likely to be.
The researchers hope that in the future, drugs, electrical stimulation or some other method of activating the D2 neurons might be used to treat alcohol addiction. Although Wang cautioned that “we are still a long way from testing this in humans”.
Source: Distinct Synaptic Strengthening of the Striatal Direct and Indirect Pathways Drives Alcohol Consumption. Yifeng Cheng, Cathy C.Y. Huang, Tengfei Ma, Xiaoyan Wei, Xuehua Wang, Jiayi Lu, Jun Wang. Biological Psychiatry, 2016; DOI: 10.1016/j.biopsych.2016.05.016.