Methylphenidate as a causal test of translational and basic neural coding hypotheses

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Abstract
Significance: Stimulants such as methylphenidate (Ritalin) are often used clinically to treat attention deficit hyperactivity disorder (ADHD) and generally to improve selective attention. Their systemic administration provides a causal manipulation of the attentional system, allowing measurements of the neuronal population changes that accompany artificially manipulated selective attention. We found that orally administering methylphenidate to rhesus monkeys selectively improved visual performance at only their attended spatial location, and that correspondingly specific changes in the shared variability of groups of neurons in visual area V4 occurred only when attention was directed toward the receptive fields of those neurons. Critically, methylphenidate changed behavior exactly when it changed the shared variability of the neuronal responses, suggesting that it may work through naturally selective cognitive mechanisms.
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Funding Information
  • US NIH (1K99NS118117-01)
  • Simons Foundation (500465)
  • US NIH (4R00EY020844-03)
  • US NIH (R01 EY022930)
  • US NIH (R01NS121913)
  • US NIH (Core Grant P30 EY008098s)
  • Whitehall Foundation (Whitehall Foundation grant)
  • Klingenstein-Simons (Klingenstein-Simons Fellowship)
  • Alfred P. Sloan Foundation (Sloan Research Fellowship)
  • McKnight Foundation (McKnight Scholar Award)
  • Simons Foundation (Simons Collaboration on the Global Brain)

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