Lasting synaptic changes underlie attention deficits caused by nicotine exposure during adolescence

Tobacco smoking and nicotine exposure during adolescence interfere with prefrontal cortex (PFC) development and result in cognitive disturbances in adult life.

In adolescent smokers, PFC activity, working-memory and attention are reduced. The present study (using a rat model) found that there was a lasting down-regulation of glutamatergic mGluR2 receptors which persisted into adulthood. The authors speculated that this reduced plasticity of glutamatergic inputs to PFC output layer V pyramidal neurons and altered information transfer in active networks underlying attention.

Restoring mGluR2 activity in vivo in the PFC of adult rats exposed to nicotine during adolescence remediated the attention deficit. By contrast, the authors found that cognitive performance, synaptic mGluR2 protein levels and glutamatergic synaptic depression were all unaffected by nicotine exposure during adulthood. The increased vulnerability to nicotine during adolescence may prompt a reconsideration of views on the etiology of attention deficits.

Counotte DS et al., Lasting synaptic changes underlie attention deficits caused by nicotine exposure during adolescence. Nature Neuroscience 14: 417-419 (2011).

http://www.nature.com/neuro/journal/v14/n4/full/nn.2770.html