Age‐related macular degeneration (AMD) is a well‐characterized and extensively studied disease. It is currently considered the leading cause of visual disability among patients over 60 years. The hallmark of early AMD is the formation of drusen, pigmentary changes at the macula, and mild to moderate vision loss. There are two forms of AMD: the “dry” and the “wet” form that is less frequent but is responsible for 90% of acute blindness due to AMD. Risk factors have been associated with AMD progression, and they are taking relevance to understand how AMD develops: (1) advanced age and the exposition to environmental factors inducing high levels of oxidative stress damaging the macula and (2) this damage, which causes inflammation inducing a vicious cycle, altogether causing central vision loss. There is neither a cure nor treatment to prevent AMD. However, there are some treatments available for the wet form of AMD. This article will review some molecular and cellular mechanisms associated with the onset of AMD focusing on feasible treatments for each related factor in the development of this pathology such as vascular endothelial growth factor, oxidative stress, failure of the clearance of proteins and organelles, and glial cell dysfunction in AMD.

Taurine is a β-amino acid present in high concentrations in different areas of the mammalian central nervous system (CNS). It participates in different physiological processes such as osmoregulation, signal transduction, antioxidant activity, trophic factor activity, modulation of calcium movements and neurotransmission. It is known that taurine is an agonist of GABA_A receptors, and their affinity depends of the subunits that conform this receptor. GABA is the main inhibitory neurotransmitter of the CNS and exerts its effect through the activation of two types of specific receptors, called GABA_A and GABA_B. In the last years, changes in the expression pattern of the GABA_A receptors subunits has been related to pathologies, such as epilepsy, depression and alcoholism, among others. This changes in the GABA_A receptors conformation might be responsible of the loss in the effectiveness of the different drugs used in clinic protocols. Therefore, considering the physiological properties of taurine and the capacity to interact with GABA_A receptors conformed by different subunits combinations, it is clear their great potential for the design of new pharmacological strategies aimed to treat the pathologies where GABA has shown a relevant participation.

Müller cells are the most abundant glial cells in the mammalian retina. Their morphology and metabolism enable them to be in close contact and interact biochemically and physically with almost all retinal cell types, including neurons, pericytes, endothelial cells, and other glial cells, influencing their physiology by releasing bioactive molecules. Studies indicate that Müller glial cells are the primary source of angiogenic growth factor secretion in the neuroretina. Because of this, over the past decade, it has been postulated that Müller glial cells play a significant role in maintaining retinal vascular homeostasis, with potential implications in vasoproliferative retinopathies. This review aims to summarize the current understanding of the mechanisms by which Müller glial cells influence retinal angiogenesis in health and disease, with a particular emphasis on three of the retinopathies with the most significant impact on visual health worldwide: diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration.

Brain edema is a pathological condition with potentially fatal consequences, related to cerebral injuries such as ischemia, chronic renal failure, uremia, and diabetes, among others. Under these pathological states, the cell volume control processes are fully compromised, because brain cells are unable to regulate the movement of water, mainly regulated by osmotic gradients. The processes involved in cell volume regulation are homeostatic mechanisms that depend on the mobilization of osmolytes (ions, organic molecules, and polyols) in the necessary direction to counteract changes in osmolyte concentration in response to water movement. The expression and coordinated function of proteins related to the cell volume regulation process, such as water channels, ion channels, and other cotransport systems in the glial cells, and considering the glial cell proportion compared to neuronal cells, leads to consider the astroglial network the main regulatory unit for water homeostasis in the central nervous system (CNS). In the last decade, several studies highlighted the pivotal role of glia in the cell volume regulation process and water homeostasis in the brain, including the retina; any malfunction of this astroglial network generates a lack of the ability to regulate the osmotic changes and water movements and consequently exacerbates the pathological condition.

Neurogenesis, the formation of new neurons in the brain, occurs throughout the lifespan in the subgranular zone of the dentate gyrus and subventricular zone (SVZ) lining the lateral ventricles of the mammal brain. In this process, gamma-aminobutyric acid (GABA) and its ionotropic receptor, the GABA_A receptor (GABA_AR), play a critical role in the proliferation, differentiation, and migration process of neural stem/progenitor cells (NPC). Taurine, a non-essential amino acid widely distributed throughout the central nervous system, increases the proliferation of SVZ progenitor cells by a mechanism that may involve GABA_AR activation. Therefore, we characterized the effects of taurine on the differentiation process of NPC expressing GABA_AR. Preincubation of NPC-SVZ with taurine increased microtubule-stabilizing proteins assessed with the doublecortin assay. Taurine, like GABA, stimulated a neuronal-like morphology of NPC-SVZ and increased the number and length of primary, secondary, and tertiary neurites compared with control NPC of the SVZ. Furthermore, neurite outgrowth was prevented when simultaneously incubating cells with taurine or GABA and the GABA_AR blocker, picrotoxin. Patch-clamp recordings revealed a series of modifications in the NPCs’ passive and active electrophysiological properties exposed to taurine, including regenerative spikes with kinetic properties similar to the action potentials of functional neurons.

Gamma‐aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system (CNS). The biological effects of GABA are mediated by activating its receptors, GABA_A or GABA_B, which are distributed across various tissues, predominantly in the brain and retina. The retina is a neural tissue responsible for receiving and transducing light stimuli. Within this tissue, GABA receptors (GABARs) primarily mediate lateral inhibition in the retina. In recent years, several studies have focused on elucidating the potential role of GABARs in retinal diseases, such as diabetic retinopathy (DR), retinitis pigmentosa (RP), glaucoma, and age‐related macular degeneration (AMD). This review aims to present the most significant findings from recent years regarding the involvement of GABA receptors in retinal pathologies. Additionally, it highlights the potential of GABA receptors as targets for developing precise therapies or adjunctive strategies for treating retinal diseases.