Faber, Elizabeth (Louise)Sah, Pankaj2015-12-132015-12-130270-6474http://hdl.handle.net/1885/81063Pyramidal 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 α-dendrotoxin- and tityustoxin-Kα-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-Ala 2-N-Me-Phe4-Glycol5-enkephalin (DAMGO) potentiates spike frequency adaptation by enhancing the α -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 A 2-arachidonic acid-lipoxygenases cascade.Keywords: arachidonic acid; calcium activated potassium channel; dendrotoxin; enkephalin[2 dextro alanine 4 methylphenylalanine 5 glycine]; guanine nucleotide binding protein; lipoxygenase; morphine; mu opiate receptor; mu opiate receptor agonist; n ethylmaleimide; Anxiolytic; Arachidonic; Channel; Kv1.2; Lipoxygenase; Nociception; Pain200410.1523/JNEUROSCI.4496-03.20042015-12-11