Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans
Picrotoxin
Gamma-Aminobutyric Acid
DOI:
10.1007/s12192-016-0701-9
Publication Date:
2016-05-27T02:15:13Z
AUTHORS (7)
ABSTRACT
The mechanisms underlying oxidative stress (OS) resistance are not completely clear. Caenorhabditis elegans (C. elegans) is a good organism model to study OS because it displays responses similar those in mammals. Among these mechanisms, the insulin/IGF-1 signaling (IIS) pathway thought affect GABAergic neurotransmission. aim of this was determine influence heat shock (HS) on activity C. elegans. For purpose, we tested effect exposure picrotoxin (PTX), gamma-aminobutyric acid (GABA), hydrogen peroxide, and HS occurrence shrinking response (SR) after nose touch stimulus N2 (WT) worms. Moreover, expression UNC-49 (GABAA receptor ortholog) EG1653 strain GABA PTX HSP-16.2 TJ375 were analyzed. 1 mM- or H2O2 0.7 mM-exposed worms displayed SR about 80 % trials. did cause SR. prompted as mM exposure. In addition, increased expression, augmented expression. Thus, results present suggest that stress, through either application shock, inactivates system, which subsequently would response, perhaps by enhancing transcription factors DAF-16 HSF-1, both regulated IIS related hsp-16.2
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