Background: Chronic exposure to cigarette
smoke produces
neuroinflammation and long-term changes in
neurotransmitter systems, especially glutamatergic systems. Objective: We examined the effects of cigarette
smoke on astroglial
glutamate transporters as well as NF-κB expression in mesocorticolimbic brain regions, prefrontal cortex (PFC) and nucleus accumbens (NAc). The behavioral consequences of cigarette
smoke exposure were assessed using open field (OF) and light/dark (LD) tests to assess withdrawal-induced anxiety-like behavior. Methods: Sprague-Dawley rats were randomly assigned to five experimental groups: a control group exposed only to standard room air, a cigarette
smoke exposed group treated with saline vehicle, two cigarette
smoke exposed groups treated with
acetylsalicylic acid (ASA) (15 mg/kg and 30 mg/kg, respectively), and a group treated only with ASA (30 mg/kg). Cigarette
smoke exposure was performed for 2 h/day, 5 days/week, for 31 days. Behavioral tests were conducted weekly, 24 h after cigarette
smoke exposure, during acute withdrawal. At the end of week 4, rats were given either saline or ASA 45 min before cigarette exposure for 11 days. Results: Cigarette
smoke increased withdrawal-induced anxiety, and 30 mg/kg ASA attenuated this effect. Cigarette
smoke exposure increased the relative
mRNA and
protein expression of nuclear factor ĸB (NFĸB) in PFC and NAc, and ASA treatment reversed this effect. Also, cigarette
smoke decreased the relative
mRNA and
protein expression of
glutamate transporter1 (GLT-1) and the
cystine-
glutamate transporter (xCT) in the PFC and the NAc, while ASA treatment normalized their expression. Conclusion: Cigarette
smoke caused
neuroinflammation, alterations in
glutamate transporter expression, and increased anxiety-like behavior, and these effects were attenuated by
acetylsalicylic acid treatment.