Open AccessContribution of a natural polymorphism, protein kinase G, modulates electroconvulsive seizure recovery in D. melanogaster
Author(s) -
Stephanie P. Kelly,
Monica G. Risley,
Leonor Miranda,
Ken DawsonScully
Publication year - 2018
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.179747
Subject(s) - drosophila melanogaster , melanogaster , electroconvulsive therapy , protein kinase a , biology , electroconvulsive shock , cgmp dependent protein kinase , neuroscience , kinase , genetics , gene , endocrinology , mitogen activated protein kinase kinase
Drosophila melanogaster is a well-characterized model for neurological disorders and is widely used for investigating causes of altered neuronal excitability leading to seizure-like behavior. One method used to analyze behavioral output of neuronal perturbance is recording the time to locomotor recovery from an electroconvulsive shock. Based on this behavior, we sought to quantify seizure susceptibility in larval D. melanogaster with differences in the enzymatic activity levels of a major protein, cGMP-dependent protein kinase (PKG). PKG, encoded by foraging, has two natural allelic variants and has previously been implicated in several important physiological characteristics including: foraging patterns, learning and memory, and environmental stress tolerance. The well-established NO/cGMP/PKG signaling pathway found in the fly, which potentially targets downstream K+ channel(s), which ultimately impacts membrane excitability; leading to our hypothesis: altering PKG enzymatic activity modulates time to recovery from an electroconvulsive seizure. Our results show that by both genetically and pharmacologically increasing PKG enzymatic activity, we can decrease the locomotor recovery time from an electroconvulsive seizure in larval D. melanogaster.