BK channels and a cGMP-dependent protein kinase (PKG) function through independent mechanisms to regulate the tolerance of synaptic transmission to acute oxidative stress at the Drosophila larval neuromuscular junction. (3rd July 2018)

• Record Type: Journal Article
• Authors: Bollinger, Wesley L.; Sial, Nadia; Dawson-Scully, Ken
• Is Part Of: Journal of neurogenetics. Volume 32:Number 3(2018)
• Page Start: 246
• Page End: 255
• Publication Date: 2018-07-03
• Subjects: Drosophila melanogaster -- oxidative stress -- cGMP-dependent protein kinase -- neuromuscular junction -- BK channels -- iberiotoxin -- synaptic transmission; Neurogenetics -- Periodicals; 616.80442
• DOI: 10.1080/01677063.2018.1500571
• Languages: English
• ISSNs: 0167-7063

Abstract

Abstract: A cGMP-dependent protein kinase (PKG) has previously been shown to regulate synaptic transmission at the Drosophila neuromuscular junction (NMJ) during acute oxidative stress, potentially through modulation of downstream K + channel kinetics; however, the specific K + channels through which PKG functions remains unclear. In this study, we hypothesized that PKG may be acting on calcium-activated large-conductance Slo K + channels, or BK channels. We found that genetic elimination and pharmacological inhibition of BK channel conductance increases synaptic transmission tolerance to acute H2 O2 -induced oxidative stress. Furthermore, we discovered that activation of PKG in BK channel loss-of-function (Slo 4 ) mutants significantly decreases time to stimulus-induced synaptic failure, providing the first evidence of PKG and BK channels functioning independently to control synaptic transmission tolerance to acute oxidative stress.