Potential Oscillations Research Articles

Oscillating Utopias

The paper focuses on two literary periods located at opposite ends of the twentieth century and examines the relationship between utopian ideas of Victorian fin de siècle and the re-emergence of utopian desires within a metamodernist context. The two periods discussed, while separated by a century of what is typically understood as progress, are both permeated by impending change and in dire need of alternatives to their respective forms of capitalism, making the appearance of utopian discourse almost inevitable. While their understanding of utopia certainly differs in many aspects, I will argue that they both recognize its oscillatory potential and neither focuses on bare facilitation of escapism or provision of blueprints, instead consciously employing hope-based utopian impulses as a method and a process by means of which various alternatives can be continuously investigated.

Trophoblast glycoprotein is required for efficient synaptic vesicle exocytosis from retinal rod bipolar cells.

Rod bipolar cells (RBCs) faithfully transmit light-driven signals from rod photoreceptors in the outer retina to third order neurons in the inner retina. Recently, significant work has focused on the role of leucine-rich repeat (LRR) proteins in synaptic development and signal transduction at RBC synapses. We previously identified trophoblast glycoprotein (TPBG) as a novel transmembrane LRR protein localized to the dendrites and axon terminals of RBCs. We examined the effects on RBC physiology and retinal processing of TPBG genetic knockout in mice using immunofluorescence and electron microscopy, electroretinogram recording, patch-clamp electrophysiology, and time-resolved membrane capacitance measurements. The scotopic electroretinogram showed a modest increase in the b-wave and a marked attenuation in oscillatory potentials in the TPBG knockout. No effect of TPBG knockout was observed on the RBC dendritic morphology, TRPM1 currents, or RBC excitability. Because scotopic oscillatory potentials primarily reflect RBC-driven rhythmic activity of the inner retina, we investigated the contribution of TPBG to downstream transmission from RBCs to third-order neurons. Using electron microscopy, we found shorter synaptic ribbons in TPBG knockout axon terminals in RBCs. Time-resolved capacitance measurements indicated that TPBG knockout reduces synaptic vesicle exocytosis and subsequent GABAergic reciprocal feedback without altering voltage-gated Ca2+ currents. TPBG is required for normal synaptic ribbon development and efficient neurotransmitter release from RBCs to downstream cells. Our results highlight a novel synaptic role for TPBG at RBC ribbon synapses and support further examination into the mechanisms by which TPBG regulates RBC physiology and circuit function.

GSK840 Alleviates Retinal Neuronal Injury by Inhibiting RIPK3/MLKL-Mediated RGC Necroptosis After Ischemia/Reperfusion.

This study aimed to explore the impact of GSK840 on retinal neuronal injury after retinal ischemia/reperfusion (IR) and its associated mechanism. We established an in vivo mouse model of IR and an in vitro model of oxygen and glucose deprivation/reoxygenation (OGDR) in primary mouse retinal ganglion cells (RGCs). GSK840, a small-molecule compound, was used to specifically inhibit RIPK3/MLKL-dependent necroptosis. Retinal structure and function evaluation was performed by using hematoxylin and eosin staining, optical coherence tomography, and electroretinography. Propidium Iodide (PI) staining was used for detection of necroptotic cell death, whereas Western blot analysis and immunofluorescence were used to assess necroptosis-related proteins and inner retinal neurons. RIPK3/MLKL-dependent necroptosis was rapidly activated in RGCs following retinal IR or OGDR. GSK840 helped maintain relatively normal inner retinal structure and thickness by preserving inner retinal neurons, particularly RGCs. Meanwhile, GSK840 ameliorated IR-induced visual dysfunction, as evidenced by the improved amplitudes of photopic negative response, a-wave, b-wave, and oscillatory potentials. And GSK840 treatment significantly reduced the population of PI+ RGCs after injury. Mechanistically, GSK840 ameliorated RGC necroptosis by inhibiting the RIPK3/MLKL pathway. GSK840 exerts protective effects against retinal neuronal injury after IR by inhibiting RIPK3/MLKL-mediated RGC necroptosis. GSK840 may represent a protective strategy for RGC degeneration in ischemic retinopathy.

Exact solution of three dimensional schrödinger equation with power function superposition potential.

Finding an analytical solution to the Schrödinger equation with power function superposition potential is essential for the development of quantum theory. For example, the harmonic oscillator potential, Coulomb potential, and Klazer potential are all classed as power function superposition potentials. In this study, the general form of the power function superposition potential was used to decompose the second-order radial Schrödinger equation with this potential into the first-order Ricatti equation. Furthermore, two forms of the power function superposition potential are constructed with an exact analytical solution, and the exact bound-state energy level formula is obtained for these two potentials. Finally, the energy levels of some of the diatomic molecules were determined through calculation. And our results are actually consistent with those obtained by other methods.

Respiratory rhythm modulates membrane potential and spiking of nonolfactory neurons.

In recent years, several studies have shown a respiratory drive of the local field potential (LFP) in numerous brain areas so that the respiratory rhythm could be considered as a master clock promoting communication between distant brain locations. However, outside of the olfactory system, it remains unknown whether the respiratory rhythm could shape membrane potential (MP) oscillations. To fill this gap, we co-recorded MP and LFP activities in different nonolfactory brain areas, medial prefrontal cortex (mPFC), primary somatosensory cortex (S1), primary visual cortex (V1), and hippocampus (HPC), in urethane-anesthetized rats. Using respiratory cycle-by-cycle analysis, we observed that respiration could modulate both MP and spiking discharges in all recorded areas during episodes that we called respiration-related oscillations (RRo). Further quantifications revealed that RRo episodes were transient in most neurons (5 consecutive respiratory cycles in average). RRo development in MP was largely correlated with the presence of respiratory modulation in the LFP. By showing that the respiratory rhythm influenced brain activities deep to the MP of nonolfactory neurons, our data support the idea that respiratory rhythm could mediate long-range communication between brain areas.NEW & NOTEWORTHY In this study, we evidenced strong respiratory-driven oscillations of neuronal membrane potential and spiking discharge in various nonolfactory areas of the mammal brain. These oscillations were found in the medial prefrontal cortex, primary somatosensory cortex, primary visual cortex, and hippocampus. These findings support the idea that respiratory rhythm could be used as a common clock to set the dynamics of large-scale neuronal networks on the same slow rhythm.

Calcium-Sensitive Subthreshold Oscillations and Electrical Coupling in Principal Cells of Mouse Dorsal Cochlear Nucleus.

In higher sensory brain regions, slow oscillations (0.5-5 Hz) associated with quiet wakefulness and attention modulate multisensory integration, predictive coding, and perception. Although often assumed to originate via thalamocortical mechanisms, the extent to which subcortical sensory pathways are independently capable of slow oscillatory activity is unclear. We find that in the first station for auditory processing, the cochlear nucleus, fusiform cells from juvenile mice (of either sex) generate robust 1-2 Hz oscillations in membrane potential and exhibit electrical resonance. Such oscillations were absent prior to the onset of hearing, intrinsically generated by hyperpolarization-activated cyclic nucleotide-gated (HCN) and persistent Na+ conductances (NaP) interacting with passive membrane properties, and reflected the intrinsic resonance properties of fusiform cells. Cx36-containing gap junctions facilitated oscillation strength and promoted pairwise synchrony of oscillations between neighboring neurons. The strength of oscillations were strikingly sensitive to external Ca2+, disappearing at concentrations >1.7 mM, due in part to the shunting effect of small-conductance calcium-activated potassium (SK) channels. This effect explains their apparent absence in previous in vitro studies of cochlear nucleus which routinely employed high-Ca2+ extracellular solution. In contrast, oscillations were amplified in reduced Ca2+ solutions, due to relief of suppression by Ca2+ of Na+ channel gating. Our results thus reveal mechanisms for synchronous oscillatory activity in auditory brainstem, suggesting that slow oscillations, and by extension their perceptual effects, may originate at the earliest stages of sensory processing.

Three-dimensional eigenvalues of harmonic oscillator and Coulomb-type potentials from one-dimensional generalized Morse potential: perturbative analysis based on generalized Laguerre polynomials

Three-dimensional eigenvalues of harmonic oscillator and Coulomb-type potentials from one-dimensional generalized Morse potential: perturbative analysis based on generalized Laguerre polynomials

Hippocampal interneuronal dysfunction and hyperexcitability in a porcine model of concussion

Cognitive impairment is a common symptom following mild traumatic brain injury (mTBI or concussion) and can persist for years in some individuals. Hippocampal slice preparations following closed-head, rotational acceleration injury in swine have previously demonstrated reduced axonal function and hippocampal circuitry disruption. However, electrophysiological changes in hippocampal neurons and their subtypes in a large animal mTBI model have not been examined. Using in vivo electrophysiology techniques, we examined laminar oscillatory field potentials and single unit activity in the hippocampal network 7 days post-injury in anesthetized minipigs. Concussion altered the electrophysiological properties of pyramidal cells and interneurons differently in area CA1. While the firing rate, spike width and amplitude of CA1 interneurons were significantly decreased post-mTBI, these parameters were unchanged in CA1 pyramidal neurons. In addition, CA1 pyramidal neurons in TBI animals were less entrained to hippocampal gamma (40–80 Hz) oscillations. Stimulation of the Schaffer collaterals also revealed hyperexcitability across the CA1 lamina post-mTBI. Computational simulations suggest that reported changes in interneuronal physiology may be due to alterations in voltage-gated sodium channels. These data demonstrate that a single concussion can lead to significant neuronal and circuit level changes in the hippocampus, which may contribute to cognitive dysfunction following mTBI.

Integrins regulate hERG1 dynamics by girdin-dependent Gαi3: signaling and modeling in cancer cells.

The hERG1 potassium channel is aberrantly over expressed in tumors and regulates the cancer cell response to integrin-dependent adhesion. We unravel a novel signaling pathway by which integrin engagement by the ECM protein fibronectin promotes hERG1 translocation to the plasma membrane and its association with β1 integrins, by activating girdin-dependent Gαi3 proteins and protein kinase B (Akt). By sequestering hERG1, β1 integrins make it avoid Rab5-mediated endocytosis, where unbound channels are degraded. The cycle of hERG1 expression determines the resting potential (Vrest) oscillations and drives the cortical f-actin dynamics and thus cell motility. To interpret the slow biphasic kinetics of hERG1/β1 integrin interplay, we developed a mathematical model based on a generic balanced inactivation-like module. Integrin-mediated cell adhesion triggers two contrary responses: a rapid stimulation of hERG1/β1 complex formation, followed by a slow inhibition which restores the initial condition. The protracted hERG1/β1 integrin cycle determines the slow time course and cyclic behavior of cell migration in cancer cells.

Vitamin A deficiency retinopathy related to medical interventions in a Swiss cohort: a case series

AIMS OF THE STUDY: Vitamin A deficiency retinopathy is a potentially blinding disease. In developed countries, vitamin A deficiency due to malnutrition is rare. However, vitamin A deficiency can be caused by malabsorption resulting from bowel resection or medication. In this retrospective study, we present five cases of vitamin A deficiency retinopathy related to malabsorption secondary to medical interventions.
 METHODS: Electronic charts over a ten-year period (2012–2022) were screened for vitamin A deficiency retinopathy. Only patients with vitamin A deficiency confirmed by laboratory tests were included. Symptoms, medical history, visual acuity, optical coherence tomography, fundus autofluorescence, electrophysiological examination, and vitamin A levels were reviewed.
 RESULTS: Five eligible cases were identified. Median age was 44.7 years (range 22.2–88.9), median duration of ocular symptoms prior to diagnosis was 14 months, and median visual acuity was 1.0 (range 0.5–1.0, Snellen, decimal). Three patients had a history of bariatric surgery, one patient had a small bowel resection and was on octreotide treatment, and one patient suffered from cystic fibrosis and had a history of small bowel resection and severe hepatopathy. Optical coherence tomography showed various abnormalities, including a reduced interdigitation zone, subretinal drusenoid deposits, and a thinned outer nuclear layer. Electroretinogram findings ranged from abnormal oscillatory potentials to non-recordable rod responses.
 CONCLUSIONS: Vitamin A deficiency retinopathy can occur following medical interventions associated with malabsorption. In cases of night blindness, vitamin A levels should be measured.

Topological defects on the energy spectra of diatomic molecules embedded with shifted Deng–Fan oscillator potential under AB flux field

AbstractA study on the effect of point like global monopole topological defects on the energy eigenvalues of the diatomic molecules , , , embedded with Shifted Deng–Fan Oscillator Potential under the influence of Aharonov–Bohm flux field has been made here. Asymptotic Iteration Method (AIM) is used to find out the bound state solutions for arbitrary states by solving the non‐relativistic Schrödinger equation. A Pekeris‐type approximation has been used to approximate the centrifugal barrier term. It is observed that, energy levels of the diatomic molecules is significantly affected by the global effects of the point like global monopole, flux field and effective potential field.

Advanced insights into gas conversion and diffusion impedance of solid oxide cells by 2D multi-physics modelling

Two-dimensional (2D) multi-physics models of solid oxide cells (SOC) reproduce distributions inside the cell during operation, and allow to implement interdependencies of heat transfer, mass transport, charge transfer, and electrochemistry. So far, this approach has mostly been utilised for transient and steady-state problems, preventing widespread application to electrochemical impedance spectroscopy, one of the main methods in experimentally analysing SOCs. In the present work, a computationally efficient alternative is outlined, surpassing these shortcomings by transforming the set of equations from the transient into the frequency form. The coupled multi-physics implemented by partial differential equations are solved numerically over a 2D domain by the finite element method, reproducing the cross section of the SOC. The model is validated with experimentally obtained polarisation curves and impedance spectra. The 2D model reproduces the experimental results and further visualises frequency-dependent oscillations of gas phase and potentials. These insights separate between impedance features from electrochemistry, gas diffusion, and gas conversion. In addition, overlapping gas conversion and diffusion impedance features at low frequencies are deconvoluted and transition frequency regions are discussed.

A dual-clock-driven model of lymphatic muscle cell pacemaking to emulate knock-out of Ano1 or IP3R.

Lymphatic system defects are involved in a wide range of diseases, including obesity, cardiovascular disease, and neurological disorders, such as Alzheimer's disease. Fluid return through the lymphatic vascular system is primarily provided by contractions of muscle cells in the walls of lymphatic vessels, which are in turn driven by electrochemical oscillations that cause rhythmic action potentials and associated surges in intracellular calcium ion concentration. There is an incomplete understanding of the mechanisms involved in these repeated events, restricting the development of pharmacological treatments for dysfunction. Previously, we proposed a model where autonomous oscillations in the membrane potential (M-clock) drove passive oscillations in the calcium concentration (C-clock). In this paper, to model more accurately what is known about the underlying physiology, we extend this model to the case where the M-clock and the C-clock oscillators are both active but coupled together, thus both driving the action potentials. This extension results from modifications to the model's description of the IP3 receptor, a key C-clock mechanism. The synchronised dual-driving clock behaviour enables the model to match IP3 receptor knock-out data, thus resolving an issue with previous models. We also use phase-plane analysis to explain the mechanisms of coupling of the dual clocks. The model has the potential to help determine mechanisms and find targets for pharmacological treatment of some causes of lymphoedema.

Optical coherence tomography in the diagnosis of glaucomatous optical neuropathy in children with primary congenital glaucoma

Purpose: to analyze morphometric, clinical and functional manifestations of glaucomatous optical neuropathy in congenital childhood glaucoma (CG).Material and methods. We examined 103 children (163 eyes) with (CG), including 54 children (86 eyes) with primary congenital glaucoma (PCG) aged 1 month to 17 years. In addition to the regular ophthalmological examination, we performed optical coherence tomography of the optic nerve head (ONH), flash visual evoked potentials, total and rhythmic electroretinogram, oscillatory potentials (OP), echobiometry of the eye axial length.Results. The thickness of the retinal nerve fiber layer peripapillary (pRNFL) ranged from 32 to 120 μm, averaging 71.67 ± 18.2 μm. The thinning was detected in 83.0% of cases, primarily in the temporal sectors (90.6%). As the condition progressed, a tendency to progressive thinning of the RNFL was detected. The minimum rim width (BMO-MRW) ranged from 87 to 336 μm and was reduced in most children (14 out of 16, 87.5%). A strong inverse correlation of the neuroretinal rim with the depth (r = -0.69) and the width (r = -0.93) of the excavation was detected. Also, a strong direct correlation was established between the minimum neuroretinal rim width reduction and the thickness of the BMO-MRW and pRNFL (r = 0.79), as well as the upper and lower temporal sectors (r = 0.81 and r = 0.88, respectively). The thickness of the ganglion cell (GC) layer varied from 8 to 23 μm and averaged 14.64 ± 4.89 μm, with a reduction recorded in most cases (64.7%). All patients showed a decrease in oscillatory potentials (OP) by 40% or more (6.31 ± 2.33) as compared to the control group (20.24 ± 6.28). Thinning of the RNFL was registered in these eyes in 90.6% of cases averagely (p < 0.05) and in the upper and the lower temporal sectors (p < 0.05).Conclusion. RNFL thickness, the minimal width of the BMO-MRW and the OP are the most sensitive criteria to assess the degree of glaucomatous optic neuropathy in children with PСG. The study of the GC layer thickness can serve as an additional diagnostic criterion of assessing the state of the ONH.

Nfia Is Critical for AII Amacrine Cell Production: Selective Bipolar Cell Dependencies and Diminished ERG.

The nuclear factor one (NFI) transcription factor genes Nfia, Nfib, and Nfix are all enriched in late-stage retinal progenitor cells, and their loss has been shown to retain these progenitors at the expense of later-generated retinal cell types. Whether they play any role in the specification of those later-generated fates is unknown, but the expression of one of these, Nfia, in a specific amacrine cell type may intimate such a role. Here, Nfia conditional knockout (Nfia-CKO) mice (both sexes) were assessed, finding a massive and largely selective absence of AII amacrine cells. There was, however, a partial reduction in type 2 cone bipolar cells (CBCs), being richly interconnected to AII cells. Counts of dying cells showed a significant increase in Nfia-CKO retinas at postnatal day (P)7, after AII cell numbers were already reduced but in advance of the loss of type 2 CBCs detected by P10. Those results suggest a role for Nfia in the specification of the AII amacrine cell fate and a dependency of the type 2 CBCs on them. Delaying the conditional loss of Nfia to the first postnatal week did not alter AII cell number nor differentiation, further suggesting that its role in AII cells is solely associated with their production. The physiological consequences of their loss were assessed using the ERG, finding the oscillatory potentials to be profoundly diminished. A slight reduction in the b-wave was also detected, attributed to an altered distribution of the terminals of rod bipolar cells, implicating a role of the AII amacrine cells in constraining their stratification.SIGNIFICANCE STATEMENT The transcription factor NFIA is shown to play a critical role in the specification of a single type of retinal amacrine cell, the AII cell. Using an Nfia-conditional knockout mouse to eliminate this population of retinal neurons, we demonstrate two selective bipolar cell dependencies on the AII cells; the terminals of rod bipolar cells become mis-stratified in the inner plexiform layer, and one type of cone bipolar cell undergoes enhanced cell death. The physiological consequence of this loss of the AII cells was also assessed, finding the cells to be a major contributor to the oscillatory potentials in the electroretinogram.

Potential Oscillations During Cobalt–Nickel Electrodeposition in the Presence of Butynediol

Potential Oscillations During Cobalt–Nickel Electrodeposition in the Presence of Butynediol

An adaptive, training‐free reduced‐order model for convection‐dominated problems based on hybrid snapshots

AbstractThe vast majority of reduced‐order models (ROMs) first obtain a low dimensional representation of the problem from high‐dimensional model (HDM) training data which is afterwards used to obtain a system of reduced complexity. Unfortunately, convection‐dominated problems generally have a slowly decaying Kolmogorov ‐width, which makes obtaining an accurate ROM built solely from training data very challenging. The accuracy of a ROM can be improved through enrichment with HDM solutions; however, due to the large computational expense of HDM evaluations for complex problems, they can only be used parsimoniously to obtain relevant computational savings. In this work, we exploit the local spatial coherence often exhibited by these problems to derive an accurate, cost‐efficient approach that repeatedly combines HDM and ROM evaluations without a separate training phase. Our approach obtains solutions at a given time step by either fully solving the HDM or by combining partial HDM and ROM solves. A dynamic sampling procedure identifies regions that require the HDM solution for global accuracy and the reminder of the flow is reconstructed using the ROM. Moreover, solutions combining both HDM and ROM solves use spatial filtering to eliminate potential spurious oscillations that may develop. We test the proposed method on inviscid compressible flow problems and demonstrate speedups up to a factor of five.

Lithium metal deposition under the geometrical confinement effect: Dendritic copper foam current collector

Dendrite-free lithium is the ultimate goal in achieving the commercial application of lithium metal anode. In this paper, Dendritic Copper Foam Current Collector (DCFC) is prepared by an electrometallurgy method to realize the homogeneous deposition of lithium metal. The deposition behavior of Cu and Li on different interfaces was studied. Firstly, the Cu dendrites constructed on the surface of Cu foam are induced and formed by the potential oscillation generated by the hydrogen evolution reaction. Secondly, the heterogeneous nucleation model reveals that the reason for the dendrite-free lithium deposition on the dendritic copper foam is the geometrical confinement effect. Compared with commercial copper foam, DCFC with hierarchical structure significantly reduces the nucleation energy and deposition overpotential of lithium metal. The in situ optical microscope observation and finite element simulation results confirm our ideas. Electrochemically, DCFC works stably after 1200 h at a lower potential of 36 mV in a DCFC@Li symmetric battery, which is much superior to 75 mV for just 340 h in Cu foam. The ideal collector with a dendritic structure has broad prospects for the practical application of lithium metal anode.

Electrophysiological Signatures of Visual Recognition Memory across All Layers of Mouse V1.

In mouse primary visual cortex (V1), familiar stimuli evoke significantly altered responses when compared with novel stimuli. This stimulus-selective response plasticity (SRP) was described originally as an increase in the magnitude of visual evoked potentials (VEPs) elicited in layer 4 (L4) by familiar phase-reversing grating stimuli. SRP is dependent on NMDA receptors (NMDARs) and has been hypothesized to reflect potentiation of thalamocortical (TC) synapses in L4. However, recent evidence indicates that the synaptic modifications that manifest as SRP do not occur on L4 principal cells. To shed light on where and how SRP is induced and expressed in male and female mice, the present study had three related aims: (1) to confirm that NMDAR are required specifically in glutamatergic principal neurons of V1, (2) to investigate the consequences of deleting NMDAR specifically in L6, and (3) to use translaminar electrophysiological recordings to characterize SRP expression in different layers of V1. We find that knock-out (KO) of NMDAR in L6 principal neurons disrupts SRP. Current-source density (CSD) analysis of the VEP depth profile shows augmentation of short latency current sinks in layers 3, 4, and 6 in response to phase reversals of familiar stimuli. Multiunit recordings demonstrate that increased peak firing occurs in response to phase reversals of familiar stimuli across all layers, but that activity between phase reversals is suppressed. Together, these data reveal important aspects of the underlying phenomenology of SRP and generate new hypotheses for the expression of experience-dependent plasticity in V1.SIGNIFICANCE STATEMENT Repeated exposure to stimuli that portend neither reward nor punishment leads to behavioral habituation, enabling organisms to dedicate attention to novel or otherwise significant features of the environment. The neural basis of this process, which is so often dysregulated in neurologic and psychiatric disorders, remains poorly understood. Learning and memory of stimulus familiarity can be studied in mouse visual cortex by measuring electrophysiological responses to simple phase-reversing grating stimuli. The current study advances knowledge of this process by documenting changes in visual evoked potentials (VEPs), neuronal spiking activity, and oscillations in the local field potentials (LFPs) across all layers of mouse visual cortex. In addition, we identify a key contribution of a specific population of neurons in layer 6 (L6) of visual cortex.

A hypothermia mimetic molecule (zr17-2) reduces ganglion cell death, gliosis, and electroretinogram distortion in male rats subjected to perinatal asphyxia.

Introduction: Perinatal asphyxia (PA) represents a major problem in perinatology and may cause visual losses, including blindness. We, and others, have shown that hypothermia prevents retinal symptoms associated to PA. In the present work, we evaluate whether a hypothermia mimetic small molecule, zr17-2, has similar effects in the context of PA. Methods: Four experimental groups were studied in male rats: Naturally born rats as controls (CTL), naturally born rats injected s.c. with 50µL of 330nmols/L zr17-2 (ZR), animals that were exposed to PA for 20min at 37°C (PA), and rats that were exposed to PA and injected with zr17-2 (PA-ZR). Forty-five days after treatment, animals were subjected to electroretinography. In addition, morphological techniques (TUNEL, H&E, multiple immunofluorescence) were applied to the retinas. Results: A reduction in the amplitude of the a- and b-wave and oscillatory potentials (OP) of the electroretinogram (ERG) was detected in PA animals. Treatment with zr17-2 resulted in a significant amelioration of these parameters (p < 0.01). In PA animals, a large number of apoptotic cells was found in the GCL. This number was significantly reduced by treatment with the small molecule (p < 0.0001). In a similar way, the thickness of the inner retina and the intensity of GFAP immunoreactivity (gliosis) increased in PA retinas (p < 0.0001). These parameters were corrected by the administration of zr17-2 (p < 0.0001). Furthermore, injection of the small molecule in the absence of PA did not modify the ERG nor the morphological parameters studied, suggesting a lack of toxicity. Discussion: In conclusion, our results indicate that a single s.c. injection of zr17-2 in asphyctic neonates may provide a novel and efficacious method to prevent the visual sequelae of PA.