57 research outputs found
Immunohistochemical localization and mRNA expression of aquaporins in the macula utriculi of patients with Meniere’s disease and acoustic neuroma
Meniere’s disease is nearly invariably associated with endolymphatic hydrops (the net accumulation of water in the inner ear endolymphatic space). Vestibular maculae utriculi were acquired from patients undergoing surgery for Meniere’s disease and acoustic neuroma and from autopsy (subjects with normal hearing and balance). Quantitative immunostaining was conducted with antibodies against aquaporins (AQPs) 1, 4, and 6, Na+K+ATPase, Na+K+2Cl co-transporter (NKCC1), and α-syntrophin. mRNA was extracted from the surgically acquired utricles from subjects with Meniere’s disease and acoustic neuroma to conduct quantitative real-time reverse transcription with polymerase chain reaction for AQP1, AQP4, and AQP6. AQP1 immunoreactivity (−IR) was located in blood vessels and fibrocytes in the underlying stroma, without any apparent alteration in Meniere’s specimens when compared with acoustic neuroma and autopsy specimens. AQP4-IR localized to the epithelial basolateral supporting cells in Meniere’s disease, acoustic neuroma, and autopsy. In specimens from subjects with Meniere’s disease, AQP4-IR was significantly decreased compared with autopsy and acoustic neuroma specimens. AQP6-IR occurred in the sub-apical vestibular supporting cells in acoustic neuroma and autopsy samples. However, in Meniere’s disease specimens, AQP6-IR was significantly increased and diffusely redistributed throughout the supporting cell cytoplasm. Na+K+ATPase, NKCC1, and α-syntrophin were expressed within sensory epithelia and were unaltered in Meniere’s disease specimens. Expression of AQP1, AQP4, or AQP6 mRNA did not differ in vestibular endorgans from patients with Meniere’s disease. Changes in AQP4 (decreased) and AQP6 (increased) expression in Meniere’s disease specimens suggest that the supporting cell might be a cellular target
GABAA Receptor Function and Binding in Stably Transfected Cells: Chronic Ethanol Treatment
Altered GABAA-Benzodiazepine Receptor Number and Pharmacology in the Adult Guinea Pig Cerebral Cortex After Chronic Prenatal Ethanol Exposure
Electrophysiological Interactions of Ethanol with GABAergic Mechanisms in the Rat Cerebellum in Vivo
Lack of evidence of the interaction of the Aβ peptide with the Wnt signaling cascade in Drosophila models of Alzheimer's disease
Cellular localization of the Huntington's disease protein and discrimination of the normal and mutated form
Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol
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