At a molecular level, smoking abstinence appears to increase the sensitized nAChRs and thereby the cholinergic neurotransmission in smokers without PEMCS. The reduced MTL activation observed in abstinent adolescent smokers without PEMCS during delayed recognition testing may result from cholinergically mediated enhancements in encoding, leading to reduced hippocampal and parahippocampal load during recognition testing185. Conversely, if adolescent smokers with PEMCS do not upregulate nAChRs while smoking and consequently experience decreased cholinergic neurotransmission during abstinence, then the increased MTL activation observed during delayed recognition testing may result from decreased efficacy of encoding, leading to increased hippocampal and parahippocampal load. Increased MTL activation observed during abstinence in the group with PEMCS during recognition testing may reflect compensatory activation in response to deficient encoding. The combined effects of prenatal and adolescent exposure to nicotine produce pronounced and lasting changes in hippocampal functioning.
