It is well known that smoking during pregnancy impairs cognitive and emotional functions in offspring. Previously, we have demonstrated that prenatal nicotine exposure (PNE) during embryonic day 14 to postnatal day 0 (E14–P0) induces the severe behavioral impairment and the reduction of the density of glutamatergic neurons in the prefrontal cortex of mice at the age of 8–12 weeks. In this study, we investigated the behavioral impairment of mice induced by PNE and examined the effects of D–cycloserine (DCS) on the behavioral impairment.
Mice at the age of 8 week were subjected to the elevated plus maze, object based attention, marble burying, and fear conditioning tasks. We found that PNE induced anxiogenic and attention deficits, and reduced the glutamate contents in the prefrontal cortex of PNE–treated mice compared to the sucrose–treated mice.
Systemic treatment (30 mg/kg s.c.) or microinjection (5 nmol/0.5 µL, both sides of the prefrontal cortex, 15° angle from A:+1.7mm, L:±1.0mm from bregma, V:-1.5 mm from the dura) of DCS attenuated behavioral impairment.
These results suggest that (1) PNE may produce the attentional and emotional deficits in mice with hypofunction of glutamatergic system in the prefrontal cortex, and (2) the activation of NMDA receptor may be useful for the treatment of behavioral impairment induced by PNE.