AI Article Synopsis
- Nicotine activates nicotinic acetylcholine receptors (nAChRs) in the brain, contributing to tobacco addiction through its rewarding effects.
- A study on rats showed that repeated exposure to whole cigarette smoke condensate (WCSC) increases locomotor activity, indicating heightened sensitivity to the drug after withdrawal.
- Blocking α4β2 nAChRs with an antagonist reduced this activity and lowered dopamine levels in the nucleus accumbens (NAc), highlighting their role in mediating tobacco's effects on behavior.
Article Abstract
Nicotine, the primary addictive substance in tobacco, produces the psychomotor, rewarding, and reinforcing effects of tobacco dependence by stimulating nicotinic acetylcholine receptors (nAChRs) in the brain. The present study determined that α4β2 nAChRs regulate locomotor sensitization by altering dopamine concentration in the nucleus accumbens (NAc) after systemic challenge exposure to whole cigarette smoke condensate (WCSC). Rats were administered subcutaneous injection of WCSC (0.2 mg/kg nicotine/day) for 7 consecutive days and then re-exposed to WCSC after 3 days of withdrawal. Challenge exposure to WCSC significantly increased locomotor activity. This increase was decreased by the subcutaneous injection of the α4β2 nAChR antagonist, DHβE (3 mg/kg), but not by the intraperitoneal injection of the α7 nAChR antagonist, MLA (5 mg/kg). In parallel with a decrease in locomotor activity, blockade of α4β2 nAChRs with DHβE decreased dopamine concentration in the NAc which was elevated by challenge exposure to WCSC. These findings suggest that challenge WCSC leads to the expression of locomotor sensitization by elevating dopamine concentration via stimulation of α4β2 nAChRs expressed in neurons of the NAc in rats.
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| http://dx.doi.org/10.1016/j.pbb.2022.173469 | DOI Listing |
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