AI Article Synopsis
- Cigarette smoking is prevalent among chronic pain patients, and chronic nicotine exposure has been linked to increased pain sensitivity in animal studies, but the exact neurobiological processes are still unclear.
- Researchers conducted experiments on mice to investigate how chronic nicotine affects the dopaminergic signaling between the ventral tegmental area (VTA) and the anterior cingulate cortex (ACC), focusing on chronic pain responses.
- They found that chronic nicotine exposure led to the development of allodynia, and inhibiting the dopaminergic pathway not only reduced this pain response but also suggested that Drd2 dopamine receptors play a significant role in this process.
Article Abstract
Background: Cigarette smoking is commonly reported among chronic pain patients in the clinic. Although chronic nicotine exposure is directly linked to nociceptive hypersensitivity in rodents, underlying neurobiological mechanisms remain unknown.
Methods: Multi-tetrode recordings in freely moving mice were used to test the activity of dopaminergic projections from the ventral tegmental area (VTA) to pyramidal neurones in the anterior cingulate cortex (ACC) in chronic nicotine-treated mice. The VTA→ACC dopaminergic pathway was inhibited by optogenetic manipulation to detect chronic nicotine-induced allodynia (pain attributable to a stimulus that does not normally provoke pain) assessed by von Frey monofilaments (force units in g).
Results: Allodynia developed concurrently with chronic (28-day) nicotine exposure in mice (0.36 g [0.0141] vs 0.05 g [0.0018], P<0.0001). Chronic nicotine activated dopaminergic projections from the VTA to pyramidal neurones in the ACC, and optogenetic inhibition of VTA dopaminergic terminals in the ACC alleviated chronic nicotine-induced allodynia in mice (0.06 g [0.0064] vs 0.28 g [0.0428], P<0.0001). Moreover, optogenetic inhibition of Drd2 dopamine receptor signalling in the ACC attenuated nicotine-induced allodynia (0.07 g [0.0082] vs 0.27 g [0.0211], P<0.0001).
Conclusions: These findings implicate a role of Drd2-mediated dopaminergic VTA→ACC pathway signalling in chronic nicotine-elicited allodynia.
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| http://dx.doi.org/10.1016/j.bja.2023.12.034 | DOI Listing |
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