The eye is the sensory organ of vision. There, the retina transforms photons into electrical signals that are sent to higher brain areas to produce visual sensations. In the light path to the retina, different types of cells and tissues are involved in maintaining the transparency of avascular structures like the cornea or lens, while others, like the retinal pigment epithelium, have a critical role in the maintenance of photoreceptor function by regenerating the visual pigment. Here, we have reviewed the roles of different ion channels expressed in ocular tissues (cornea, conjunctiva and neurons innervating the ocular surface, lens, retina, retinal pigment epithelium, and the inflow and outflow systems of the aqueous humor) that are involved in ocular disease pathophysiologies and those whose deletion or pharmacological modulation leads to specific diseases of the eye. These include pathologies such as retinitis pigmentosa, macular degeneration, achromatopsia, glaucoma, cataracts, dry eye, or keratoconjunctivitis among others. Several disease-associated ion channels are potential targets for pharmacological intervention or other therapeutic approaches, thus highlighting the importance of these channels in ocular physiology and pathophysiology.
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http://dx.doi.org/10.1016/bs.apcsb.2015.11.006 | DOI Listing |
Front Neuroinform
January 2025
Centre Borelli, Université Paris Cité, UMR 9010, CNRS, Paris, France.
This article develops a fundamental insight into the behavior of neuronal membranes, focusing on their responses to stimuli measured with power spectra in the frequency domain. It explores the use of linear and nonlinear (quadratic sinusoidal analysis) approaches to characterize neuronal function. It further delves into the random theory of internal noise of biological neurons and the use of stochastic Markov models to investigate these fluctuations.
View Article and Find Full Text PDFSovrem Tekhnologii Med
January 2025
MD, DSc, Professor, Chief Researcher, Laboratory of Molecular Genetic Testing of Therapeutic Diseases; Institution of Internal and Preventive Medicine - Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 175/1 B. Bogatkova St., Novosibirsk, 630089, Russia.
Unlabelled: was to search for the associations of benign unconjugated hyperbilirubinemia phenotype with rs1799945 (H63D), rs1800562 (C282Y), rs1800730 (S65C) mutations of gene, rs113993960 (ΔF508) of gene, rs28929474 (PIZ), rs17580 (PIS) mutations of gene.
Material And Methods: The study design is case-control. The group with Gilbert's syndrome (GS) phenotype (n=414; mean age - 36.
Nat Commun
January 2025
College of Life Sciences, Shaanxi Normal University, 710119, Xi'an, China.
Ferroptosis is a form of iron-dependent programmed cell death, which is distinct from apoptosis, necrosis, and autophagy. Mitochondria play a critical role in initiating and amplifying ferroptosis in cancer cells. Voltage-Dependent Anion Channel 1 (VDAC1) embedded in the mitochondrial outer membrane, exerts roles in regulation of ferroptosis.
View Article and Find Full Text PDFJ Neurosci
January 2025
Carney Institute for Brain Science, Brown University, Providence, RI 02912
The neuromuscular junction (NMJ) is the linchpin of nerve-evoked muscle contraction. Broadly, the function of the NMJ is to transduce nerve action potentials into muscle fiber action potentials (MFAPs). Efficient neuromuscular transmission requires both cholinergic signaling, responsible for generation of endplate potentials (EPPs), and excitation, the amplification of the EPP by postsynaptic voltage-gated sodium channels (Nav1.
View Article and Find Full Text PDFJ Neurosci
January 2025
Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, Ontario, Canada
Action potentials (spikes) are regenerated at each node of Ranvier during saltatory transmission along a myelinated axon. The high density of voltage-gated sodium channels required by nodes to reliably transmit spikes increases the risk of ectopic spike generation in the axon. Here we show that ectopic spiking is avoided because K1 channels prevent nodes from responding to slow depolarization; instead, axons respond selectively to rapid depolarization because K1 channels implement a high-pass filter.
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