EFFICIENCIES OF BIPOLAR CELLS

There is a great potential of energy saving in bipolar cells. Based on research for several years, a theoretical analysis of energy saving in bipolar cells is given, and some practical data presented.

Postnatal development of rat retina:a continuous observation and comparison between the organotypic retinal explant model and in vivo development

The organotypic retinal explant culture has been established for more than a decade and offers a range of unique advantages compared with in vivo experiments and cell cultures.However,the lack of systematic and continuous comparison between in vivo retinal development and the organotypic retinal explant culture makes this model controversial in postnatal retinal development studies.Thus,we aimed to verify the feasibility of using this model for postnatal retinal development studies by comparing it with the in vivo retina.In this study,we showed that postnatal retinal explants undergo normal development,and exhibit a consistent structure and timeline with retinas in vivo.Initially,we used SOX2 and PAX6 immunostaining to identify retinal progenitor cells.We then examined cell proliferation and migration by immunostaining with Ki-67 and doublecortin,respectively.Ki-67-and doublecortin-positive cells decreased in both in vivo and explants during postnatal retinogenesis,and exhibited a high degree of similarity in abundance and distribution between groups.Additionally,we used Ceh-10 homeodomain-containing homolog,glutamate-ammonia ligase(glutamine synthetase),neuronal nuclei,and ionized calcium-binding adapter molecule 1 immunostaining to examine the emergence of bipolar cells,Müller glia,mature neurons,and microglia,respectively.The timing and spatial patterns of the emergence of these cell types were remarkably consistent between in vivo and explant retinas.Our study showed that the organotypic retinal explant culture model had a high degree of consistency with the progression of in vivo early postnatal retina development.The findings confirm the accuracy and credibility of this model and support its use for long-term,systematic,and continuous observation.

Two mathematical frameworks for vesicle release from a ribbon synapse of a retinal bipolar cell

Objective:bipolar cells(BCs)communicate with amacrine and ganglion cells of the retina via both transient and sustained neurotransmitter release in ribbon synapses.Reconstructing the published quantitative release data from electrical soma stimulation(voltage clamp experiments)of rat rod BCs were used to develop two simple models to predict the number of released vesicles as time series.In the experiment,the currents coming to the All amacrine cell originating from releasing vesicles from the rod BC were recorded using paired-recordings in whole-cell voltage-clamp method.Method:one of the models is based directly on terminal transmembrane voltage,so-called ‘model’,whereas the temporally exacter modelCa includes changes of intracellular calcium concentrations at terminals.Result:the intracellular calcium concentration method replicates a 0.43 ms signal delay for the transient release to pulsatile stimulation as a consequence of calcium channel dynamics in the presynaptic membrane,while the modelV has no signal delay.Both models produce the quite similar results in low stimuli amplitudes.However,for large stimulation intensities that may be done during extracellular stimulations in retinal implants,the modelCa predicts that the reversal potential of calcium limits the number of transiently released vesicles.Adding sodium and potassium ion channels to the axon of the cell enable to study the impact of spikes on the transient release in BC ribbons.Conclusion:a spike elicited by somatic stimulation causes the rapid release of all vesicles that are available for transient release,while a non-spiking BC with a similar morphometry needs stronger stimuli for any transient vesicle release.During extracellular stimulation,there was almost no difference in transient release between the active and passive cells because in both cases the terminal membrane of the cell senses the same potentials originating from the microelectrode.An exception was found for long pulses when the spike has the possibility to generate a higher terminal voltage than the passive cell.Simulated periodic 5 Hz stimulation showed a reduced transient release of 3 vesicles per stimulus,which is a recovery effect.

Conductive and corrosion behaviors of silver-doped carbon-coated stainless steel as PEMFC bipolar plates

Ni–Cr enrichment on stainless steel SS316 L resulting from chemical activation enabled the deposition of carbon by spraying a stable suspension of carbon nanoparticles; trace Ag was deposited in situ to prepare a thin continuous Ag-doped carbon film on a porous carbon-coated SS316 L substrate. The corrosion resistance of this film in 0.5 mol·L^（-1） H_2SO_4 solution containing 5 ppm F- at 80°C was investigated using polarization tests. The results showed that the surface treatment of the SS316 L strongly affected the adhesion of the carbon coating to the stainless steel. Compared to the bare SS316 L, the Ag-doped carbon-coated SS316 L bipolar plate was remarkably more stable in both the anode and cathode environments of proton exchange membrane fuel cell（PEMFC） and the interface contact resistance between the specimen and Toray 060 carbon paper was reduced from 333.0 m？·cm^2 to 21.6 m？·cm^2 at a compaction pressure of 1.2 MPa.

HYDRAULIC MODEL OF A NEW BIPOLAR CELL FOR ALUMINUM PRODUCTION

The electrolyte circulations in monopolar cell and two-compartment bipolar cell with submerged electrodes were described by a hydraulic model.The influence of current density,electrode tilt,anode-cathode distance(ACD)and immersion depth of electrodes on the electrolyte circulation velocities between electrodes had been studied.Results demonstrated that the flow rates in the two compartments of bipolar cell were very different,which provided important information for the structure design of bipolar cell.

Optimal transcorneal electrical stimulation parameters for preserving photoreceptors in a mouse model of retinitis pigmentosa

Retinitis pigmentosa is a hereditary retinal disease that affects rod and cone photoreceptors,leading to progressive photoreceptor loss.Previous research supports the beneficial effect of electrical stimulation on photoreceptor survival.This study aims to identify the most effective electrical stimulation parameters and functional advantages of transcorneal electrical stimulation(tcES)in mice affected by inherited retinal degeneration.Additionally,the study seeked to analyze the electric field that reaches the retina in both eyes in mice and post-mortem humans.In this study,we recorded waveforms and voltages directed to the retina during transcorneal electrical stimulation in C57BL/6J mice using an intraocular needle probe with rectangular,sine,and ramp waveforms.To investigate the functional effects of electrical stimulation on photoreceptors,we used human retinal explant cultures and rhodopsin knockout(Rho^(-/-))mice,demonstrating progressive photoreceptor degeneration with age.Human retinal explants isolated from the donors’eyes were then subjected to electrical stimulation and cultured for 48 hours to simulate the neurodegenerative environment in vitro.Photoreceptor density was evaluated by rhodopsin immunolabeling.In vivo Rho^(-/-)mice were subjected to two 5-day series of daily transcorneal electrical stimulation using rectangular and ramp waveforms.Retinal function and visual perception of mice were evaluated by electroretinography and optomotor response(OMR),respectively.Immunolabeling was used to assess the morphological and biochemical changes of the photoreceptor and bipolar cells in mouse retinas.Oscilloscope recordings indicated effective delivery of rectangular,sine,and ramp waveforms to the retina by transcorneal electrical stimulation,of which the ramp waveform required the lowest voltage.Evaluation of the total conductive resistance of the post-mortem human compared to the mouse eyes indicated higher cornea-to-retina resistance in human eyes.The temperature recordings during and after electrical stimulation indicated no significant temperature change in vivo and only a subtle temperature increase in vitro(~0.5-1.5°C).Electrical stimulation increased photoreceptor survival in human retinal explant cultures,particularly at the ramp waveform.Transcorneal electrical stimulation(rectangular+ramp)waveforms significantly improved the survival and function of S and M-cones and enhanced visual acuity based on the optomotor response results.Histology and immunolabeling demonstrated increased photoreceptor survival,improved outer nuclear layer thickness,and increased bipolar cell sprouting in Rho^(-/-)mice.These results indicate that transcorneal electrical stimulation effectively delivers the electrical field to the retina,improves photoreceptor survival in both human and mouse retinas,and increases visual function in Rho^(-/-)mice.Combined rectangular and ramp waveform stimulation can promote photoreceptor survival in a minimally invasive fashion.

Neural and Müller glial adaptation of the retina to photoreceptor degeneration

The majority of inherited retinal degenerative diseases and dry age-related macular degeneration are characterized by decay of the outer retina and photoreceptors,which leads to progressive loss of vision.The inner retina,including second-and third-order retinal neurons,also shows aberrant structural changes at all stages of degeneration.Müller glia,the major glial cells maintain retinal homeostasis,activating and rearranging immediately in response to photoreceptor stress.These phenomena are collectively known as retinal remodeling and are anatomically well described,but their impact on visual function is less well characterized.Retinal remodeling has traditionally been considered a detrimental chain of events that decreases visual function.However,emerging evidence from functional assays suggests that remodeling could also be a part of a survival mechanism wherein the inner retina responds plastically to outer retinal degeneration.The visual system’s first synapses between the photoreceptors and bipolar cells undergo rewiring and functionally compensate to maintain normal signal output to the brain.Distinct classes of retinal ganglion cells remain even after the massive loss of photoreceptors.Müller glia possess the regenerative potential for retinal recovery and possibly exert adaptive transcriptional changes in response to neuronal loss.These types of homeostatic changes could potentially explain the well-maintained visual function observed in patients with inherited retinal degenerative diseases who display prominent anatomic retinal pathology.This review will focus on our current understanding of retinal neuronal and Müller glial adaptation for the potential preservation of retinal activity during photoreceptor degeneration.Targeting retinal self-compensatory responses could help generate universal strategies to delay sensory disease progression.

Roles of the ocular pressure, pressure-sensitive ion channel, and elasticity in pressure-induced retinal diseases

The intraocular pressure inside the human eye maintains 10–21 mmHg above the atmospheric pressure.Elevation of intraocular pressure is highly correlated with the retinopathy in glaucoma,and changes in the exterior pressure during mountain hiking,air traveling,and diving may also induce vision decline and retinopathy.The pathophysiological mechanism of these pressure-induced retinal disorders has not been completely clear.Retinal neurons express pressure-sensitive channels intrinsically sensitive to pressure and membrane stretch,such as the transient receptor potential channel(TRP)family permeable to Ca^2+and Na^+and the two-pore domain K channel family.Recent data have shown that pressure excites the primate retinal bipolar cell by opening TRP vanilloid 4 to mediate transient depolarizing currents,and TRP vanilloid 4 agonists enhance the membrane excitability of primate retinal ganglion cells.The eyeball wall is constructed primarily by the sclera and cornea of low elasticity,and the flow rate of the aqueous humor and intraocular pressure both fluctuate,but the mathematical relationship between the ocular elasticity,aqueous humor volume,and intraocular pressure has not been established.This review will briefly review recent literature on the pressure-related retinal pathophysiology in glaucoma and other pressure-induced retinal disorders,the elasticity of ocular tissues,and pressure-sensitive cation channels in retinal neurons.Emerging data support the global volume and the elasticity and thickness of the sclera and cornea as variables to affect the intraocular pressure level like the volume of the aqueous humor.Recent results also suggest some potential routes for TRPs to mediate retinal ganglion cell dysfunction:TRP opening upon intraocular pressure elevation and membrane stretch,enhancing glutamate release from bipolar cells,increasing intracellular Na^+,Ca^2+concentration in retinal ganglion cells and extracellular glutamate concentration,inactivating voltage-gated Na^+channels,and causing excitotoxicity and dysfunction of retinal ganglion cells.Further studies on these routes likely identify novel targets and therapeutic strategies for the treatment of pressure-induced retinal disorders.