Chronic exposure to nicotine is associated with reduced reward-related activity in the striatum but not the midbrain.

What Was Tested

This randomized controlled trial looks at Therapeutic nicotine (patch, non-peptide).

The reinforcing effects of nicotine are mediated by brain regions that also support temporal difference error (TDE) processing; yet, the impact of nicotine on TDE is undetermined.

Who Took Part

PubMed indexes the participants as adults, both men and women.

Dependent smokers (n = 21) and matched control subjects (n = 21) were trained to associate a juice reward with a visual cue in a classical conditioning paradigm.

Subjects subsequently underwent functional magnetic resonance imaging sessions in which they were exposed to trials where they either received juice as temporally predicted or where the juice was withheld (negative TDE) and later received unexpectedly (positive TDE).

How the Study Was Run

The design is described as randomized and placebo-controlled.

The participants were allocated by chance, so the Therapeutic nicotine (patch, non-peptide) group and the comparison group should start out alike.

A placebo (an inactive look-alike) gave the Therapeutic nicotine (patch, non-peptide) group a baseline to be compared against.

Analysis focused on regions along the trajectory of mesocorticolimbic and nigrostriatal dopaminergic pathways.

What Was Measured

The subject headings attached to it are Case-Control Studies, Conditioning, Classical, Corpus Striatum, Cues, Functional Neuroimaging, Magnetic Resonance Imaging and Mesencephalon.

What This Means in Plain Language

The paper is a randomized and placebo-controlled study of Therapeutic nicotine (patch, non-peptide).

Its findings take up roughly 4 sentences of the abstract and are left out here on purpose; the source paper is the place to read them.

The publication is from 2012 (Biological psychiatry), a journal based in United States.

More context: the Therapeutic nicotine (patch, non-peptide) compound page, all human trials.