Effects of methylphenidate on regional brain glucose metabolism in humans: Relationship to dopamine D2 receptors

Nora D. Volkow, Gene Jack Wang, Joanna S. Fowler, Jean Logan, Burton Angrist, Robert Hitzemann, Jeffrey Lieberman, Naomi Pappas

Research output: Contribution to journalArticle

143 Citations (Scopus)

Abstract

Objective: The authors' goals were to determine whether baseline dopamine activity contributes to response to methylphenidate and to assess the pattern of metabolic responses associated with enhanced dopamine activity. Method: They used positron emission tomography with 2-deoxy- 2[18F]fluoro-D-glucose to evaluate the effects of two sequential doses of methylphenidate on brain metabolism in 15 healthy subjects. Dopamine D2 receptor availability was measured with [11C]raclopride to evaluate its relation to methylphenidate-induced metabolic changes. Results: Methylphenidate increased brain metabolism in six subjects, decreased it in two, and did not change it in seven; however, it consistently increased cerebellar metabolism. Methylphenidate significantly increased 'relative 1' (region relative to the whole brain) metabolism in the cerebellum and decreased it in the basal ganglia. Regional metabolic changes in the cerebellum and the frontal and temporal cortices were significantly correlated with D2 availability. Frontal and temporal metabolism were increased in subjects with high D2 receptors and decreased in subjects with low D2 receptors. Conclusions: Methylphenidate induced variable changes in brain metabolism, but it consistently increased cerebellar metabolism. It also induced a significant reduction in relative metabolism in the basal ganglia. The significant association between metabolic changes in the frontal and temporal cortices and in the cerebellum and D2 receptors suggests that methylphenidate's metabolic effects in these brain regions are due in part to dopamine changes and that differences in D2 receptors may be one of the mechanisms accounting for the variability in response to methylphenidate.

Original languageEnglish (US)
Pages (from-to)50-55
Number of pages6
JournalAmerican Journal of Psychiatry
Volume154
Issue number1
StatePublished - 1997
Externally publishedYes

Fingerprint

Methylphenidate
Dopamine D2 Receptors
Glucose
Brain
Cerebellum
Dopamine
Frontal Lobe
Temporal Lobe
Basal Ganglia
Raclopride
Fluorodeoxyglucose F18
Positron-Emission Tomography
Healthy Volunteers

ASJC Scopus subject areas

  • Psychiatry and Mental health

Cite this

Volkow, N. D., Wang, G. J., Fowler, J. S., Logan, J., Angrist, B., Hitzemann, R., ... Pappas, N. (1997). Effects of methylphenidate on regional brain glucose metabolism in humans: Relationship to dopamine D2 receptors. American Journal of Psychiatry, 154(1), 50-55.

Effects of methylphenidate on regional brain glucose metabolism in humans : Relationship to dopamine D2 receptors. / Volkow, Nora D.; Wang, Gene Jack; Fowler, Joanna S.; Logan, Jean; Angrist, Burton; Hitzemann, Robert; Lieberman, Jeffrey; Pappas, Naomi.

In: American Journal of Psychiatry, Vol. 154, No. 1, 1997, p. 50-55.

Research output: Contribution to journalArticle

Volkow, ND, Wang, GJ, Fowler, JS, Logan, J, Angrist, B, Hitzemann, R, Lieberman, J & Pappas, N 1997, 'Effects of methylphenidate on regional brain glucose metabolism in humans: Relationship to dopamine D2 receptors', American Journal of Psychiatry, vol. 154, no. 1, pp. 50-55.
Volkow, Nora D. ; Wang, Gene Jack ; Fowler, Joanna S. ; Logan, Jean ; Angrist, Burton ; Hitzemann, Robert ; Lieberman, Jeffrey ; Pappas, Naomi. / Effects of methylphenidate on regional brain glucose metabolism in humans : Relationship to dopamine D2 receptors. In: American Journal of Psychiatry. 1997 ; Vol. 154, No. 1. pp. 50-55.
@article{4b352a88b9e04ac9a41e1c1a1d00a9a7,
title = "Effects of methylphenidate on regional brain glucose metabolism in humans: Relationship to dopamine D2 receptors",
abstract = "Objective: The authors' goals were to determine whether baseline dopamine activity contributes to response to methylphenidate and to assess the pattern of metabolic responses associated with enhanced dopamine activity. Method: They used positron emission tomography with 2-deoxy- 2[18F]fluoro-D-glucose to evaluate the effects of two sequential doses of methylphenidate on brain metabolism in 15 healthy subjects. Dopamine D2 receptor availability was measured with [11C]raclopride to evaluate its relation to methylphenidate-induced metabolic changes. Results: Methylphenidate increased brain metabolism in six subjects, decreased it in two, and did not change it in seven; however, it consistently increased cerebellar metabolism. Methylphenidate significantly increased 'relative 1' (region relative to the whole brain) metabolism in the cerebellum and decreased it in the basal ganglia. Regional metabolic changes in the cerebellum and the frontal and temporal cortices were significantly correlated with D2 availability. Frontal and temporal metabolism were increased in subjects with high D2 receptors and decreased in subjects with low D2 receptors. Conclusions: Methylphenidate induced variable changes in brain metabolism, but it consistently increased cerebellar metabolism. It also induced a significant reduction in relative metabolism in the basal ganglia. The significant association between metabolic changes in the frontal and temporal cortices and in the cerebellum and D2 receptors suggests that methylphenidate's metabolic effects in these brain regions are due in part to dopamine changes and that differences in D2 receptors may be one of the mechanisms accounting for the variability in response to methylphenidate.",
author = "Volkow, {Nora D.} and Wang, {Gene Jack} and Fowler, {Joanna S.} and Jean Logan and Burton Angrist and Robert Hitzemann and Jeffrey Lieberman and Naomi Pappas",
year = "1997",
language = "English (US)",
volume = "154",
pages = "50--55",
journal = "American Journal of Psychiatry",
issn = "0002-953X",
publisher = "American Psychiatric Association",
number = "1",

}

TY - JOUR

T1 - Effects of methylphenidate on regional brain glucose metabolism in humans

T2 - Relationship to dopamine D2 receptors

AU - Volkow, Nora D.

AU - Wang, Gene Jack

AU - Fowler, Joanna S.

AU - Logan, Jean

AU - Angrist, Burton

AU - Hitzemann, Robert

AU - Lieberman, Jeffrey

AU - Pappas, Naomi

PY - 1997

Y1 - 1997

N2 - Objective: The authors' goals were to determine whether baseline dopamine activity contributes to response to methylphenidate and to assess the pattern of metabolic responses associated with enhanced dopamine activity. Method: They used positron emission tomography with 2-deoxy- 2[18F]fluoro-D-glucose to evaluate the effects of two sequential doses of methylphenidate on brain metabolism in 15 healthy subjects. Dopamine D2 receptor availability was measured with [11C]raclopride to evaluate its relation to methylphenidate-induced metabolic changes. Results: Methylphenidate increased brain metabolism in six subjects, decreased it in two, and did not change it in seven; however, it consistently increased cerebellar metabolism. Methylphenidate significantly increased 'relative 1' (region relative to the whole brain) metabolism in the cerebellum and decreased it in the basal ganglia. Regional metabolic changes in the cerebellum and the frontal and temporal cortices were significantly correlated with D2 availability. Frontal and temporal metabolism were increased in subjects with high D2 receptors and decreased in subjects with low D2 receptors. Conclusions: Methylphenidate induced variable changes in brain metabolism, but it consistently increased cerebellar metabolism. It also induced a significant reduction in relative metabolism in the basal ganglia. The significant association between metabolic changes in the frontal and temporal cortices and in the cerebellum and D2 receptors suggests that methylphenidate's metabolic effects in these brain regions are due in part to dopamine changes and that differences in D2 receptors may be one of the mechanisms accounting for the variability in response to methylphenidate.

AB - Objective: The authors' goals were to determine whether baseline dopamine activity contributes to response to methylphenidate and to assess the pattern of metabolic responses associated with enhanced dopamine activity. Method: They used positron emission tomography with 2-deoxy- 2[18F]fluoro-D-glucose to evaluate the effects of two sequential doses of methylphenidate on brain metabolism in 15 healthy subjects. Dopamine D2 receptor availability was measured with [11C]raclopride to evaluate its relation to methylphenidate-induced metabolic changes. Results: Methylphenidate increased brain metabolism in six subjects, decreased it in two, and did not change it in seven; however, it consistently increased cerebellar metabolism. Methylphenidate significantly increased 'relative 1' (region relative to the whole brain) metabolism in the cerebellum and decreased it in the basal ganglia. Regional metabolic changes in the cerebellum and the frontal and temporal cortices were significantly correlated with D2 availability. Frontal and temporal metabolism were increased in subjects with high D2 receptors and decreased in subjects with low D2 receptors. Conclusions: Methylphenidate induced variable changes in brain metabolism, but it consistently increased cerebellar metabolism. It also induced a significant reduction in relative metabolism in the basal ganglia. The significant association between metabolic changes in the frontal and temporal cortices and in the cerebellum and D2 receptors suggests that methylphenidate's metabolic effects in these brain regions are due in part to dopamine changes and that differences in D2 receptors may be one of the mechanisms accounting for the variability in response to methylphenidate.

UR - http://www.scopus.com/inward/record.url?scp=0031032748&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031032748&partnerID=8YFLogxK

M3 - Article

C2 - 8988958

AN - SCOPUS:0031032748

VL - 154

SP - 50

EP - 55

JO - American Journal of Psychiatry

JF - American Journal of Psychiatry

SN - 0002-953X

IS - 1

ER -