Mechanism of action of methylphenidate: insights from PET imaging studies

J Atten Disord. 2002:6 Suppl 1:S31-43. doi: 10.1177/070674370200601s05.

Abstract

Methylphenidate (MPH) is the most commonly prescribed drug for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD). We have used Positron Emission Tomography (PET) to investigate the mechanism of action of MPH in the human brain. We have shown (a) that oral MPH reaches peak concentration in the brain 60-90 minutes after its administration, (b) that therapeutic doses of MPH block more than 50% of the dopamine transporters (DAT), and (c) that of the two enantiomers that compose MPH, it is d-threo-methylphenidate (d-MPH) and not l-threo-methylphenidate (l-MPH) that binds to the DAT. We have also shown that therapeutic doses of MPH significantly enhance extracellular dopamine (DA) in the basal ganglia, which is an effect that appears to be modulated by the rate of DA release and that is affected by age (older subjects show less effect). Thus, we postulate (a) that MPH's therapeutic effects are in part due to amplification of DA signals, (b) that variability in responses is in part due to differences in DA tone between subjects, and (c) that MPH's effects are context dependent. Because DA enhances task specific neuronal signaling and decreases noise, we also postulate that MPH-induced increases in DA could improve attention and decrease distractibility; and that since DA modulates motivation, the increases in DA would also enhance the saliency of the task facilitating the 'interest it elicits' and thus improving performance.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Attention Deficit Disorder with Hyperactivity / diagnostic imaging
  • Attention Deficit Disorder with Hyperactivity / drug therapy*
  • Basal Ganglia / diagnostic imaging
  • Basal Ganglia / drug effects
  • Brain / diagnostic imaging
  • Brain / drug effects*
  • Brain Mapping
  • Central Nervous System Stimulants / adverse effects
  • Central Nervous System Stimulants / pharmacokinetics
  • Central Nervous System Stimulants / therapeutic use*
  • Child
  • Dopamine / metabolism
  • Dopamine Plasma Membrane Transport Proteins
  • Humans
  • Membrane Glycoproteins*
  • Membrane Transport Modulators
  • Membrane Transport Proteins / antagonists & inhibitors
  • Membrane Transport Proteins / metabolism
  • Methylphenidate / adverse effects
  • Methylphenidate / pharmacokinetics
  • Methylphenidate / therapeutic use*
  • Middle Aged
  • Nerve Tissue Proteins*
  • Stereoisomerism
  • Tomography, Emission-Computed*
  • Treatment Outcome

Substances

  • Central Nervous System Stimulants
  • Dopamine Plasma Membrane Transport Proteins
  • Membrane Glycoproteins
  • Membrane Transport Modulators
  • Membrane Transport Proteins
  • Nerve Tissue Proteins
  • SLC6A3 protein, human
  • Methylphenidate
  • Dopamine