Title : Enhanced GABAergic synaptic transmission at VLPAG neurons and potent modulation by oxycodone in a bone cancer pain model.

Pub. Date : 2015 Apr

PMID : 25521524






5 Functional Relationships(s)
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1 KEY RESULTS: The supraspinal antinociceptive effects of oxycodone, but not morphine, were abolished by blocking G protein-gated inwardly rectifying potassium1 (Kir 3.1) channels. Oxycodone potassium inwardly rectifying channel subfamily J member 3 Homo sapiens
2 Following treatment with oxycodone and morphine, IPSCs were reduced in the FBC model, and the inhibition of presynaptic GABA release by oxycodone, but not morphine was enhanced and dependent on Kir 3.1 channels. Oxycodone potassium inwardly rectifying channel subfamily J member 3 Homo sapiens
3 Following treatment with oxycodone and morphine, IPSCs were reduced in the FBC model, and the inhibition of presynaptic GABA release by oxycodone, but not morphine was enhanced and dependent on Kir 3.1 channels. Oxycodone potassium inwardly rectifying channel subfamily J member 3 Homo sapiens
4 CONCLUSION AND IMPLICATIONS: Our results demonstrate that Kir 3.1 channels are important for supraspinal antinociception and presynaptic GABA release inhibition by oxycodone in the FBC model. Oxycodone potassium inwardly rectifying channel subfamily J member 3 Homo sapiens
5 Enhanced GABAergic synaptic transmission at VLPAG neurons in the FBC model is an important site of supraspinal antinociception by oxycodone via Kir 3.1 channel activation. Oxycodone potassium inwardly rectifying channel subfamily J member 3 Homo sapiens