Heat acclimation prevents neurobehavioral and physiological disorders in mice exposed to chronic aircraft noise

Abstract

We aimed to test whether heat acclimation (HA) would protect against aircraft noise (AN)-induced neurobehavioral and physiological disorders in mice. A total of 90 adult male mice were equally divided into three groups: control (c) plus non-AN group, c plus AN group, and HA plus AN group. Neurobehavioral performances included passive avoidance tasks (to assess learning and memory function), Y-maze tests (to assess spatial memory ability), and novel object recognition tests. Physiological functions included stress responses, inflammation, and oxidative stress, which were determined biochemically. The severity of endotoxemia was determined by measuring the serum levels of lipopolysaccharide. Both gut barrier and blood-brain barrier permeability were determined by fluorescein isothiocyanate and Evans Blue dye measurement, respectively. Compared to c+non-AN mice, the c+AN mice displayed neurobehavioral disorders along with exacerbated stress reactions, gut barrier disruption, endotoxemia, blood-brain barrier disruption, and hippocampal inflammation and oxidative stress. Compared to c+AN mice, the HA+AN mice had significantly less severity of all the abovementioned behavioral and physiological impairments. These results suggest that HA counteracts neurobehavioral and physiological disorders in mice exposed to aircraft noise.

Keywords: aircraft noise; blood–brain barrier disruption; endotoxemia; gut barrier disruption; heat acclimation; hippocampus; neurobehavioral disorders.

FIGURE 1

Experimental scheme. Mice undergoing HA or C with AN or without AN (non‐AN) were assigned to three different experimental paradigms. In experiment 1, 1 day following the last aircraft noise (AN) exposure, we first determined the values of both systolic blood pressure (SBP) and heat rate (HR) in C + non‐AN (n = 8), C + AN (n = 10), and HA + AN (n = 10) groups of mice. Then, these groups of mice were subjected to neurobehavioral tests. One day following the neurobehavioral trials, these groups of mice were euthanized and their blood and tissue samples were collected for determination of values of pro‐inflammatory cytokines, oxidative damage markers, stress indicators, and lipopolysaccharide (LPS). In our experiment 2 and experiment 3, the measurements of gut barrier permeability and blood–brain barrier (BBB) permeability were determined respectively in the C+non‐AN group (n = 10 each), C+AN group (n = 10 each), and HA+AN group of mice (n = 10 each).

FIGURE 2

Effects of AN on neurobehavioral functions in mice. Mice were subjected to a battery of neurobehavioral performances (passive avoidance task, Y‐maze tests, and NOR tests). Values are presented as mean ± SD of n = 10 for each group.

FIGURE 3

Systolic blood pressure (SBP), heart rate (HR), plasma ACTH, plasma corticosterone, and plasma noradrenaline values in C+non‐AN mice, C+AN mice, and HA+AN mice. The values were obtained 7 days after initiation of AN. Bars are the mean ± SD of n = 10 for each group.

FIGURE 4

Effects of aircraft noise (AN) on the levels of IL‐6, TNF‐α, and IL‐1β in the heart, duodenum and hippocampus in C+non‐AN mice, C+AN, and HA+AN. The values were obtained 7 days after the iniation of AN. Bars are the mean ± SD of n = 10 for each group.

FIGURE 5

Effects of AN on the levels of 8‐OHdG, MDA, H₂O₂, SOD, GSH, and T‐AOC in the mouse heart, duodenum, and hippocampus in C+non‐AN mice, C+AN mice, and HA+AN mice. The values were obtained 7 days after the initiation of AN. Bars are the mean ± SD of n = 10 for each group.

FIGURE 6

Effect of AN on the gut barrier permeability, the blood–brain barrier permeability, and plasma levels of LPS in C+non‐AN mice, C+AN mice, and HA+AN mice. Values are expressed as mean ± SD of n = 10 per group.