Abstract:With the development of industrialization in recent years, infrasound has become an important component of public noise. To date, diverse studies have revealed the negative effects of infrasound on the central nervous system (CNS), especially the learning and memory ability. It is widely reported that environmental enrichment (EE) ameliorates the learning and memory deficits in different models of brain injury. Therefore, the present study was designed to determine the possible benefits of pre-exposure to EE i… Show more
“…As described in our previous study [ 25 , 26 ], the infrasound system comprised an infrasound generator, a power amplifier, an infrasonic cabin, an infrasonic sensor, and a data collection system. The infrasound generator generates infrasonic waves at a sound pressure of 90–140 dB, with a frequency range of 2–20 Hz.…”
As a kind of environmental noise, infrasonic noise has negative effects on various human organs. To date, research has shown that infrasound impairs cognitive function, especially the ability for learning and memory. Previously, we demonstrated that impaired learning and memory induced by infrasound was closely related with glia activation; however, the underlying mechanisms remain unclear. Connexin 43 hemichannels (Cx43 HCs), which are mainly expressed in hippocampal astrocytes, are activated under pathological conditions, lending support to the hypothesis that Cx43 HCs might function in the impaired learning and memory induced by infrasound. This study revealed that that blocking hippocampal Cx43 HCs or downregulating hippocampal Cx43 expression significantly alleviated impaired learning and memory induced by infrasound. We also observed that infrasound exposure led to the abundant release of glutamate and ATP through Cx43 HCs. In addition, the abundant release of glutamate and ATP depended on proinflammatory cytokines. Our finds suggested that the enhanced release of ATP and glutamate by astroglial Cx43 HCs may be involved in the learning and memory deficits caused by infrasound exposure.
“…As described in our previous study [ 25 , 26 ], the infrasound system comprised an infrasound generator, a power amplifier, an infrasonic cabin, an infrasonic sensor, and a data collection system. The infrasound generator generates infrasonic waves at a sound pressure of 90–140 dB, with a frequency range of 2–20 Hz.…”
As a kind of environmental noise, infrasonic noise has negative effects on various human organs. To date, research has shown that infrasound impairs cognitive function, especially the ability for learning and memory. Previously, we demonstrated that impaired learning and memory induced by infrasound was closely related with glia activation; however, the underlying mechanisms remain unclear. Connexin 43 hemichannels (Cx43 HCs), which are mainly expressed in hippocampal astrocytes, are activated under pathological conditions, lending support to the hypothesis that Cx43 HCs might function in the impaired learning and memory induced by infrasound. This study revealed that that blocking hippocampal Cx43 HCs or downregulating hippocampal Cx43 expression significantly alleviated impaired learning and memory induced by infrasound. We also observed that infrasound exposure led to the abundant release of glutamate and ATP through Cx43 HCs. In addition, the abundant release of glutamate and ATP depended on proinflammatory cytokines. Our finds suggested that the enhanced release of ATP and glutamate by astroglial Cx43 HCs may be involved in the learning and memory deficits caused by infrasound exposure.
“…Inflammatory mediators and apoptosis-related molecules in the brain or blood were measured using ELISAs. The brain tissues were obtained according to our past study [35]. Briefly, the isolated brain was homogenized in normal saline, followed by centrifugation for 10 min at 4 °C and 2000 rpm.…”
“…The extent of lipid peroxidation was measured by determining the level of thiobarbituric acidreactive substances (TBARS), as previously described [35,36]. Isolated brain tissue was sonicated in 10% (w/v) radioimmunoprecipitation assay (RIPA) buffer added with a protease inhibitor cocktail (Sigma, St. Louis, MO, USA).…”
Section: Measurement Of Oxidant Activity 261 Lipid Peroxidationmentioning
confidence: 99%
“…Tissue was subjected sonication for homogenization by sonication in cold 50 mM NaH 2 PO 4 and 1 mM EDTA buffer at pH 7.5. The, homogenates were then subjected to centrifugation for 10 min at 4 °C and 10,000 × g. According to Barsotti's method [35,37], a spectrophotometer was used to determine AOPP levels at 340 nm.…”
Section: Advanced Oxidation Protein Products (Aopps)mentioning
confidence: 99%
“…In vivo, NO's final and stable end products are nitrates and nitrites, whose sum (NOx) represents total NO production. A colorimetric assay (Cayman Chemical Company, Ann Arbor, MI, USA) was used to determine NOx [35,38]. In sample homogenates, nitrates were converted to nitrites using nitrate reductase and NADPH.…”
Background: One of the most serious complications of sepsis is sepsis-associated encephalopathy (SAE), which impairs the cognition ability of survivors. Environmental enrichment (EE) has been demonstrated to alleviate cognition deficits under many kinds of brain injury conditions. However, EE's effects on SAE remain unknown. Therefore, this study aimed to determine EE's effect on cognition disorders under SAE conditions and the underlying mechanism. Materials and Methods: Adult male rats, subject to SAE or not, were housed under a standard environment (SE) or EE for 30 days. Subsequently, the rats were subjected to cognitive tests, such as the novel object recognition (NOR) test, the Morris water maze (MWM) test, an Open Field (OF) test, the elevated plus maze (EPM) test, and a sensory neglect (SN) test. Neuroinflammation, apoptosis, and oxidative stress changes in the brain were also detected. Results: The results revealed that SAE impaired somatesthesia, recognition memory, spatial learning and memory, and exploratory activity, which were significantly improved by EE housing. EE also prevented SAE-induced anxiety-like behavior. In addition, EE housing capable induced a decrease in pro-inflammatory cytokines, and an increase in anti-inflammatory cytokines and antioxidant properties in the brain. Moreover, EE housing exerted an anti-apoptosis function by upregulating the level of B-cell lymphoma/leukemia-2 (Bcl-2) level and downregulating the level of p53 level in the hippocampus. Conclusions: The results of the present study indicated that EE exerts a neuroprotective function on cognitive ability in SAE rats. The effect is achieved by increasing antioxidants, and anti-inflammatory and antiapoptotic capacities. EE can effectively rescue SAE-induced cognitive deficits.
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