Postembedding immunocytochemistry was used to compare the distribution of GABA and glycine immunoreactive labelling in the cochlear nucleus, in particular the number of immunolabeled synaptic boutons apposing the cell body profiles of three major neuronal types. The proportions and absolute numbers of glycine immunoreactive puncta were greatest on fusiform cell body profiles. Glycine immunoreactive puncta also predominated on spherical cell body profiles, although GABA immunoreactive boutons were more abundant than on fusiform cells. Octopus cell body profiles were apposed by the fewest immunoreactive puncta. Puncta colabeled for glycine and GABA were frequently observed on all three cell types. These findings suggest that each major cell type possesses a distinct pattern of glycinergic and GABAergic input, with glycinergic input predominating. Since both tuberculoventral and cartwheel neurons were immunolabeled and are known to project intrinsically, it is clear that a large percentage of glycinergic and GABAergic input to cochlear nucleus neurons originates from intrinsic sources.
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BMC Infect Dis
January 2025
Department of Dermatology, Showa University School of Medicine, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo, 142-8555, Japan.
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January 2025
Health Management Center, the First Affiliated Hospital of Zhejiang University School of Medicine, No.79 Qingchun Road, Shangcheng District, Hangzhou, Zhejiang, China.
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View Article and Find Full Text PDFExpert Opin Pharmacother
January 2025
The Association of Diabetes Investigators, California, CA, USA.
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View Article and Find Full Text PDFToxicol Appl Pharmacol
January 2025
Department of Preventive Medicine, Shantou University Medical College, Shantou 515041, Guangdong, China. Electronic address:
Background: Bisphenol F (BPF), a substitute for bisphenol A (BPA), is widely used in consumer products, increasing the potential for environmental exposure. Our study investigated the reproductive effects of BPF on adult male zebrafish and explored its toxicological mechanisms, as well as its intergenerational effects.
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Neurobiol Dis
January 2025
Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK S7K 0M7, Canada; Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, SK S7N 0X8, Canada. Electronic address:
RNA binding protein dysfunction is a pathogenic feature of multiple neurological diseases, including multiple sclerosis (MS). Neurodegeneration (the loss of, or damage to neurons and axons) is the primary driver of disease progression in MS. Herein, we utilized a novel, neuron-specific model of neurodegeneration by transducing primary mouse neurons with mutant forms of the RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) identified from MS patients, including one within the M9-nuclear localization sequence of hnRNP A1 (A1(P275S)) and a second in the prion-like domain of hnRNP A1 (A1(F263S)) to test the hypothesis that neuronal hnRNP A1 dysfunction drives neurodegeneration in MS.
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