Actions of norepinephrine in the cerebral cortex and thalamus: implications for function of the central noradrenergic system

Prog Brain Res. 1991;88:293-305. doi: 10.1016/s0079-6123(08)63817-0.


Norepinephrine (NE) has potent and long-lasting ionic effects on cortical and thalamic neurons. In cortical pyramidal cells, activation of beta-adrenergic receptors results in an enhanced excitability and responsiveness to depolarizing inputs. This enhanced excitability is expressed as a reduction in spike frequency adaptation and is mediated by a marked suppression of a slow Ca(++)-activated potassium current known as IAHP. In the thalamus, application of NE results in the suppression of ongoing rhythmic burst activity and a switch to the single spike firing mode of action potential generation. This effect is mediated through an alpha 1-adrenergic suppression of a resting leak potassium current, IKL, and through a beta-adrenoceptor-mediated enhancement of the hyperpolarization activated cation current Ih. Together with the actions of other neuromodulatory neurotransmitters (i.e., acetylcholine, histamine, serotonin) these effects facilitate the switch of these neurons from a state of rhythmic oscillation and low excitability during drowsiness and slow-wave sleep to a state of increased excitability and responsiveness during periods of waking, attentiveness and cognition.

Publication types

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

MeSH terms

  • Action Potentials / drug effects
  • Adrenergic Fibers / physiology
  • Arousal / physiology*
  • Cations
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / physiology*
  • Ion Channel Gating / drug effects
  • Ion Channels / drug effects
  • Locus Coeruleus / physiology*
  • Models, Neurological
  • Neurotransmitter Agents / pharmacology
  • Norepinephrine / pharmacology
  • Norepinephrine / physiology*
  • Receptors, Adrenergic / classification
  • Receptors, Adrenergic / drug effects
  • Receptors, Adrenergic / physiology
  • Sleep Stages / physiology
  • Thalamus / drug effects
  • Thalamus / physiology*


  • Cations
  • Ion Channels
  • Neurotransmitter Agents
  • Receptors, Adrenergic
  • Norepinephrine