Analysis of information sources in references of the Wikipedia article "Caffeine dependence" in English language version.
Astrid Nehlig and colleagues present evidence that in animals caffeine does not trigger metabolic increases or dopamine release in brain areas involved in reinforcement and reward. A single photon emission computed tomography (SPECT) assessment of brain activation in humans showed that caffeine activates regions involved in the control of vigilance, anxiety, and cardiovascular regulation but did not affect areas involved in reinforcement and reward.
the D1 receptor is not involved in the rewarding effects of caffeine. ... The current data indicates that caffeine has aversive effects at high doses and neither rewarding nor unpleasant effects at low doses. Previous work in rats has indicated that caffeine induces mild preferences at low doses (Brockwell et al., 1991; Bedingfield et al., 1998; Patkina & Zvartau, 1998) and aversions at high doses ... Indeed the rewarding effects of caffeine seen by Brockwell et al.(1991) were at one dose and small. This is similar to our current data; the lower doses of caffeine on our dose-response curve are weakly, but non-significantly rewarding. Also consistent, the rewarding effects of caffeine in humans are mild or absent in individuals with limited caffeine experience
We show a significant increase in D2/D3R availability in striatum with caffeine administration, which indicates that caffeine at doses consumed by humans does not increase DA in striatum. Instead we interpret our findings to indicate that caffeine's DA-enhancing effects in the human brain are indirect and mediated by an increase in D2/D3R levels and/or changes in D2/D3R affinity.
the D1 receptor is not involved in the rewarding effects of caffeine. ... The current data indicates that caffeine has aversive effects at high doses and neither rewarding nor unpleasant effects at low doses. Previous work in rats has indicated that caffeine induces mild preferences at low doses (Brockwell et al., 1991; Bedingfield et al., 1998; Patkina & Zvartau, 1998) and aversions at high doses ... Indeed the rewarding effects of caffeine seen by Brockwell et al.(1991) were at one dose and small. This is similar to our current data; the lower doses of caffeine on our dose-response curve are weakly, but non-significantly rewarding. Also consistent, the rewarding effects of caffeine in humans are mild or absent in individuals with limited caffeine experience
We show a significant increase in D2/D3R availability in striatum with caffeine administration, which indicates that caffeine at doses consumed by humans does not increase DA in striatum. Instead we interpret our findings to indicate that caffeine's DA-enhancing effects in the human brain are indirect and mediated by an increase in D2/D3R levels and/or changes in D2/D3R affinity.
the D1 receptor is not involved in the rewarding effects of caffeine. ... The current data indicates that caffeine has aversive effects at high doses and neither rewarding nor unpleasant effects at low doses. Previous work in rats has indicated that caffeine induces mild preferences at low doses (Brockwell et al., 1991; Bedingfield et al., 1998; Patkina & Zvartau, 1998) and aversions at high doses ... Indeed the rewarding effects of caffeine seen by Brockwell et al.(1991) were at one dose and small. This is similar to our current data; the lower doses of caffeine on our dose-response curve are weakly, but non-significantly rewarding. Also consistent, the rewarding effects of caffeine in humans are mild or absent in individuals with limited caffeine experience
We show a significant increase in D2/D3R availability in striatum with caffeine administration, which indicates that caffeine at doses consumed by humans does not increase DA in striatum. Instead we interpret our findings to indicate that caffeine's DA-enhancing effects in the human brain are indirect and mediated by an increase in D2/D3R levels and/or changes in D2/D3R affinity.
