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PubMed1989

Changes in the distribution of insulin-like growth factor I, thioredoxin, thioredoxin reductase and ribonucleotide reductase during the development of the retina.

The postnatal development of the rat retina offers good opportunities to follow migration and differentiation of neuroectodermal cells. In this study we have analyzed, by immunohistochemical methods, the distribution of several protein antigens and the trophic peptide insulin-like growth factor I (IGF-I; somatomedin-C). The latter contains disulfide bonds, which in vitro are reduced by the thioredoxin system, i.e. thioredoxin, thioredoxin reductase and NADPH. Ribonucleotide reductase provides growing cells with deoxyribonucleotides, necessary for DNA synthesis, and thioredoxin is an in vitro hydrogen donor. By immunofluorescence IGF-I immunoreactivity was observed throughout the Müller neuroglial cells in the developing retina, but only to a very small extent in the mature retina. Nerve cells showed transient expression of IGF-I during their development. The IGF-I immunoreactivity is likely to be due to local synthesis, since we could demonstrate retinal IGF-I mRNA. Treatment with the transport-blocking agent colchicine caused the Müller glial cells and the retinal pigment epithelium cells to become IGF-I immunoreactive. Thioredoxin and thioredoxin reductase immunoreactivities are confined to neurons and photoreceptor cells in the developing retina. Ribonucleotide reductase subunit M1 immunoreactivity was only observed during the first postnatal week in proliferating neuroectodermal cells. In conclusion, IGF-I and ribonucleotide reductase subunit M1 immunoreactivities are transiently expressed by neuroectodermal cells in the developing rat retina. In contrast, the proteins of the thioredoxin system are demonstrable also in the mature retina.

Animals↗
PubMed1989

Interphotoreceptor retinoid-binding protein (IRBP) in the postnatal developing rds mutant mouse retina: EM immunocytochemical localization.

The distribution of IRBP was examined in postnatal developing retinas of rds (020/A) mutant mice and Balb/c controls by EM immunocytochemistry. Light labeling for IRBP was detected in mutant and control retinas by postnatal day 9 (P9) largely in the interphotoreceptor matrix (IPM). At P14, some photoreceptors in the rds retina showed a higher density of label in the Golgi for IRBP than neighboring cells and those of controls processed simultaneously. This high density of label for IRBP was observed also in the Golgi of a small population of photoreceptor cells at P18, P19 and P21 in rds retinas. These cells were found to represent approximately 3-5% of the photoreceptor population. The density of label for IRBP at the apical RPE region was obviously low in the rds retinas by P18, P19 and P21. However, this same region in controls of the same ages was densely labeled for IRBP. The low density of labeling at the apical RPE region in the rds retinas may indicate a change in the rate of synthesis, secretion, distribution and/or degradation in the IPM. The high density of intracellular labeling in a small population of cells may be indicative of impaired secretion, an increase in IRBP synthesis or the initiation of photoreceptor deterioration. Whether the differences observed in the distribution of IRBP in the rds mutant are primary or secondary effects of the genetic lesion remains undetermined.

Animals↗
PubMed2001

Gradual and partial loss of corner cone-occupied area in the retina of rainbow trout.

Several studies have indicated that the rainbow trout (Oncorhynchus mykiss) loses ultraviolet (UV) sensitivity and the associated UV-sensitive corner cones when the animal transforms from a small (parr) juvenile to a larger, silver-coloured, smolt. Similar changes supposedly take place when parr juveniles are treated with thyroid hormone (T(4)) or retinoic acid. In contrast to previous investigations, this study shows that parr juveniles lack corner cones throughout the lower half of the ventral retina, suggesting that corner cones cease to be incorporated into the ventral retina some time after hatching. This uneven incorporation of corner cones across the retina, when combined with retinal growth, creates a progressively smaller area of lower retina occupied by corner cones. Because in previous studies, the stimulating illumination was directed primarily at the ventral retina, the reported age-dependent changes in UV or polarization sensitivities can be explained by differences in the area of corner cones that was illuminated, and not necessarily by a loss of corner cones. This study also shows: (1) that the double cones from non-ventral mosaics of parr rainbow trout may change in cross-sectional shape, altering the mosaic formation from a square to a row, (2) the existence of a 'pure' (non-changing) square mosaic in the ventral retina, and (3) a potential method, based on differential staining of cone nuclei, to classify paired cones into double or twin cones.

Animals↗
PubMed1999

L-arginine transport in retinas from streptozotocin diabetic rats: correlation with the level of IL-1 beta and NO synthase activity.

Several evidences suggest that the pro-inflammatory cytokines IL-1 beta and the radical NO are implicated as effectors molecules in the pancreatic beta-cells dysfunction; an event preceding the pathogenesis of diabetes. IL-1 beta induces the expression of the inducible isoform of NO synthase (iNOS), which use L-arginine as substrate to overproduce NO. However, it is not known whether these events may participate in the development of diabetic retinopathy, which is the main cause of blindness. In this work, we found an increased level of IL-1 beta in retinas from streptozotocin-induced (STZ) diabetic rats. We also observed that the activity of the NO synthase (NOS) and the L-arginine uptake are enhanced in retinas from STZ-induced diabetic rats as compared to retinas from control rats. We found that the uptake of L-arginine in retinas from control and diabetic rats occurs through a transporter resembling the Y + system, i.e. it is saturable, not affected over the pH range 6.5 to 7.4, and is independent of the extracellular Na+. Nevertheless, the L-arginine transport in retinas from diabetic rats occurs through a carrier with lower affinity (K(m) = 25 microM) and higher capacity (Vmax = 295 +/- 22.4 pmol L-arginine/mg protein) than in retinas from control rats (K(m) = 5 microM and Vmax = 158 +/- 12.8 pmol L-arginine/mg protein) which is correlated with the increased NOS activity and consequent depletion of the intracellular pool of L-arginine.

Animals↗
PubMed1987

Synapse formation in retina is influenced by molecules that identify cell position.

Molecules that identify cell type and position in the nervous system were detected by monoclonal antibodies. One molecule, TOP, is distributed in a 35-fold topographic gradient from the dorsoposterior margin to the ventroanterior margin of avian retina. The gradient is present in young embryos, increases with retinal growth, and persists in the adult. TOP molecules are present on most or all cells of retina. The number of TOP molecules detected per cell varies continuously along the axis of the antigen gradient. Thus, TOP can be used to identify position in the plane of retina along that axis. Other antigens that identify cell type and position across the thickness of retina also were detected. Molecules that mark such cellular organization may represent a neuronal recognition system. Antibodies were used to examine the role of markers of cell position in development of the nervous system. Antibody to TOP from hybridoma cells that were injected into in vivo embryo eyes diffused into the retina and bound in a topographic gradient of Ab.TOP complexes. Synapse formation in retina was inhibited in the presence of anti-TOP antibody. This suggests that TOP is involved in synapse formation and that recognition of position by neurons is necessary for normal synapse formation.

Animals↗
PubMed2000

Connexin expression in the retina.

Here, we review recent results from our laboratory on connexin expression in mouse retina in the context of previous results with other vertebrate species. In mouse retina, four different connexin proteins were detected by immunoblot and immunofluorescence: connexin (Cx)-36, -37, -43 and -45. Cx36 and Cx45 immunoreactive signals were found in the inner and outer plexiform layer, both of which are known to show interneuronal gap junctions. Cx43 was detected in the ganglion cell layer, presumably in astrocytes, where it appeared to be colocalized with glial fibrillary acid protein. Cx37 was expressed in retinal endothelial cells. Additionally, Cx26, -31, -32 and -40 mRNAs were detected in retina by RT-PCR but none of the corresponding proteins were found. In order to exclude cross reactions of the corresponding antibodies, retinae from targeted connexin-deficient mice (Cx31 -/-, Cx32 -/- and Cx40 -/-) were used as negative controls for immunoblot and immunofluorescence analyses of wild-type retina. Further detailed investigation of cell type specific connexin expression in the mouse retina will be necessary for functional analyses of targeted mouse mutants with defects in connexins expressed in retinal neuronal cells.

Animals↗
PubMed2001

Sources and sink of retinoic acid in the embryonic chick retina: distribution of aldehyde dehydrogenase activities, CRABP-I, and sites of retinoic acid inactivation.

Previous experiments in mice and zebrafish led to the hypothesis that an asymmetric distribution of the transcriptional activator retinoic acid (RA) causes ventral-dorsal polarity in the vertebrate eye anlage. A high concentration of RA in the ventral retinal neuroepithelium has been suggested to induce developmental events that finally establish topographic order in the retinotectal projection along the vertical eye axis. In the present study we have investigated potential sources and sinks of RA during embryonic development of the chick retina. At embryonic day (E)1 to E2, when the spatial determination of the eye primordia takes place, no RA synthesis by aldehyde dehydrogenases was detectable, and neither immunoreactivity for retinaldehyde dehydrogenase RALDH-2 nor for cellular retinoic acid binding protein CRABP-I was observed. These components of RA signal transduction appeared in the eye between E3 and E5. At later stages, RA-measurements with a reporter cell line showed highest synthesis in the retinal pigment epithelium (RPE) and at the ventral and dorsal poles of the retina. RA degradation occurred mostly in a horizontal region in the middle of the retina with only small differences along the nasal-temporal axis. CRABP-I immunoreactivity appeared first in differentiating retinal ganglion cells with no indication of a spatial gradient across the ventral-dorsal eye axis. RA-production depended on three NAD+-dependent enzyme activities, which could be competitively inhibited by citral. One enzyme, located in the dorsal retina (corresponding to mouse RALDH-1), and one enzyme in the RPE (RALDH-2) were aldehyde dehydrogenases of the same molecular weight (monomers about 55 kDa) but with different isoelectric points (6.5-6.9; 4.9-5.4). The third RA-synthesizing activity (pI 6.0-6.3) was limited to the ventral retina, and likely corresponded to mouse RALDH-3. The restricted localization of retinoid-metabolizing activities along the dorsal-ventral axis of the embryonic chick retina does support the idea that RA is involved in dorsal-ventral eye patterning. However, the late time of appearance of aldehyde dehydrogenase activities and CRABP-I points to functions in cellular differentiation that are distinct from the initiation of the dorsal-ventral polarity.

Aldehyde Dehydrogenase↗
PubMed2001

Expression pattern of a newt Notch homologue in regenerating newt retina.

We isolated part of a newt Notch homologue, N-Notch, from regenerating newt retina. The spatio-temporal pattern of N-Notch expression was studied by in situ hybridization at different stages of newt retinal regeneration. Proliferating cells were confirmed by the injection of bromodeoxyuridine (BrdU). In the early stage of regeneration, when the retina was one to two cells thick, all proliferating retinal progenitors expressed N-Notch. As the thickness of the retina increased with regeneration, N-Notch expression decreased in BrdU-positive cells on the vitreal side of the retina. Subsequently, presumptive retinal ganglion cells that were BrdU-negative cells appeared at the vitreal edge of the regenerating retina. These differentiating cells did not express N-Notch. Later, N-Notch expression decreased in the BrdU-positive cells on the scleral surface of the retina. Subsequently, presumptive photoreceptor cells that were BrdU-negative cells appeared in this region. These differentiating cells also did not express N-Notch. The proliferating retinal progenitors ceased expressing N-Notch and then stopped dividing during the differentiation of ganglion cells and photoreceptor cells. It was found that retinal regeneration involves the expression of an important developmental signaling molecule, Notch, in retinal progenitors and the expression of Notch ceased as cell differentiation proceeded during retinal regeneration.

Amino Acid Sequence↗
PubMed2003

Transient muscarinic calcium mobilisation in transdifferentiating as in reaggregating embryonic chick retinae.

Two independent in vitro regeneration systems of the embryonic chick retina (E4-5) were used to study the mobilisation of intracellular calcium by the neurotransmitters acetylcholine (ACh) and glutamate, as measured by Fura-2 fluorescence changes. Retinal pigment epithelium (RPE) explants under the influence of basic fibroblast growth factor transdifferentiate into a retina-like tissue with normal laminar organisation, while rosetted spheres reaggregated from fully dispersed cells of the embryonic retina will achieve only an inferior tissue organisation, characterised by regions of an inverted retina [Layer et al., Neuroreport 12 (2001) A39-46]. ACh induced a pronounced Ca(2+) response in young explants, and a similar but less pronounced response in reaggregates; this response decreased almost entirely after 1 week in culture. In contrast, a Ca(2+) response to glutamate became detectable later, continuously increasing during this period. The response to ACh was strictly mediated by muscarinic ACh receptors (mAChRs), since it was inhibited by preincubation with atropine, but not tubocurarine; correspondingly, it was mimicked by muscarine, but not nicotine. Studies with mAChR blockers, preferentially acting on the m1-, m2-, or m3-receptor subtypes, suggested that the muscarine-induced Ca(2+) response is mediated by m1- and/or m3-type mAChRs, but not by the m2-type. These results show that (i) similar to the in vivo retina, in both a transdifferentiating and a reaggregating system an early muscarinic Ca(2+) response is active, which (ii) roughly parallels periods of cell proliferation, and (iii)-as evidenced by the reaggregates-does not depend on any tissue pre-organisation. In contrast, a response to glutamate becomes prominent only when tissue differentiation commences. This is the first demonstration of a physiological response in regenerating chick retinas, supporting their validity as models both of retinal development and regeneration.

Acetylcholine↗
PubMed1997

Developmental localization of retina cognin synthesis by in situ hybridization.

Retina cognin (R-cognin) is a 50 kDa protein involved in cell recognition and neuronal differentiation during development of the embryonic chick retina. Initial characterization of a partial cDNA encoding R-cognin revealed a striking similarity to the cDNA encoding protein disulfide isomerase (PDI), a 57 kDa multifunctional protein. The exact nature of the relationship between R-cognin and PDI is not known; however, both proteins appear to be encoded by the same gene. In the present study, we developed cRNA probes to examine the expression of R-cognin and PDI transcripts in embryonic chick retina and liver. In the retina, the amount of transcript decreased with embryonic age, in parallel to a similar decrease in R-cognin protein. In the liver, where PDI is prominently expressed, the amount of transcript was not developmentally regulated. The spatial and temporal pattern of expression of the R-cognin-encoding retinal transcript was examined by in situ hybridization. R-cognin mRNA was expressed in cells across the retina early in retinogenesis, but became restricted to the cells of the inner retina later in development. This pattern of expression was the same as the developmental pattern of R-cognin protein [Dobi et al., Invest. Ophthalmol. Vis. Sci. 27, (1986) p. 323-329], thus, demonstrating that this secreted protein functions at the surface of the cells where it is transcribed.

Animals↗
PubMed1999

Histone H1(o) expression in the developing cat retina.

Histone H1(o) is a subtype of the non-core H1 histones located in the linker region of DNA between nucleosome cores and postulated to be involved in the regulation of gene expression. Studies in both the mouse retina and rat brain have correlated the terminal differentiation of cell types in these tissues to the expression of H1(o)a The expression of H1(o) in mouse retina occurs after light exposure suggesting that light may trigger the expression of H1(o). The aims of the present research were to: (1) describe the relationship of the appearance of H1(o) protein immunoreactivity to the formation of cell types and layers in the cat retina; and (2) determine whether H1(o) may be dependent on exposure to light or on other postnatal developmental events. We find the nuclei of ganglion, amacrine, and prospective bipolar cells contain H1(o) immunoreactivity before birth, prior to the terminal differentiation of these cells. In the cat retina, expression of H1(o) occurs prior to light exposure. These results show that the expression of H1 degrees protein is not required for the terminal differentiation of retinal cell types in the cat. Additionally, we find no requirement for light exposure prior to H1(o) expression. These findings are at variance with the findings in the mouse retina and are inconsistent with any cross species requirement for the expression of this histone in the terminal differentiation of cell types in the retina.

Aging↗
PubMed1999

Postnatal development of NK1, NK2, and NK3 neurokinin receptors expression in the rat retina.

The biological effects of tachykinins are mediated by three distinct receptors, the neurokinin 1 receptor (NK1-R), NK2-R, and NK3-R. There is no information available concerning the development of these receptors in the retina. In the present study, we investigated the localization of tachykinin receptors, using antisera directed against NK1-R, NK2-R, and NK3-R in the adult and developing rat retinas. Numerous NK1-R immunoreactive (NK1-R IR) cells were already observed in the proximal part of the neuroblastic layer in the retina at postnatal day 5 (P5). The distribution and intensity of NK1-R IR cells and processes in the inner nuclear layer (INL) and inner plexiform layer (IPL) at P10 were similar to those of adult retina. Most NK1-R IR cells located in the proximal part of INL, which were morphologically amacrine cells. In the contrast to the early expression of NK1-R IR cells, no NK3-R IR structures existed in the neuronal elements of the retina until P10. NK3-R IR processes were first detected in the outer plexiform layer (OPL) at P10. At P15, NK3-R IR somata were slightly stained in the distal and middle parts of the INL, and NK3-R IR processes were present in the OPL and the upper part of the IPL. During P15-P30, the number of NK3-R IR somata located in the INL remarkably increased. These NK3-R IR cells were morphologically bipolar and amacrine cells. This study provides differential cellular distribution of NK1-R IR cells and NK3-R IR cells in the INL of the rat retina. Our findings suggest that NK1-R and NK3-R are involved in different visual circuits and retinal maturation, and NK3-R may play previously unknown important roles in the visual processes of the rat.

Aging↗
PubMed2002

Localization of adenylyl cyclase proteins in the rodent retina.

The isoforms of adenylyl cyclase that mediate cyclic AMP signaling pathways in the retina are, for the most part, unknown. Therefore, the protein expression patterns of adenylyl cyclase isoforms in the rodent retina were characterized immunocytochemically using antibodies directed against Ca(2+)-stimulated (AC1, AC3 and AC8), Ca(2+)-inhibited (AC9) and Ca(2+)-insensitive (AC2, AC4, AC7) isoforms of adenylyl cyclase. The ganglion cell layer and the inner nuclear layer (INL) were immunoreactive for both Ca(2+)-sensitive (AC1, AC3) and Ca(2+)-insensitive (AC2, AC4) isoforms of adenylyl cyclase. Antibodies against isoforms from all three classes of adenylyl cyclase labeled the inner plexiform layer. In the outer retina, antibodies against Ca(2+)-insensitive isoforms labeled photoreceptors and the outer plexiform layer (OPL). Radial elements in the ONL and INL were AC4-immunoreactive and the nerve fibre layer and optic nerve were AC2-, AC4- and AC9-immunoreactive. Antibodies against AC7 did not label rodent neural retina. These data indicate that there is a heterogeneous distribution of adenylyl cyclase isoforms throughout the rodent retina. Nonetheless, there is a general indication of a greater expression of Ca(2+)-insensitive adenylyl cyclase isoforms in the outer retina, particularly within photoreceptors.

Adenylyl Cyclases↗
PubMed1998

Expression patterns of voltage-dependent calcium channel alpha 1 subunits (alpha 1A-alpha 1E) mRNA in rat retina.

The transcript levels of the genes encoding for the different alpha1 (alpha1A-alpha1E) subunits of voltage-dependent calcium channels (VDCCs) were studied in the retina of the rat using RT-PCR, Northern blotting, and in situ hybridization. Abundant expression of alpha1A and alpha1B was found with RT-PCR and on Northern blots of total retina RNA, corresponding with high expression levels in all nuclear layers (outer and inner nuclear layers and the ganglion cell layer) of the retina. VDCC alpha1D mRNA was also present in all nuclear layers of the retina but at less abundant levels than alpha1A or alpha1B. Expression level of alpha1C in the retina was low as deduced from a faint Northern blot signal and a moderate yield after PCR amplification. VDCC alpha1E specific amplification of retinal cDNA yielded a longer product (designated alpha1E-L) than obtained from the hippocampus. Nucleotide sequencing of this PCR product revealed a 129 bp insert which is largely homologous (97%) with a previously described insert in the same position in human alpha1E cDNA. In situ hybridization in rat brain showed a differential expression pattern of the long and short variants of alpha1E mRNA. Northern blotting of retinal RNA confirmed the absence of the short variant (alpha1E-S), while alpha1E-L was present at low levels. In situ hybridization detected a significant level of expression of alpha1E-L in the inner nuclear layer. The prevalent expression of alpha1A and alpha1B, and to a lesser extent, of alpha1D, indicates that P/Q-, N-, and L-type calcium currents play a prominent role in the various cell types involved in the retinal signal-transduction pathway. The absence of alpha1C transcript in the retina suggests that the slowly inactivating L-type calcium currents involved in neurotransmitter release from the terminals of photoreceptors and bipolar cells may be encoded by the alpha1D isoform.

Alternative Splicing↗
PubMed1997

Expression of beta 1-4 N-acetylgalactosaminyltransferase gene in the developing rat brain and retina: mRNA, protein immunoreactivity and enzyme activity.

The developmental pattern of expression of the UDP-GalNAc:GM3 N-acetylgalactosaminyltransferase (GalNAc-T) gene was examined in the rat brain and retina. A GalNAc-T cDNA cloned from a rat olfactory bulb cDNA library was used as a probe for Northern blot and in situ hybridization experiments and a rabbit polyclonal antibody to rat GalNAc-T peptide was used for Western blot analysis. In Northern blot experiments, a single approximately 3 kb transcript was detected both in brain and retina. In brain, the abundance of this transcript increased from E15 to PN1-5 and then declined while, in retina, it increased steadily from PN1 to PN13-24. The developmental trends of GalNAc-T mRNA expression, GalNAc-T immunoreactive protein and GalNAc-T activity were comparable in brain. In retina, however, GalNAc-T activity and GalNAc-T peptide immunoreactivity followed developmental patterns that were similar between them and different from that of the specific mRNA. Results suggest that post-transcriptional controls of the GalNAc-T gene expression operate in the rat CNS, which are particularly evident in retina. The expression of the GalNAc-T gene in glial and neuronal cells was examined in rat retina cell cultures by in situ hybridization. The GalNAc-T mRNA was abundant in GM1+/GD3+ neurons and almost absent in the flat, GM1-/GD3+ Müller glia-derived cells.

Animals↗
PubMed1998

Developmental regulation of group III metabotropic glutamate receptors modulating adenylate cyclase activity in the avian retina.

The regulation of adenylate cyclase by neurotransmitters is observed in early development of the chick retina. In the present work we show that L-2-amine-4-phosphonobutyric acid (L-AP4), the major agonist of group III metabotropic glutamate receptors (mGluRs), inhibits the accumulation of cyclic AMP induced by forskolin in the chick retina. This effect is observed after 8 days of development (E8), is maximal from E12-E17 and decreases at the post-hatching period (PH). The inhibition is also observed in cultures of retinal cells incubated for 2-8 days. We have also investigated the interaction between group III mGluRs and other receptors coupled to adenylate cyclase in the developing retina. The inhibition by L-AP4 is partially additive with that induced by the A1 adenosine agonist Cyclohexyladenosine and is not observed when cyclic AMP levels are increased with 2-chloroadenosine or dopamine. The group II mGluR agonist trans-(1S,3R)-1-amino-cyclopentanedicarboxylic acid has an inhibitory effect only on PH retinas, indicating that group II and group III mGluRs have a differential ontogenesis in this tissue. The results show that Group III mGluRs are expressed early during chick retina development and do not interact with other receptors known to be coupled to adenylate cyclase in the developing retina.

Adenylyl Cyclase Inhibitors↗
PubMed1999

Expression of beta-amyloid precursor and Bcl-2 proto-oncogene proteins in rat retinas after intravitreal injection of aminoadipic acid.

In order to investigate the role of glia in relation to factors that affect the expression of beta-amyloid precursor protein (betaAPP) and B cell lymphoma oncogene protein (Bcl-2) in the central nervous tissue, the patterns of expression of betaAPP and Bcl-2 in developing and mature rat retinas were studied immunocytochemically after intravitreal injection of alpha-aminoadipic acid (alpha-AAA), a glutamate analogue and gliotoxin that is known to cause injury of retinal Müller glial cells. In normal developing retinas, betaAPP and Bcl-2 were expressed primarily but transiently in a small number of neurons in the ganglion cell layer during the first postnatal week. Immunoreactivity of betaAPP and Bcl-2 appeared in the endfeet and proximal part of the radial processes of Müller glial cells from the second postnatal week onwards. In rats that received intravitreal injection of alpha-AAA at birth, there was a loss of immunoreactivity to vimentin, and a delayed expressed on betaAPP or Bcl-2 in Muller glial cells until 3-5 weeks post-injection. Immunoreactive neurons were also observed in the inner retina especially in the ganglion cell layer from 5 to 35 days after injection. A significant reduction in numerical density of cells with large somata in the ganglion cell layer was observed in the neonatally injected retinas at P56, which was accompanied by an increased immunostaining in radial processes of Müller glial cells. In contrast, no detectable changes in the expression of betaAPP and Bcl-2 were observed in retina that received alpha-AAA as adults. These results indicate that the gliotoxin alpha-AAA has long lasting effects on the expression of betaAPP and Bcl-2 in Müller glial cells as well as neurons in the developing but not mature retinas. The loss of vimentin and delayed expression of betaAPP and Bcl-2 in developing Müller glial cells suggests that the metabolic integrity of Müller cells was temporarily compromised, which may have adverse effects on developing neurons that are vulnerable or dependent on trophic support from the Müller glial cells.

2-Aminoadipic Acid↗
PubMed2002

Nitric oxide synthase expression in the transient ischemic rat retina: neuroprotection of betaxolol.

Betaxolol is a beta-adrenergic blocker but its neuroprotective action is generally thought to be due to its calcium channel blocking properties. In this study, we investigated neuronal cell damage and changes in the expression of neuronal nitric oxide synthase (nNOS) immunoreactivity in the ischemic retina and its relationship to the neuroprotection of betaxolol treatment after ischemic injury. Using the retina after ischemia, the expression of nNOS was studied by immunocytochemistry. In control retinas, two types of amacrine cells and a class of displaced amacrine cells were nNOS-labeled. After ischemia/reperfusion, the number of nNOS immunoreactive cells increased in both the ganglion cell layer and the inner nuclear layer compared to the control retinas. However, when experiments were carried out on animals that had been treated with betaxolol twice daily after ischemia/reperfusion, the number of nNOS immunoreactive cells decreased compared to the untreated ischemic retinas. These results suggest that an increase in nNOS expression could be associated with the degenerative changes in the ischemic retina, and that betaxolol treatment appears to play a role in protecting retinal tissue from ischemic damage.

Amacrine Cells↗