TRPV4-induced Neurofilament Injury Contributes to Memory Impairment after High Intensity and Low Frequency Noise Exposures

Objective Exposure to high intensity, low frequency noise(HI-LFN) causes vibroacoustic disease(VAD),with memory deficit as a primary non-auditory symptomatic effect of VAD. However, the underlying mechanism of the memory deficit is unknown. This study aimed to characterize potential mechanisms involving morphological changes of neurons and nerve fibers in the hippocampus, after exposure to HILFN.Methods Adult wild-type and transient receptor potential vanilloid subtype 4 knockout(TRPV4^(-/-)) mice were used for construction of the HI-LFN injury model. The new object recognition task and the Morris water maze test were used to measure the memory of these animals. Hemoxylin and eosin and immunofluorescence staining were used to examine morphological changes of the hippocampus after exposure to HI-LFN.Results The expression of TRPV4 was significantly upregulated in the hippocampus after HI-LFN exposure. Furthermore, memory deficits correlated with lower densities of neurons and neurofilamentpositive nerve fibers in the cornu ammonis 1(CA1) and dentate gyrus(DG) hippocampal areas in wildtype mice. However, TRPV4^(-/-)mice showed better performance in memory tests and more integrated neurofilament-positive nerve fibers in the CA1 and DG areas after HI-LFN exposure.Conclusion TRPV4 up-regulation induced neurofilament positive nerve fiber injury in the hippocampus,which was a possible mechanism for memory impairment and cognitive decline resulting from HI-LFN exposure. Together, these results identified a promising therapeutic target for treating cognitive dysfunction in VAD patients.

20-Hydroxyecdysone Improves Neuronal Differentiation of Adult Hippocampal Neural Stem Cells in High Power Microwave Radiation-Exposed Rats

Objective The hippocampus is thought to be a vulnerable target of microwave exposure.The aim of the present study was to investigate whether 20-hydroxyecdysone(20E)acted as a fate regulator of adult rat hippocampal neural stem cells(NSCs).Furthermore,we investigated if 20E attenuated high power microwave(HMP)radiation-induced learning and memory deficits.Methods Sixty male Sprague-Dawley rats were randomly divided into three groups:normal controls,radiation treated,and radiation+20E treated.Rats in the radiation and radiation+20E treatment groups were exposed to HPM radiation from a microwave emission system.The learning and memory abilities of the rats were assessed using the Morris water maze test.Primary adult rat hippocampal NSCs were isolated in vitro and cultured to evaluate their proliferation and differentiation.In addition,hematoxylin&eosin staining,western blotting,and immunofluorescence were used to detect changes in the rat brain and the proliferation and differentiation of the adult rat hippocampal NSCs after HPM radiation exposure.Results The results showed that 20E induced neuronal differentiation of adult hippocampal NSCs from HPM radiation-exposed rats via the Wnt3a/β-catenin signaling pathway in vitro.Furthermore,20E facilitated neurogenesis in the subgranular zone of the rat brain following HPM radiation exposure.Administration of 20E attenuated learning and memory deficits in HPM radiation-exposed rats and frizzled-related protein(FRZB)reduced the 20E-induced nuclear translocation ofβ-catenin,while FRZB treatment also reversed 20E-induced neuronal differentiation of NSCs in vitro.Conclusion These results suggested that 20E was a fate regulator of adult rat hippocampal NSCs,where it played a role in attenuating HPM radiation-induced learning and memory deficits.

A three-dimensional matrix system containing melatonin and neural stem cells repairs damage from traumatic brain injury in rats

Brain lesions can cause neural stem cells to activate,proliferate,diffe rentiate,and migrate to the injured area.However,after traumatic brain injury,brain tissue defects and microenvironment changes greatly affect the survival and growth of neural stem cells;the resulting reduction in the number of neural stem cells impedes effective repair of the injured area.Melatonin can promote the survival,proliferation,and differentiation of neural stem cells under adverse conditions such as oxidative stress or hypoxia that can occur after traumatic brain injury.Therefore,we investigated the therapeutic effects of melatonin combined with neural stem cells on traumatic brain injury in rats.First,in vitro studies confirmed that melatonin promoted the survival of neural stem cells deprived of oxygen and glucose.Then,we established a three-dimensional Matrigel-based transplantation system containing melatonin and neural stem cells and then used it to treat traumatic brain injury in rats.We found that treatment with the Matrigel system containing melatonin and neural stem cells decreased brain lesion volume,increased the number of surviving neuro ns,and improved recove ry of neurological function compared with treatment with Matrigel alone,neural stem cells alone,Matrigel and neural stem cells combined,and Matrigel and melatonin combined.Our findings suggest that the three-dimensional Matrigelbased transplantation system containing melatonin and neural stem cells is a potential treatment for traumatic brain injury.

Targeting ASIC1a Promotes Neural Progenitor Cell Migration and Neurogenesis in Ischemic Stroke

Cell replacement therapy using neural progenitor cells(NPCs)has been shown to be an effective treatment for ischemic stroke.However,the therapeutic effect is unsatisfactory due to the imbalanced homeostasis of the local microenvironment after ischemia.Microenvironmental acidosis is a common imbalanced homeostasis in the penumbra and could activate acid-sensing ion channels 1a(ASIC1a),a subunit of proton-gated cation channels following ischemic stroke.However,the role of ASIC1a in NPCs post-ischemia remains elusive.Here,our results indicated that ASIC1a was expressed in NPCs with channel functionality,which could be activated by extracellular acidification.Further evidence revealed that ASIC1a activation inhibited NPC migration and neurogenesis through RhoA signaling-mediated reorganization of filopodia formation,which could be primarily reversed by pharmacological or genetic disruption of ASIC1a.In vivo data showed that the knockout of the ASIC1a gene facilitated NPC migration and neurogenesis in the penumbra to improve behavioral recovery after stroke.

Terahertz two-pixel imaging based on complementary compressive sensing

A compact terahertz(THz) imaging system based on complementary compressive sensing has been proposed using two single-pixel detectors. By using a mechanical spatial light modulator, sampling in the transmission and reflection orientations was achieved simultaneously, which allows imaging with negative mask values. The improvement of THz image quality and anti-noise performance has been verified experimentally compared with the traditional reconstructed image, and is in good agreement with the numerical simulation. The demonstrated imaging system, with the advantages of high imaging quality and strong anti-noise property, opens up possibilities for new applications in the THz region.