Activation of lateral geniculate neurons by norepinephrine: Mediation by an α-adrenergic receptor

Michael A Rogawski, George K. Aghajanian

Research output: Contribution to journalArticlepeer-review

94 Scopus citations


Adrenergic receptors in the vicinity of neurons in the lateral geniculate nucleus (LGN) of the rat were pharmacologically characterized using extracellular single-cell recording and microiontophoretic techniques. Application of norepinephrine (NE) at low iontophoretic currents (1-15 nA) produced a delayed activation of most LGN neurons. This activation was mimicked by various sympathomimetic amines. The relative potency series of agonists was typical of postsynaptic α-adrenergic receptors: epinephrine> NE > phenylephrine ≥ α-methylnorepinephrine > dopamine > isoproterenol. The α-antagonists phentolamine, piperoxane and WB-4101, when applied at low iontophoretic currents (<10 nA), produced a selective, dose-dependent and reversible blockade of the response to NE. The β-antagonist sotalol had weak and variable effects at these currents. At low currents, the presynaptic α-agonist clonidine was also able to block the response to NE but, at higher currents, produced a partial activation of some units, suggesting that it is a weak agonist. The ability of sympathomimetic amines to activate LGN neurons correlates well with their reported affinities for brain α1-adrenoceptors labeled with [3H]WB-4101. It is concluded that NE activates neurons in the LGN via a postsynaptic or α1-adrenergic receptor.

Original languageEnglish (US)
Pages (from-to)345-359
Number of pages15
JournalBrain Research
Issue number2
StatePublished - Jan 27 1980
Externally publishedYes


  • lateral geniculate nucleus
  • microiontophoresis
  • norepinephrine
  • sympathomimetic amine
  • α-adrenergic agonist
  • α-adrenergic receptor

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)


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