Pre-synaptic Neuronal Changes of AII Amacrine Cells in the Streptozotocin-induced Diabetic Rat Retina / 대한해부학회지

It has been previously reported that parvalbumin expression was downregulated in AII amacrine cells, while upregulated in a subset of cone bipolar cells electrically synapse with AII amacrine cell in the streptozotocin-induced diabetic rat retina. In the present study, we aimed to trace biochemical changes of pre-synaptic neurons to AII amacrine cells in rat retina following diabetic injury. Diabetic condition was induced by streptozotocin injection into Sprague-Dawley rats aged of 8 weeks. The experimental term of induced diabetes was set at 1, 4, 12 and 24 weeks. Changes of pre-synaptic neurons were evaluated by immunohistochemistry and Western blot analysis with anti-protein kinase C (PKC)-alpha and anti-tyrosine hydroxylase (TH) antibodies. Rod bipolar cells immunolocalized with PKC-alpha antibody extended their enlarged axon terminals into stratum 5 of the inner plexiform layer. In later diabetes, the axon was shorten and its terminals of rod bipolar cell are slightly enlarged. The protein levels of PKC-alpha were slightly increased along with the duration of diabetes. TH immunoreactive neurons are morphologically classified into two subtypes of amacrine cells in the inner nuclear layer: one (type 1) has large soma with long and primary dendrites, classified with dopaminergic, and the other (type 2) has small soma with dendritic arborization. In the outermost inner plexiform layer, ring-like structures being composed of type 1 cell processes were densely distributed. In diabetic retina, the intensity of TH immunoreactivity in type 1 neurons was reduced. In accordance with morphological changes, the protein levels of TH were reduced during diabetes. These results demonstrate that TH immunoreactive dopaminergic amacrine cells are more susceptible to diabetic injury than the rod bipolar cells in the rat retina and may suggest that downregulation of parvalbumin expression in AII amacrine cells of diabetic retina is mainly due to dysfunction of pre-synaptic dopaminergic amacrine cells.

Immunocytochemical Study on the Development of the Rod Pathway in the Rat Retina / 대한해부학회지

Rod bipolar cells constitute the second-order neuron in the rod pathway. Previous investigations of the rat retina have evaluated the development of other components of the rod pathway namely the AII amacrine cell and GABAergic amacrine cell populations. To gain further insights into the maturation of this retinal circuitry, we studied the development of rod bipolar cells, immunocytochemistry with antibodies directed to the protein kinase C (PKC), in the rat retina. PKC immunoreactivity first appeared in postnatal day 9 (P9), faint PKC immunoreactivity was observed in the cell bodies located at the distal inner nuclear layer (INL), dendrites in the outer plexiform layer (OPL) and immunoreactive bands in the proximal inner plexiform layer (IPL). PKC immunoreactive cells and terminal bulbs at P10 show stronger immunostaining. At P15, the time of eye opening, PKC immunoreactive cells display stronger immunostaining than those of P10 and more mature characteristics like in the adult retina. Double fluorescence immunocytochemistry using an antiserum against parvalbumin, a marker for the AII amacrine cells, or GABA revealed that PKC immunoreactive rod bipolar cell terminals make contact with AII amacrine cells and GABAergic neurons in the proximal IPL from P9. Given these results, the different components of the rod pathway follow a similar pattern of maturation, presumably allowing the rod pathway to function at the early developmental stage of retina.