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Noise-induced ribbon synapse loss in the mouse basal cochlear region does not reduce inner hair cell exocytosis.
Front Cell Neurosci
January 2025
Experimental Otology Group, InnerEarLab, Department of Otolaryngology, University Medical Center Göttingen, Göttingen, Germany.
Noise-induced hearing loss is one of the most common forms of hearing loss in adults and also one of the most common occupational diseases. Extensive previous work has shown that the highly sensitive synapses of the inner hair cells (IHCs) may be the first target for irreparable damage and permanent loss in the noise-exposed cochlea, more precisely in the cochlear base. However, how such synaptic loss affects the synaptic physiology of the IHCs in this particularly vulnerable part of the cochlea has not yet been investigated.
View Article and Find Full Text PDFHemispheric Asymmetry of Intracortical Myelin Orientation in the Mouse Auditory Cortex.
Eur J Neurosci
January 2025
Faculty of Life Sciences, Leipzig University, Leipzig, Germany.
Communication sound processing in mouse AC is lateralized. Both left and right AC are highly specialised and differ in auditory stimulus representation, functional connectivity and field topography. Previous studies have highlighted intracortical functional circuits that explain hemispheric stimulus preference.
View Article and Find Full Text PDFAdvances in mechanotransduction and sonobiology: effects of audible acoustic waves and low-vibration stimulations on mammalian cells.
Biophys Rev
December 2024
Department of Optics, Pharmacology and Anatomy, University of Alicante, San Vicente del Raspeig, Spain.
In recent decades, research on mechanotransduction has advanced considerably, focusing on the effects of audible acoustic waves (AAWs) and low-vibration stimulation (LVS), which has propelled the field of sonobiology forward. Taken together, the current evidence demonstrates the influence of these biosignals on key cellular processes, such as growth, differentiation and migration in mammalian cells, emphasizing the determining role of specific physical parameters during stimulation, such as frequency, sound pressure level/amplitude and exposure time. These mechanical waves interact with various cellular elements, including ion channels, primary cilia, cell-cell adhesion receptors, cell-matrix and extracellular matrix proteins, and focal adhesion complexes.
View Article and Find Full Text PDFSatellite microglia: marker of traumatic brain injury and regulator of neuronal excitability.
J Neuroinflammation
January 2025
Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, 98104, USA.
Traumatic brain injury is a leading cause of chronic neurologic disability and a risk factor for development of neurodegenerative disease. However, little is known regarding the pathophysiology of human traumatic brain injury, especially in the window after acute injury and the later life development of progressive neurodegenerative disease. Given the proposed mechanisms of toxic protein production and neuroinflammation as possible initiators or contributors to progressive pathology, we examined phosphorylated tau accumulation, microgliosis and astrogliosis using immunostaining in the orbitofrontal cortex, a region often vulnerable across traumatic brain injury exposures, in an age and sex-matched cohort of community traumatic brain injury including both mild and severe cases in midlife.
View Article and Find Full Text PDFInsights Into the Local Heating Effects in Triple-Cation Mixed-Halide Perovskite Cells: Charge Dynamics, Coherent Phonons, Anion Segregation.
Small
January 2025
Faculty of Physics and Astronomy, Adam Mickiewicz University, Poznan, 61-614, Poland.
The behavior of triple-cation mixed halide perovskite solar cells (PSCs) under ultrashort laser pulse irradiation at varying fluences is investigated, with a focus on local heating effects observed in femtosecond transient absorption (TA) studies. The carrier cooling time constant is found to increase from 230 fs at 2 µJ cm⁻ to 1.3 ps at 2 mJ cm⁻ while the charge population decay accelerates from tens of nanoseconds to the picosecond range within the same fluence range.
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