Short- and long-term consequences of nicotine exposure during adolescence for prefrontal cortex neuronal network function

Abstract

More than 70% of adolescents report to have smoked a cigarette at least once. At the adolescent stage the brain has not completed its maturation. The prefrontal cortex (PFC), the brain area responsible for executive functions and attention performance, is one of the last brain areas to mature and is still developing during adolescence. Smoking during adolescence increases the risk of developing psychiatric disorders and cognitive impairment in later life. In addition, adolescent smokers suffer from attention deficits, which aggravate with the years of smoking. Recent studies in rodents reveal the molecular changes induced by adolescent nicotine exposure that alter the functioning of synapses in the PFC and that underlie the lasting effects on cognitive function. Here we provide an overview of these recent findings.

Figure 1.

Schematic representation of the short-term and long-term adaptations in prefrontal cortex (PFC) neuronal networks caused by nicotine exposure during adolescence. The upper panels show the sequence of adaptations in nAChR and mGluR2 protein levels and the resulting changes in inhibition and excitation and attention behavior from control conditions (saline) to nicotine exposure during adolescence (short-term effects of nicotine) and 5 weeks following nicotine exposure (long-term effects of nicotine). The lower panels show the effects of mGluR2 agonists and antagonists in saline and nicotine-exposed animals. Applying mGluR2 antagonists to the adult medial PFC reduces mGluR2 function and short-term depression of glutamatergic synapses and reduces attention performance of the animal. Providing mGluR2 agonists to the medial PFC of adult rats that were exposed to nicotine during adolescence increases mGluR2 function at glutamatergic synapses and improves attention performance.