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The Journal of Neuroscience, March 24, 2004, 24(12):3031-3039; doi:10.1523/JNEUROSCI.4496-03.2004

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Cellular/Molecular
Opioids Inhibit Lateral Amygdala Pyramidal Neurons by Enhancing a Dendritic Potassium Current

E. S. Louise Faber^1,2 and Pankaj Sah^1,2

¹Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia, and ²The Queensland Brain Institute, University of Queensland, Brisbane QLD 4072, Australia

Pyramidal neurons in the lateral amygdala discharge trains of action potentials that show marked spike frequency adaptation, which is primarily mediated by activation of a slow calcium-activated potassium current. We show here that these neurons also express an -dendrotoxin- and tityustoxin-K-sensitive voltage-dependent potassium current that plays a key role in the control of spike discharge frequency. This current is selectively targeted to the primary apical dendrite of these neurons. Activation of µ-opioid receptors by application of morphine or D-Ala²-N-Me-Phe⁴-Glycol⁵-enkephalin (DAMGO) potentiates spike frequency adaptation by enhancing the -dendrotoxin-sensitive potassium current. The effects of µ-opioid agonists on spike frequency adaptation were blocked by inhibiting G-proteins with N-ethylmaleimide (NEM) and by blocking phospholipase A₂. Application of arachidonic acid mimicked the actions of DAMGO or morphine. These results show that µ-opioid receptor activation enhances spike frequency adaptation in lateral amygdala neurons by modulating a voltage-dependent potassium channel containing Kv1.2 subunits, through activation of the phospholipase A₂–arachidonic acid–lipoxygenases cascade.

Key words: anxiolytic; arachidonic; channel; nociception; pain; lipoxygenase; Kv1.2

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Received Oct 3, 2003; revised February 3, 2004; accepted February 5, 2004.

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