Alfa2-adrenoblockers attenuate the elevated plasma cholesterol, anxiety levels and restore impaired spatial memory of rats under the chronic noise exposure

Manukyan, Ashkhen; Grigoryan, Artem; Hunanyan, Lilit; Harutyunyan, Hayk; Manukyan, Mariam Varos; Mkrtchyan, V.S.; Melkonyan, Magda M

doi:10.1016/j.scitotenv.2020.140390

Cited by 11 publications

(6 citation statements)

References 46 publications

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“… 2 , 38 This study used white noise because it contains all frequencies across the audible spectrum and has been commonly used in laboratory experiments to mimic environmental noise. 16 , 39 , 40 Similar protocols (85–90 dB SPL, 4–12 h/d, 21–56 d) have been used to examine the effects of noise on sleep 41 and stress hormones 42 in rats and insulin resistance 43 and immunity 44 in mice. Our previous discovery of acute, white noise–evoked mouse escape implied that sudden noise may be linked to negative emotion.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Anxiety-Like Behaviors and Neural Circuitry following Chronic Moderate Noise Exposure in Mice

Peng,

Mao,

Tai

et al. 2023

Environ Health Perspect

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Background: Commonly encountered nontraumatic, moderate noise is increasingly implicated in anxiety; however, the neural substrates underlying this process remain unclear. Objectives: We investigated the neural circuit mechanism through which chronic exposure to moderate-level noise causes anxiety-like behaviors. Methods: Mice were exposed to chronic, moderate white noise [85 decibel (dB) sound pressure level (SPL)], 4 h/d for 4 wk to induce anxiety-like behaviors, which were assessed by open field, elevated plus maze, light-dark box, and social interaction tests. Viral tracing, immunofluorescence confocal imaging, and brain slice patch-clamp recordings were used to characterize projections from auditory brain regions to the lateral amygdala. Neuronal activities were characterized by in vivo multielectrode and fiber photometry recordings in awake mice. Optogenetics and chemogenetics were used to manipulate specific neural circuitry. Results: Mice chronically (4 wk) exposed to moderate noise (85 dB SPL, 4 h/d) demonstrated greater neuronal activity in the lateral amygdala (LA), and the LA played a critical role in noise-induced anxiety-like behavior in these model mice. Viral tracing showed that the LA received monosynaptic projections from the medial geniculate body (MG) and auditory cortex (ACx). Optogenetic excitation of the or circuits acutely evoked anxiety-like behaviors, whereas their chemogenetic inactivation abolished noise-induced anxiety-like behavior. Moreover, mice chronically exposed to moderate noise were more susceptible to acute stress, with more neuronal firing in the LA, even after noise withdrawal. Discussion: Mice exposed to 4 wk of moderate noise (85 dB SPL, 4 h/d) demonstrated behavioral and physiological differences compared to controls. The neural circuit mechanisms involved greater excitation from glutamatergic neurons of the MG and ACx to LA neurons under chronic, moderate noise exposure, which ultimately promoted anxiety-like behaviors. Our findings support the hypothesis that nontraumatic noise pollution is a potentially serious but unrecognized public health concern. https://doi.org/10.1289/EHP12532

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Section: Introductionmentioning

confidence: 99%

Characterization of Anxiety-Like Behaviors and Neural Circuitry following Chronic Moderate Noise Exposure in Mice

Peng,

Mao,

Tai

et al. 2023

Environ Health Perspect

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“…It should be also noticed, under the proper conditions both catecholamines can be regenerated to their original form so their functions can be restored [30]. So, according to our previous data, one of the main advantages of α 2adrenoblocker action is its regulatory effect on lipoprotein metabolism [28]. Environmental noise has its stress-realizing effects through the direct connections to the neural mechanisms via the autonomic nervous system [31], and also different mediated connections to the cerebral centers responsible for the principal physiological and behavioral effects of organism [32].…”

Section: Discussionmentioning

confidence: 78%

“…Reduction of the noise impact by α 2 -adrenoblockers was expressed by less level of MDA in the EM, in the 3rd and the 4th groups. Low level of MDA in these groups was caused by regulatory properties of α 2adrenoblockers [11,28] compared with the 1st group after 7, 30 and 60 days of noise exposure.…”

Section: Discussionmentioning

confidence: 99%

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Adrenergic alpha-2 receptor antagonists regulate noise–induced metabolic and cognitive changes in rats

Manukyan

Grigoryan

Hunanyan

et al. 2020

Preprint

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Background: Noise is a modern life wide-spread stressor produced by urban traffic and the industrial environment. The noise stress causes central nervous system’s dysfunction and neurotransmission impairment in the brain, as well as changes the hormones levels which potentially result in psychological and behavioral problems. Underscoring the implications of the chronic stress, the aim of our investigation was to study the level of the malondialdehyde (MDA) in the plasma and erythrocytes’ membrane (EM), as well as the behavioral characteristics of experimental animals, and the influences of the α2-adrenoblockers to evident their modulating effect during noise exposure. Results: The obtained results imply increase of plasma and erythrocytes’ membrane MDA content which is an indicator of oxidative stress development. At the same time the noise impact decreases cognitive functions. Conclusion: The use of α2-adrenoblockers to the noise-exposed animals by the specific tests revealed a regulatory effect on the noise time-dependent delay in behavioral activity manifested by disorientation, increased anxiety, the spatial memory deficit. Reduction of the noise impact by α2-adrenoblockers was expressed by less level of MDA in the EM, in the 3rd and the 4th groups.

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“…SV2C deletion resulted in dopamine loss and sports injury, which triggered anxietyand depression-like behavior and memory disorders in rats (Lapmanee et al, 2017;Rai et al, 2017). The evaluation of cognitive function is based mainly on locomotor activity, spatial memory, and anxiety (Manukyan et al, 2020); the Morris water maze and NORT tests revealed that locomotor and behavioral activity was impaired with lower miR-96 levels. Therefore, in concert with the previously published reports, we put forth out findings that demonstrate that the expression of miR-96 and SV2C is altered in mice induced with depression-like behaviors and memory disorders, highlighting their roles in depression.…”

Section: Discussionmentioning

confidence: 99%

miR-96 Inhibits SV2C to Promote Depression-Like Behavior and Memory Disorders in Mice

Sun¹,

Bai²,

Lin³

et al. 2021

Front. Behav. Neurosci.

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Accumulating evidence continues to emphasize the role of microRNAs as significant contributors to depression-like behavior and memory disorders. The current study aimed to investigate the mechanism by which miR-96 influences depression-like behavior and memory deficit in mice. A depression-like behavior and memory disorder mouse model was initially established by means of intraperitoneal injection with lipopolysaccharide. Memory deficits in the mice were evaluated using the Novel Object Recognition Test and Morris water maze experiments, whereas the Sucrose Preference Experiment and forced swimming experiments were performed to identify depression-like behavior in mice. The levels of tumor necrosis factor-α, malondialdehyde, superoxide dismutase, glutathione, and the monoamine transmitters 5-hydroxytryptamine and dopamine were subsequently detected in the serum. Reverse transcription-quantitative polymerase chain reaction and Western blot analysis evaluated the expression of miR-96 and SV2C expression in the CA1 hippocampal region of the mice. Finally, the relationship of miR-96 and SV2C was verified by dual-luciferase reporter gene assay. Our data indicated that the expression of miR-96 was increased, whereas that of SV2C was decreased in the CA1 region of mice exhibiting depression-like behavior and memory impairment. When miR-96 was downregulated or SV2C was overexpressed via intra-cerebroventricular injection with a miR-96 antagonist (miR-96 antagomir) or overexpression of SV2C vector, the Novel Object Recognition Test and sucrose preference index were increased, whereas the escape latency, the number of water maze platform crossings, and the immobility time of the mice were decreased. The serum levels of tumor necrosis factor-α, interleukin-1β, and malondialdehyde in the mouse CA1 region of mice were reduced, whereas the levels of superoxide dismutase and glutathione were elevated after the downregulation of miR-96 or overexpression of SV2C. Collectively, our study demonstrates that miR-96 negatively regulates the expression of SV2C, which consequently leads to depression-like behavior and memory impairment in mice. Our findings highlight the potential of miR-96-targeted therapeutics.

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Alfa2-adrenoblockers attenuate the elevated plasma cholesterol, anxiety levels and restore impaired spatial memory of rats under the chronic noise exposure

Cited by 11 publications

References 46 publications

Characterization of Anxiety-Like Behaviors and Neural Circuitry following Chronic Moderate Noise Exposure in Mice

Characterization of Anxiety-Like Behaviors and Neural Circuitry following Chronic Moderate Noise Exposure in Mice

Adrenergic alpha-2 receptor antagonists regulate noise–induced metabolic and cognitive changes in rats

miR-96 Inhibits SV2C to Promote Depression-Like Behavior and Memory Disorders in Mice

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