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Brain Sciences
Special Issues
Retinal Neurochemistry and Development
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Retinal Neurochemistry and Development

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: 20 November 2025 | Viewed by 2784

Special Issue Editors

Prof. Dr. Roberto Paes-de-Carvalho

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Guest Editor
Department of Neurobiology and Program of Neurosciences, Institute of Biology, Fluminense Federal University, Niterói, Brazil
Interests: neurochemistry and developmental neurobiology
Dr. Sriparna Majumdar

E-Mail Website
Guest Editor
1. Department of Psychology, Santa Clara University, Santa Clara, CA, USA
2. Computer Science Department, City College of San Francisco, San Francisco, CA, USA
Interests: immunohistochemistry; electrophysiology; neural network; mammalian brain and retina; data science; computational models

Special Issue Information

Dear Colleagues,

The retina is a tissue specialized in transducing light stimuli into electrical signals that are transmitted to brain visual centers. Most neurotransmitters and signaling molecules, such as hormones and neurotrophins, including excitatory and inhibitory synaptic transmitters present in the brain, are also present in the retina, making it an excellent model for studying nervous system functions. Nervous system development is also studied using the retina both in vivo and in culture, making it the ideal substrate to study cellular interactions between different types of neurons and between neurons and glial cells. This Special Issue welcomes articles and reviews at the frontier of neurochemistry and developmental neurobiology of the retina, especially involving distinct neurotransmitters, receptors, and signaling pathways related to neural functions, such as synaptic transmission and developmental processes such as neurogenesis, cell survival, differentiation, and neuron–glia interaction. Electrophysiological evidence and mathematical and computational models of neural development are also welcome.

Prof. Dr. Roberto Paes-de-Carvalho
Dr. Sriparna Majumdar
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • retina
  • neurochemistry
  • development
  • neurotransmitter
  • signaling pathways
  • cultures
  • neuron–glia interactions
  • synapses
  • neuronal differentiation
  • neuritogenesis

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Published Papers (3 papers)

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16 pages, 2662 KiB  
Article
Vitamin C Modulates the PI3K/AKT Pathway via Glutamate and Nitric Oxide in Developing Avian Retina Cells in Culture
by Aline T. Duarte-Silva, Ivan Domith, Isabele Gonçalves-da-Silva and Roberto Paes-de-Carvalho
Brain Sci. 2025, 15(4), 369; https://doi.org/10.3390/brainsci15040369 - 2 Apr 2025
Viewed by 505
Abstract
Background: In addition to its known antioxidant function, the reduced form of vitamin C, ascorbate, also acts as a neuromodulator in the nervous system. Previous work showed a reciprocal interaction of ascorbate with glutamate in chicken embryo retinal cultures. Ascorbate modulates extracellular glutamate [...] Read more.
Background: In addition to its known antioxidant function, the reduced form of vitamin C, ascorbate, also acts as a neuromodulator in the nervous system. Previous work showed a reciprocal interaction of ascorbate with glutamate in chicken embryo retinal cultures. Ascorbate modulates extracellular glutamate levels by inhibiting excitatory amino acid transporter 3 and promoting the activation of NMDA receptors and the consequent activation of intracellular signaling pathways involved in transcription and survival. Objective: In the present work, we investigated the regulation of AKT phosphorylation by ascorbate in chicken embryo retina cultures. Methodology: Cultures of chicken embryo retina cells were tested using Western blot, immunocytochemistry, fluorescent probe transfection, and cellular imaging techniques. Results: Our results show that ascorbate induces a concentration and time-dependent increase in AKT phosphorylation via the accumulation of extracellular glutamate, the activation of glutamate receptors, and the activation of the PI3K pathway. Ascorbate produces an increase in intracellular calcium accumulation and, accordingly, AKT phosphorylation by ascorbate is blocked by the calcium chelator BAPTA-AM. Moreover, AKT phosphorylation is also blocked by the nitric oxide synthase inhibitor 7-nitroindazole, indicating that it is mediated by calcium and nitric oxide-dependent mechanisms. Conclusions: We demonstrate that ascorbate modulates the PI3K/AKT pathway in retinal cultures through the activation of glutamate receptors and NO production in a calcium-dependent manner. Given that previous research has shown that glutamate induces ascorbate release in retinal cultures, our findings emphasize the significance of the reciprocal interactions between ascorbate and glutamate in retinal development. These findings provide further evidence supporting the role of ascorbate as a neuromodulator in retinal development. Full article
(This article belongs to the Special Issue Retinal Neurochemistry and Development)
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Graphical abstract

19 pages, 11999 KiB  
Article
Cannabinoids Activate Endoplasmic Reticulum Stress Response and Promote the Death of Avian Retinal Müller Cells in Culture
by Ana Lúcia Marques Ventura, Thayane Martins Silva and Guilherme Rapozeiro França
Brain Sci. 2025, 15(3), 291; https://doi.org/10.3390/brainsci15030291 - 10 Mar 2025
Viewed by 668
Abstract
Background/Objectives: Activation of cannabinoid CB1 or CB2 receptors induces the death of glial progenitors from the chick retina in culture. Here, by using an enriched retinal glial cell culture, we characterized some mechanisms underlying glial death promoted by cannabinoids. Methods and Results: Retinal [...] Read more.
Background/Objectives: Activation of cannabinoid CB1 or CB2 receptors induces the death of glial progenitors from the chick retina in culture. Here, by using an enriched retinal glial cell culture, we characterized some mechanisms underlying glial death promoted by cannabinoids. Methods and Results: Retinal cultures obtained from 8-day-old (E8) chick embryos and maintained for 12–15 days (C12–15) were used. MTT assays revealed that the CB1/CB2 agonist WIN 55,212-2 (WIN) decreased cell viability in the cultures in a time-dependent manner, with a concomitant increase in extracellular LDH activity, suggesting membrane integrity loss. Cell death was also dose-dependently induced by cannabidiol (CBD), Δ9-tetrahydrocannabinol (THC), and CP55940, another CB1/CB2 agonist. In contrast to WIN-induced cell death that was not blocked by either antagonist, the deleterious effect of CBD was blocked by the CB2 receptor antagonist SR144528, but not by PF514273, a CB1 receptor antagonist. WIN-treated cultures showed glial cells with large vacuoles in cytoplasm that were absent in cultures incubated with WIN plus 4-phenyl-butyrate (PBA), a chemical chaperone. Since cannabinoids induced the phosphorylation of eukaryotic initiation factor 2-alfa (eIF2α), these results suggest a process of endoplasmic reticulum (ER) swelling and stress. Incubation of the cultures with WIN for 4 h induced a ~five-fold increase in the number of cells labeled with the ROS indicator CM-H2DCFDA. WIN induced the phosphorylation of JNK but not of p38 in the cultures, and also induced an increase in the number of glial cells expressing cleaved-caspase 3 (c-CASP3). The decrease in cell viability and the expression of c-CASP3 was blocked by salubrinal, an inhibitor of eIF2α dephosphorylation. Conclusions: These data suggest that cannabinoids induce the apoptosis of glial cells in culture by promoting ROS production, ER stress, JNK phosphorylation, and caspase-3 processing. The graphical abstract was created at Biorender.com. Full article
(This article belongs to the Special Issue Retinal Neurochemistry and Development)
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Graphical abstract

14 pages, 4556 KiB  
Article
Ouabain Counteracts Retinal Ganglion Cell Death Through Modulation of BDNF and IL-1 Signaling Pathways
by Amanda Candida da Rocha Oliveira, Camila Saggioro Figueiredo, Ícaro Raony, Juliana Salles Von-Held-Ventura, Marcelo Gomes Granja, Thalita Mázala-de-Oliveira, Vinícius Henrique Pedrosa-Soares, Aline Araujo dos Santos and Elizabeth Giestal-de-Araujo
Brain Sci. 2025, 15(2), 123; https://doi.org/10.3390/brainsci15020123 - 26 Jan 2025
Viewed by 899
Abstract
Background: Ouabain is a steroid hormone that binds to the sodium pump (Na+, K+-ATPase) at physiological (nanomolar) concentrations, activating different signaling pathways. This interaction has been shown to prevent the axotomy-induced death of retinal ganglion cells (RGCs), although the [...] Read more.
Background: Ouabain is a steroid hormone that binds to the sodium pump (Na+, K+-ATPase) at physiological (nanomolar) concentrations, activating different signaling pathways. This interaction has been shown to prevent the axotomy-induced death of retinal ganglion cells (RGCs), although the underlying mechanisms remain unclear. Objective: In this study, we investigated potential mechanisms by which ouabain promotes RGC survival using primary cultures of rat neural retina. Results: Our findings indicate that ouabain regulates brain-derived neurotrophic factor (BDNF) signaling in retinal cells via matrix metalloproteinase-9-mediated processing of proBDNF to mature BDNF (mBDNF) and by increasing the phosphorylation of the mBDNF receptor, tropomyosin-related receptor kinase B. Ouabain also enhances the maturation of interleukin (IL)-1β through the increased activation of caspase-1, which mediates the processing of proIL-1β into IL-1β, and transiently upregulates both IL-1 receptor and IL-1 receptor antagonist (IL-1Ra). Treatment using either IL-1β or IL-1Ra alone is sufficient to enhance RGC survival similarly to that achieved with ouabain. Finally, we further show that ouabain prevents RGC death through a complex signaling mechanism shared by BDNF and IL-1β, which includes the activation of the Src and protein kinase C pathways. Conclusions: Collectively, these results suggest that ouabain stimulates the maturation and signaling of both BDNF and IL-1β, which act as key mediators of RGC survival. Full article
(This article belongs to the Special Issue Retinal Neurochemistry and Development)
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