Title : Spinal AMP kinase activity differentially regulates phrenic motor plasticity.

Pub. Date : 2020 Mar 1

PMID : 31971473






3 Functional Relationships(s)
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1 Consistent with our hypothesis, spinal AMPK activation with 2-deoxyglucose (2-DG) or metformin blocked 5-HT7, but not 5-HT2A receptor-induced pMF; in both cases, pMF inhibition was reversed by spinal administration of the AMPK inhibitor compound C. Thus, AMPK differentially regulates cellular mechanisms of serotonin-induced phrenic motor plasticity. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
2 Consistent with our hypothesis, spinal AMPK activation with 2-deoxyglucose (2-DG) or metformin blocked 5-HT7, but not 5-HT2A receptor-induced pMF; in both cases, pMF inhibition was reversed by spinal administration of the AMPK inhibitor compound C. Thus, AMPK differentially regulates cellular mechanisms of serotonin-induced phrenic motor plasticity. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
3 Consistent with our hypothesis, spinal AMPK activation with 2-deoxyglucose (2-DG) or metformin blocked 5-HT7, but not 5-HT2A receptor-induced pMF; in both cases, pMF inhibition was reversed by spinal administration of the AMPK inhibitor compound C. Thus, AMPK differentially regulates cellular mechanisms of serotonin-induced phrenic motor plasticity. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus