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BLA neurons were retrogradely labeled with a fluorescent tracer injected into the CeA of rats. Whole cell voltage-clamp recordings were performed on labeled BLA neurons in brain slices. The specific \u03bc opioid receptor agonist, (d-Ala<jats:sup>2<\/jats:sup>, N-Me-Phe<jats:sup>4<\/jats:sup>,Gly<jats:sup>5<\/jats:sup>-ol)-enkephalin (DAMGO, 1 \u03bcM), significantly reduced the frequency of miniature inhibitory postsynaptic currents (mIPSCs) in 77% of cells tested. DAMGO also significantly decreased the peak amplitude of evoked IPSCs in 75% of cells examined. However, DAMGO did not significantly alter the frequency of mEPSCs or the peak amplitude of evoked EPSCs in 90% and 75% of labeled cells, respectively. Bath application of the Kv channel blockers, 4-AP (Kv1.1, 1.2, 1.3, 1.5, 1.6, 3.1, 3.2), \u03b1-dendrotoxin (Kv1.1, 1.2, 1.6), dendrotoxin-K (Kv1.1), or tityustoxin-K\u03b1 (Kv1.2) each blocked the inhibitory effect of DAMGO on mIPSCs. Double immunofluorescence labeling showed that some of the immunoreactivities of Kv1.1 and Kv1.2 were colocalized with synaptophysin in the BLA. This study provides new information that activation of presynaptic \u03bc opioid receptors primarily attenuates GABAergic synaptic inputs to CeA-projecting neurons in the BLA through a signaling mechanism involving Kv1.1 and Kv1.2 channels. <\/jats:p>","DOI":"10.1152\/jn.01004.2005","type":"journal-article","created":{"date-parts":[[2005,11,23]],"date-time":"2005-11-23T20:34:25Z","timestamp":1132778065000},"page":"2032-2041","source":"Crossref","is-referenced-by-count":52,"title":["\u03bc Opioid Receptor Activation Inhibits GABAergic Inputs to Basolateral Amygdala Neurons Through Kv1.1\/1.2 Channels"],"prefix":"10.1152","volume":"95","author":[{"given":"Thomas F.","family":"Finnegan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shao-Rui","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui-Lin","family":"Pan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nlm.2004.10.001"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.102.042135"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(02)00061-8"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1990.63.3.473"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1007\/BF00269454"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1002\/cne.902730407"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1999.tb11293.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-4522(01)00361-X"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1002\/cne.1154"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1096-9861(19960408)367:3<375::AID-CNE5>3.0.CO;2-2"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.046250"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.050120"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4496-03.2004"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1038\/306684a0"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Finnegan TF, Chen SR, and Pan HL. 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