No abstract

Mouse models of retinal degeneration are useful tools to study therapeutic approaches for patients affected by hereditary retinal dystrophies. We have studied degeneration in the rd10 mice both by immunocytochemistry and TUNEL-labeling of retinal cells, and through electrophysiological recordings. The cell degeneration in the retina of rd10 mice produced appreciable morphological changes in rod and cone cells by P20. Retinal cell death is clearly observed in the central retina and it peaked at P25 when there were 800 TUNEL-positive cells per mm(2). In the central retina, only one row of photoreceptors remained in the outer nuclear layer by P40 and there was a remarkable deterioration of bipolar cell dendrites postsynaptic to photoreceptors. The axon terminals of bipolar cells also underwent atrophy and the inner retina was subject to further changes, including a reduction and disorganization of AII amacrine cell population. Glutamate sensitivity was tested in rod bipolar cells with the single cell patch-clamp technique in slice preparations, although at P60 no significant differences were observed with age-matched controls. Thus, we conclude that rod and cone degeneration in the rd10 mouse model is followed by deterioration of their postsynaptic cells and the cells in the inner retina. However, the functional preservation of receptors for photoreceptor transmission in bipolar cells may open new therapeutic possibilities.

No abstract

The dopaminergic amacrine cells of the cat retina have been stained by immunocytochemistry using an antibody to tyrosine hydroxylase (Toh). The complete population of Toh+ cells has been studied by light microscopy of retinal wholemounts to evaluate morphological details of dendritic structure and branching patterns. Selected Toh+ amacrine cells have been studied by serial-section electron microscopy to analyse synaptic input and output relationships. The majority of Toh+ amacrine cells occur in the amacrine cell layer of the retina and have their dendrites ramifying and forming the characteristic rings in stratum 1 of the inner plexiform layer. A minority of Toh+ cells have cell bodies displaced to the ganglion cell layer but their dendrites also stratify in stratum 1. All Toh+ cells have some dendritic branches running in stratum 2 as well as in stratum 1, and frequently they have long 'axon-like' processes (500-1000 microns long) dipping down to run in stratum 5 before passing up to rejoin the major dendritic arbors in stratum 1. In addition Toh+ stained processes follow blood vessels in the inner plexiform layer and in the ganglion cell layer. A population of Toh+ cells found in the inferior retina appears to give rise to stained processes that pass to the outer plexiform layer and therein to run for as far as one millimeter. Electron microscopy reveals that Toh+ amacrine cells are postsynaptic to amacrine cells and a few bipolar cell terminals in stratum 1 of the inner plexiform layer and are primarily presynaptic to AII amacrine cell bodies and lobular appendages, and to another type of amacrine cell body and amacrine dendrites hypothesized to be the A17 amacrine cell. The Toh+ dendrites in stratum 2 are presynaptic to AII lobular appendages primarily. Stained 'axon-like' processes running in stratum 5 prove to be presynaptic to AII amacrine dendrites as they approach the rod bipolar axon terminals and they may also be presynaptic to the rod bipolar terminal itself. The Toh+ stained dendrites that have been followed in the outer plexiform layer run along the top of the B-type horizontal cell somata and may have small synapses upon them. The only clear synapses seen in the outer plexiform layer are from the Toh+ profiles upon vesicle filled amacrine-like profiles that are in turn presynaptic to bipolar cell dendrites in the outer plexiform layer. We presume the cells postsynaptic to the Toh+ dendrites in the outer plexiform layer are interplexiform cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Discomfort in dry eye is possibly caused by an augmented ongoing activity in corneal cold neurons secondary to dryness-induced alterations in sodium and potassium channel expression.