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Book ; Online: Encoding Visual Features by Parallel Ganglion Cell Initiated Pathways in the Healthy, Diseased and Artificial Retina

Völgyi, Béla / Völgyi, Béla / Kenyon, Garrett T. / Marshak, David W. / Sagdullaev, Botir

2019

Keywords	Science: general issues ; Neurosciences ; Retina ; ganglion cell ; encoding ; Decoding ; signaling ; visual feature
Size	1 electronic resource (115 pages)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT021230818
ISBN	9782889631056 ; 2889631052
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Molecular Biology of Retinal Ganglion Cells.

Völgyi, Béla

Cells

2020 Volume 9, Issue 11

Abstract: The main goal of this thematic issue was to bring both original research papers and reviews together to provide an insight into the rather broad topic of molecular biology of retinal ganglion cells (RGCs) [ ... ]. ...

Abstract	The main goal of this thematic issue was to bring both original research papers and reviews together to provide an insight into the rather broad topic of molecular biology of retinal ganglion cells (RGCs) [...].
MeSH term(s)	Humans ; Molecular Biology ; Optic Nerve Diseases/metabolism ; Research ; Retinal Ganglion Cells/metabolism
Language	English
Publishing date	2020-11-15
Publishing country	Switzerland
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9112483
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Molecular Mechanisms of Retinal Degeneration and How to Avoid It.

Kovács-Öller, Tamás / Völgyi, Béla

International journal of molecular sciences

2023 Volume 24, Issue 10

Abstract: Vision is the most important sensory modality in vertebrates in general, and as such, it is the most feared sense to lose [ ... ]. ...

Abstract	Vision is the most important sensory modality in vertebrates in general, and as such, it is the most feared sense to lose [...].
MeSH term(s)	Animals ; Humans ; Retinal Degeneration/genetics ; Vertebrates ; Vision, Ocular
Language	English
Publishing date	2023-05-15
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24108752
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Extrinsic and Intrinsic Factors Determine Expression Levels of Gap Junction-Forming Connexins in the Mammalian Retina.

Kovács-Öller, Tamás / Szarka, Gergely / Hoffmann, Gyula / Péntek, Loretta / Valentin, Gréta / Ross, Liliana / Völgyi, Béla

Biomolecules

2023 Volume 13, Issue 7

Abstract: Gap junctions (GJs) are not static bridges; instead, GJs as well as the molecular building block connexin (Cx) proteins undergo major expression changes in the degenerating retinal tissue. Various progressive diseases, including retinitis pigmentosa, ... ...

Abstract	Gap junctions (GJs) are not static bridges; instead, GJs as well as the molecular building block connexin (Cx) proteins undergo major expression changes in the degenerating retinal tissue. Various progressive diseases, including retinitis pigmentosa, glaucoma, age-related retinal degeneration, etc., affect neurons of the retina and thus their neuronal connections endure irreversible changes as well. Although Cx expression changes might be the hallmarks of tissue deterioration, GJs are not static bridges and as such they undergo adaptive changes even in healthy tissue to respond to the ever-changing environment. It is, therefore, imperative to determine these latter adaptive changes in GJ functionality as well as in their morphology and Cx makeup to identify and distinguish them from alterations following tissue deterioration. In this review, we summarize GJ alterations that take place in healthy retinal tissue and occur on three different time scales: throughout the entire lifespan, during daily changes and as a result of quick changes of light adaptation.
MeSH term(s)	Animals ; Connexins/genetics ; Connexins/metabolism ; Gap Junctions/metabolism ; Retina/metabolism ; Neurons/metabolism ; Mammals/metabolism
Chemical Substances	Connexins
Language	English
Publishing date	2023-07-13
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13071119
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: LED-Induced Microglial Activation and Rise in Caspase3 Suggest a Reorganization in the Retina.

Balogh, Boglárka / Szarka, Gergely / Tengölics, Ádám J / Hoffmann, Gyula / Völgyi, Béla / Kovács-Öller, Tamás

International journal of molecular sciences

2021 Volume 22, Issue 19

Abstract: Vision is our primary sense as the human eye is the gateway for more than 65% of information reaching the human brain. Today's increased exposure to different wavelengths and intensities of light from light emitting diode (LED) sources could induce ... ...

Abstract	Vision is our primary sense as the human eye is the gateway for more than 65% of information reaching the human brain. Today's increased exposure to different wavelengths and intensities of light from light emitting diode (LED) sources could induce retinal degeneration and accompanying neuronal cell death. Damage induced by chronic phototoxic reactions occurring in the retina accumulates over years and it has been suggested as being responsible for the etiology of many debilitating ocular conditions. In this work, we examined how LED stimulation affects vision by monitoring changes in the expression of death and survival factors as well as microglial activation in LED-induced damage (LID) of the retinal tissue. We found an LED-exposure-induced increase in the mRNA levels of major apoptosis-related markers BAX, Bcl-2, and Caspase-3 and accompanying widespread microglial and Caspase-3 activation. Everyday LED light exposure was accounted for in all the described changes in the retinal tissue of mice in this study, indicating that overuse of non-filtered direct LED light can have detrimental effects on the human retina as well.
MeSH term(s)	Animals ; Caspase 3/metabolism ; Humans ; Light/adverse effects ; Mice ; Microglia/metabolism ; Microglia/pathology ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Retina/metabolism ; Retina/pathology ; Retinal Degeneration/metabolism ; Retinal Degeneration/pathology ; bcl-2-Associated X Protein/metabolism
Chemical Substances	Bax protein, mouse ; Proto-Oncogene Proteins c-bcl-2 ; bcl-2-Associated X Protein ; Bcl2 protein, mouse (114100-40-2) ; Casp3 protein, mouse (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2021-09-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms221910418
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The role of gap junctions in cell death and neuromodulation in the retina.

Szarka, Gergely / Balogh, Márton / Tengölics, Ádám J / Ganczer, Alma / Völgyi, Béla / Kovács-Öller, Tamás

Neural regeneration research

2021 Volume 16, Issue 10, Page(s) 1911–1920

Abstract: Vision altering diseases, such as glaucoma, diabetic retinopathy, age-related macular degeneration, myopia, retinal vascular disease, traumatic brain injuries and others cripple many lives and are projected to continue to cause anguish in the foreseeable ...

Abstract	Vision altering diseases, such as glaucoma, diabetic retinopathy, age-related macular degeneration, myopia, retinal vascular disease, traumatic brain injuries and others cripple many lives and are projected to continue to cause anguish in the foreseeable future. Gap junctions serve as an emerging target for neuromodulation and possible regeneration as they directly connect healthy and/or diseased cells, thereby playing a crucial role in pathophysiology. Since they are permeable for macromolecules, able to cross the cellular barriers, they show duality in illness as a cause and as a therapeutic target. In this review, we take recent advancements in gap junction neuromodulation (pharmacological blockade, gene therapy, electrical and light stimulation) into account, to show the gap junction's role in neuronal cell death and the possible routes of rescuing neuronal and glial cells in the retina succeeding illness or injury.
Language	English
Publishing date	2021-02-28
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.308069
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Transience of the Retinal Output Is Determined by a Great Variety of Circuit Elements.

Ganczer, Alma / Szarka, Gergely / Balogh, Márton / Hoffmann, Gyula / Tengölics, Ádám Jonatán / Kenyon, Garrett / Kovács-Öller, Tamás / Völgyi, Béla

Cells

2022 Volume 11, Issue 5

Abstract: Retinal ganglion cells (RGCs) encrypt stimulus features of the visual scene in action potentials and convey them toward higher visual centers in the brain. Although there are many visual features to encode, our recent understanding is that the ~46 ... ...

Abstract	Retinal ganglion cells (RGCs) encrypt stimulus features of the visual scene in action potentials and convey them toward higher visual centers in the brain. Although there are many visual features to encode, our recent understanding is that the ~46 different functional subtypes of RGCs in the retina share this task. In this scheme, each RGC subtype establishes a separate, parallel signaling route for a specific visual feature (e.g., contrast, the direction of motion, luminosity), through which information is conveyed. The efficiency of encoding depends on several factors, including signal strength, adaptational levels, and the actual efficacy of the underlying retinal microcircuits. Upon collecting inputs across their respective receptive field, RGCs perform further analysis (e.g., summation, subtraction, weighting) before they generate the final output spike train, which itself is characterized by multiple different features, such as the number of spikes, the inter-spike intervals, response delay, and the rundown time (transience) of the response. These specific kinetic features are essential for target postsynaptic neurons in the brain in order to effectively decode and interpret signals, thereby forming visual perception. We review recent knowledge regarding circuit elements of the mammalian retina that participate in shaping RGC response transience for optimal visual signaling.
MeSH term(s)	Action Potentials ; Animals ; Brain ; Mammals ; Retina ; Retinal Ganglion Cells ; Visual Perception
Language	English
Publishing date	2022-02-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11050810
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Editorial: Encoding Visual Features by Parallel Ganglion Cell Initiated Pathways in the Healthy, Diseased and Artificial Retina.

Völgyi, Béla / Kenyon, Garrett T / Marshak, David W / Sagdullaev, Botir

Frontiers in cellular neuroscience

2019 Volume 13, Page(s) 229

Language	English
Publishing date	2019-05-24
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2019.00229
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Traumatic Brain Injury Induces Microglial and Caspase3 Activation in the Retina.

Kovács-Öller, Tamás / Zempléni, Renáta / Balogh, Boglárka / Szarka, Gergely / Fazekas, Bálint / Tengölics, Ádám J / Amrein, Krisztina / Czeiter, Endre / Hernádi, István / Büki, András / Völgyi, Béla

International journal of molecular sciences

2023 Volume 24, Issue 5

Abstract: Traumatic brain injury (TBI) is among the main causes of sudden death after head trauma. These injuries can result in severe degeneration and neuronal cell death in the CNS, including the retina, which is a crucial part of the brain responsible for ... ...

Abstract	Traumatic brain injury (TBI) is among the main causes of sudden death after head trauma. These injuries can result in severe degeneration and neuronal cell death in the CNS, including the retina, which is a crucial part of the brain responsible for perceiving and transmitting visual information. The long-term effects of mild-repetitive TBI (rmTBI) are far less studied thus far, even though damage induced by repetitive injuries occurring in the brain is more common, especially amongst athletes. rmTBI can also have a detrimental effect on the retina and the pathophysiology of these injuries is likely to differ from severe TBI (sTBI) retinal injury. Here, we show how rmTBI and sTBI can differentially affect the retina. Our results indicate an increase in the number of activated microglial cells and Caspase3-positive cells in the retina in both traumatic models, suggesting a rise in the level of inflammation and cell death after TBI. The pattern of microglial activation appears distributed and widespread but differs amongst the various retinal layers. sTBI induced microglial activation in both the superficial and deep retinal layers. In contrast to sTBI, no significant change occurred following the repetitive mild injury in the superficial layer, only the deep layer (spanning from the inner nuclear layer to the outer plexiform layer) shows microglial activation. This difference suggests that alternate response mechanisms play a role in the case of the different TBI incidents. The Caspase3 activation pattern showed a uniform increase in both the superficial and deep layers of the retina. This suggests a different action in the course of the disease in sTBI and rmTBI models and points to the need for new diagnostic procedures. Our present results suggest that the retina might serve as such a model of head injuries since the retinal tissue reacts to both forms of TBI and is the most accessible part of the human brain.
MeSH term(s)	Animals ; Humans ; Brain Concussion/metabolism ; Brain Injuries, Traumatic/metabolism ; Disease Models, Animal ; Inflammation/metabolism ; Microglia/metabolism ; Retina/metabolism ; Caspase 3
Chemical Substances	Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2023-02-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24054451
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Imatinib Sets Pericyte Mosaic in the Retina.

Kovács-Öller, Tamás / Ivanova, Elena / Szarka, Gergely / Tengölics, Ádám J / Völgyi, Béla / Sagdullaev, Botir T

International journal of molecular sciences

2020 Volume 21, Issue 7

Abstract: The nervous system demands an adequate oxygen and metabolite exchange, making pericytes (PCs), the only vasoactive cells on the capillaries, essential to neural function. Loss of PCs is a hallmark of multiple diseases, including diabetes, Alzheimer's, ... ...

Abstract	The nervous system demands an adequate oxygen and metabolite exchange, making pericytes (PCs), the only vasoactive cells on the capillaries, essential to neural function. Loss of PCs is a hallmark of multiple diseases, including diabetes, Alzheimer's, amyotrophic lateral sclerosis (ALS) and Parkinson's. Platelet-derived growth factor receptors (PDGFRs) have been shown to be critical to PC function and survival. However, how PDGFR-mediated PC activity affects vascular homeostasis is not fully understood. Here, we tested the hypothesis that imatinib, a chemotherapeutic agent and a potent PDGFR inhibitor, alters PC distribution and thus induces vascular atrophy. We performed a morphometric analysis of the vascular elements in sham control and imatinib-treated NG2-DsRed mice. Vascular morphology and the integrity of the blood-retina barrier (BRB) were evaluated using blood albumin labeling. We found that imatinib decreased the number of PCs and blood vessel (BV) coverage in all retinal vascular layers; this was accompanied by a shrinkage of BV diameters. Surprisingly, the total length of capillaries was not altered, suggesting a preferential effect of imatinib on PCs. Furthermore, blood-retina barrier disruption was not evident. In conclusion, our data suggest that imatinib could help in treating neurovascular diseases and serve as a model for PC loss, without BRB disruption.
MeSH term(s)	Animals ; Blood-Retinal Barrier/cytology ; Blood-Retinal Barrier/drug effects ; Imatinib Mesylate/pharmacology ; Mice ; Mice, Inbred C57BL ; Pericytes/drug effects ; Pericytes/metabolism ; Protein Kinase Inhibitors/pharmacology ; Receptors, Platelet-Derived Growth Factor/antagonists & inhibitors ; Receptors, Platelet-Derived Growth Factor/metabolism
Chemical Substances	Protein Kinase Inhibitors ; Imatinib Mesylate (8A1O1M485B) ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2020-04-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21072522
Database	MEDical Literature Analysis and Retrieval System OnLINE

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