Activation of lateral geniculate neurons by norepinephrine: mediation by an alpha-adrenergic receptor

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 alpha-adrenergic receptors: epinephrine greater than NE greater than phenylephrine greater than or equal to alpha-methylnorepinephrine greater than dopamine greater than isoproterenol. The alpha-antagonists phentolamine, piperoxane and WB-4101, when applied at low iontophoretic currents (less than 10 nA), produced a selective, dose-dependent and reversible blockade of the response to NE. The beta-antagonist sotalol had weak and variable effects at these currents. At low currents, the presynaptic alpha-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 alpha1-adrenoceptors labeled with [3H]WB-4101. It is concluded that NE activates neurons in the LGN via a postsynaptic or alpha1-adrenergic receptor.