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Planed frozen-hydrated (FH) bulk biological samples of chicken retina were analysed by X-ray elemental imaging in a scanning electron microscope and reanalysed after freeze-drying in the microscope column. Sequential elemental imaging of the same bulk sample in this way provides improved information on element distributions. There was no evidence of element redistribution during the freeze-drying process. Quantitative elemental images were obtained and interpreted to deduce relative and absolute element concentrations in different regions of the retina. Water concentrations were determined from the difference in oxygen concentrations at 15 kV and 5 kV in FH and freeze-dried (FD) samples, respectively. Two accelerating voltages were used to maintain similar X-ray excitation volumes. Water concentrations were also estimated by relating measured oxygen concentration in FH samples to the concentration of oxygen in solutions of a generalized protein in water and by comparing concentrations of phosphorous or sulphur in the FH and FD states., (© 2011 The Authors Journal of Microscopy © 2011 Royal Microscopical Society.)

Background and Purpose: The nitric oxide system has two proposed sites and mechanisms of action within the ocular growth/refractive compensation platform-neuromodulatory effects on retinal physiology, and vascular/smooth muscle effects in the choroid. The relative contribution of these mechanisms are tested here with drugs that perturb the nitric oxide system and with slow flicker modulation of the ON and OFF pathways of the retina., Experimental Approach: Intravitreal injection of saline or 900 nmol N(G) -nitro-L-arginine methyl ester or L-arginine in saline was followed by monocular defocus with ±10 D lens (or no lens), from days 5-9 under standard diurnal (SD) or daytime 1 Hz ramped flicker conditions. Biometric, electrophysiological and histological analyses were conducted., Key Results: After 4 days of SD conditions, both drugs enhanced electroretinogram (ERG) b-wave cf. d-wave amplitudes compared with saline and reduced refractive compensation to -10 D lenses. Under flicker conditions compensation to +10 D lenses was suppressed. Choroidal thinning was observed in the drug, no lens groups under SD conditions, whereas choroidal thickening was seen in most groups under flicker conditions, irrespective of refractive outcomes., Conclusions and Implications: As choroidal thickness was not predictive of final refractive compensation across any of the variables of drug, defocus sign or light condition, it is unlikely that choroidal thickness is a primary mechanism underlying refractive compensation across the range of parameters of this study. Rather, the changes in refractive compensation observed under these particular drug and light conditions are more likely due to a neuromodulatory action on retinal ON and OFF pathways., (© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.)

Many diverse retinal disorders are characterized by retinal edema; yet, little experimental attention has been given to understanding the fundamental mechanisms underlying and contributing to these fluid-based disorders. Water transport in and out of cells is achieved by specialized membrane channels, with most rapid water transport regulated by transmembrane water channels known as aquaporins (AQPs). The predominant AQP in the mammalian retina is AQP4, which is expressed on the Müller glial cells. Müller cells have previously been shown to modulate neuronal activity by modifying the concentrations of ions, neurotransmitters, and other neuroactive substances within the extracellular space between the inner and the outer limiting membrane. In doing so, Müller cells maintain extracellular homeostasis, especially with regard to the spatial buffering of extracellular potassium (K+) via inward rectifying K+ channels (Kir channels). Recent studies of water transport and the spatial buffering of K+ through glial cells have highlighted the involvement of both AQP4 and Kir channels in regulating the extracellular environment in the brain and retina. As both glial functions are associated with neuronal activation, controversy exists in the literature as to whether the relationship is functionally dependent. It is argued in this review that as AQP4 channels are likely to be the conduit for facilitating fluid homeostasis in the inner retina during light activation, AQP4 channels are also likely to play a consequent role in the regulation of ocular volume and growth. Recent research has already shown that the level of AQP4 expression is associated with environmentally driven manipulations of light activity on the retina and the development of myopia.