Hyperalgesia in mice lacking the Kv1.1 potassium channel gene

• Published in: Neuroscience letters Vol. 251; no. 2; pp. 121 - 124
• Main Authors: Clark, J.David, Tempel, Bruce L
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 24.07.1998; Elsevier
• Subjects: Animals; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Hyperalgesia; Hyperalgesia - genetics; Hyperalgesia - metabolism; Kv1.1; Kv1.1 Potassium Channel; Mice; Mice, Inbred C3H; Mice, Knockout; Morphine; Null mutant; Potassium channels; Potassium Channels - deficiency; Potassium Channels - genetics; Potassium Channels, Voltage-Gated; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors; Vertebrates: nervous system and sense organs; Morphine; Potassium channels; Kv1.1; Hyperalgesia; Null mutant; Nociception; Analgesia; Vertebrata; Mammalia; Gene; Mouse; Rodentia; Ionic channel; Mutation; Potassium
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(98)00516-3

Hyperalgesia and morphine induced antinociception were measured in mice lacking the gene for the Shaker-like voltage-gated potassium channel Kv1.1 alpha subunit. The effects of varying gene dosage were studied by comparing homozygous null (−/−) versus heterozygous (±) and wildtype (+/+) littermates. Hyperalgesia was measured using the paw flick assay, hot plate assay and formalin induced hind paw licking. It was observed that null mutant animals had significantly shorter latencies to response in the paw flick (36%) and hot plate (27%) assays while their licking times after hind paw injection of formalin was increased in both the first (74%) and second (65%) phases of the response compared to wildtype controls. Morphine induced antinociception in Kv1.1 null mutant animals was blunted. These studies indicate that Kv1.1 plays an important role in nociceptive and antinociceptive signaling pathways.