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. Author manuscript; available in PMC: 2022 Apr 29.
Published in final edited form as: Life Sci. 2021 Oct 26;289:120094. doi: 10.1016/j.lfs.2021.120094

Fig. 1.

Fig. 1.

GW exposure model and endpoints. Four experimental groups of adult mice were used: a sham treated control (CON), a sham treated control that received restraint stress (CON/S), and two GW groups that received one of two doses of PB P.O.: 6.5 mg/kg b.i.d. (GW1) and 8.7 mg/kg (GW2), plus topical DEET and PER as well as 5 min restraint stress. The exposure regimen was given 5 days/week followed by 2 day rest for 4 weeks. Animals were tested on metabolic, behavior and exercise endpoints as described. We tested the persistence of phenotype by testing for selected behaviors at various post-treatment time points T1 (PT 25–70), T2 (PT 70–94), T3 (94–199). Metabolic endpoints assessed include insulin sensitivity (IP ITT), post-exercise blood lactate and glucose, body weight and composition (QMR). Behavior tests included: SUOK, elevated plus maze (EPM), forced swim test (FST), tail suspension test (TST), novel object recognition test (NORT), sucrose splash test (SST), passive avoidance test (PAT), exercise endurance (EE), Rotarod, Barnes maze (BM), hot plate test (HPT). Mice were tested initially (1×) and repeat-tested on selected behaviors once (2×) and twice (3×) to determine onset and persistence of latently-emerging GW pathology as described in captions of figures below. DEET, N,N-diethyl-meta-toluamide; PB, pyridostigmine bromide; PER, permethrin; PT, post-treatment; QMR, quantitative magnetic resonance; T, time point; TRT, treatment; GW1, 6.5 mg/kg b.i.d.; GW2, 8.7 mg/kg.