Visual perception remains stable across saccadic eye movements, despite the concurrent strongly disruptive visual flow. This stability is partially associated with a reduction in visual sensitivity, known as saccadic suppression, which already starts in the retina with reduced ganglion cell sensitivity. However, the retinal circuit mechanisms giving rise to such suppression remain unknown. Here, we describe these mechanisms using electrophysiology in mouse, pig, and macaque retina, 2-photon calcium imaging, computational modeling, and human psychophysics. We find that sequential stimuli, like those that naturally occur during saccades, trigger three independent suppressive mechanisms in the retina. The main mechanism is triggered by contrast-reversing sequential stimuli and originates within the receptive field center of ganglion cells. It does not involve inhibition or other known suppressive mechanisms like saturation or adaptation. Instead, it relies on temporal filtering of the inherently slow response of cone photoreceptors coupled with downstream nonlinearities. Two further mechanisms of suppression are present predominantly in ON ganglion cells and originate in the receptive field surround, highlighting another disparity between ON and OFF ganglion cells. The mechanisms uncovered here likely play a role in shaping the retinal output following eye movements and other natural viewing conditions where sequential stimulation is ubiquitous.
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http://dx.doi.org/10.1038/s42003-022-03526-2 | DOI Listing |
Invest Ophthalmol Vis Sci
January 2025
Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Química Biológica Ranwel Caputto. Córdoba, Argentina.
Purpose: Stress granules (SGs) are cytoplasmic biocondensates formed in response to various cellular stressors, contributing to cell survival. Although implicated in diverse pathologies, their role in retinal degeneration (RD) remains unclear. We aimed to investigate SG formation in the retina and its induction by excessive LED light in an RD model.
View Article and Find Full Text PDFJ Neurol
January 2025
Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
Background: Previous investigations on optical coherence tomography (OCT) in multiple sclerosis (MS) focused on generalizable macular and peri-papillary regions without considering the anatomic variations of the retinal layer thickness.
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Methods: In this cross-sectional study, 214 people with MS (pwMS) and 57 age- and sex-matched healthy controls (HCs) were enrolled.
J Neurol
January 2025
Department of Medical and Surgical Sciences, University of Foggia, 71122, Foggia, Italy.
Background: Multiple sclerosis (MS) involves a complex interplay between immune-mediated inflammation and neurodegeneration. Recent advances in biomarker research have provided new insights into the molecular underpinnings of MS, including ferritin, neurogranin, Triggering Receptor Expressed on Myeloid cells 2 (TREM2), and neurofilaments light chain.
Objectives: This pilot study aims to investigate the levels of these biomarkers in the cerebrospinal fluid (CSF) of MS patients and explore their associations with clinical, cognitive, and optical coherence tomography (OCT) parameters.
Elife
January 2025
Department of Neurology, University of Iowa, Iowa City, United States.
The role of striatal pathways in cognitive processing is unclear. We studied dorsomedial striatal cognitive processing during interval timing, an elementary cognitive task that requires mice to estimate intervals of several seconds and involves working memory for temporal rules as well as attention to the passage of time. We harnessed optogenetic tagging to record from striatal D2-dopamine receptor-expressing medium spiny neurons (D2-MSNs) in the indirect pathway and from D1-dopamine receptor-expressing MSNs (D1-MSNs) in the direct pathway.
View Article and Find Full Text PDFExtracell Vesicles Circ Nucl Acids
December 2024
Department of Diagnostic and Biological Sciences, University of Minnesota, Minneapolis, MN 55455, USA.
The effective management of cancer pain continues to be a challenge because of our limited understanding of cancer pain mechanisms and, in particular, how cancer cells interact with neurons to produce pain. In a study published in , Inyang used a mouse model of human papillomavirus (HPV1)-induced oropharyngeal squamous cell carcinoma to show a role for cancer cell-derived extracellular vesicles (cancer sEVs) in cancer pain. They found that inhibiting the release of sEVs reduced spontaneous and evoked pain behaviors, and that pain produced by sEVs is due to activation of TRPV1 channels.
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