The contribution of alpha 2-noradrenergic mechanisms of prefrontal cortical cognitive function. Potential significance for attention-deficit hyperactivity disorder

Arch Gen Psychiatry. 1996 May;53(5):448-55. doi: 10.1001/archpsyc.1996.01830050084013.

Abstract

This article aims to review research in nonhuman primates demonstrating that norepinephrine can enhance the cognitive functioning of the prefrontal cortex through actions at alpha 2 A-adrenergic receptors postjunctional to noradrenergic terminals. As prefrontal cortex cognitive deficits are prominent in several psychiatric disorders, including attention-deficit hyperactivity disorder, these basic findings may have relevance for the development of novel pharmacotherapies.

Publication types

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

MeSH terms

  • Adrenergic alpha-Agonists / therapeutic use
  • Animals
  • Attention Deficit Disorder with Hyperactivity / physiopathology*
  • Clonidine / pharmacology
  • Clonidine / therapeutic use
  • Cognition Disorders / drug therapy
  • Guanfacine / pharmacology
  • Guanfacine / therapeutic use
  • Haplorhini
  • Humans
  • Locus Coeruleus / drug effects
  • Locus Coeruleus / physiology
  • Models, Neurological
  • Neural Pathways / drug effects
  • Neural Pathways / physiology
  • Norepinephrine / pharmacology*
  • Norepinephrine / physiology
  • Prefrontal Cortex / drug effects
  • Prefrontal Cortex / physiology*
  • Receptors, Adrenergic, alpha-2 / drug effects
  • Receptors, Adrenergic, alpha-2 / physiology*

Substances

  • Adrenergic alpha-Agonists
  • Receptors, Adrenergic, alpha-2
  • Guanfacine
  • Clonidine
  • Norepinephrine