“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.”

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Although it is well known that the neurotransmitter dopamine is involved in addiction, this study goes further, showing that the dopamine D1 receptor also plays an important role in addiction. The team found that periodic consumption of large amounts of alcohol acts on D1 neurons, making them much more excitable, which means that they activate with less stimulation.

“If these neurons are excited, you will want to drink alcohol,” Wang said. “You’ll have a craving.” That is to say, when neurons with D1 receptors are activated, they compel you to perform an action — reaching for another bottle of tequila, in this case. This then creates a cycle, where drinking causes easier activation, and activation causes more drinking.

These changes in activation of D1 neurons might be related to the physical changes happening at the sub-cellular level in brains that have been exposed to alcohol. They have longer branching and more of the mature, mushroom-shaped spines — the type that stores long-term memories — than their abstaining counterparts.

alcohol triggers a cell type-specific functional and structural plasticity in the DMS, contributing to mechanisms that drive alcohol consumption…D1R signaling in the dorsal striatum stimulates LTP induction whereas dopamine activation of D2Rs inhibits NMDAR activity

In summary, our results suggest that repeated cycles of alcohol drinking and the activation of D1Rs result in sustained functional and structural alterations preferentially in the D1R MSNs of the DMS, which in turn lead to aberrant synaptic and structural plasticity that may contribute to pathological alcohol-related phenotypes.

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