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PubMed2004

Role of purpurin as a retinol-binding protein in goldfish retina during the early stage of optic nerve regeneration: its priming action on neurite outgrowth.

Unlike mammals, the fish optic nerve can regenerate after injury. So far, many growth or trophic factors have been shown as an axon-regenerating molecule. However, it is totally unknown what substance regulates or triggers the activity of these factors on axonal elongation. Therefore, we constructed a goldfish retina cDNA library prepared from the retina treated with optic nerve transection 5 d previously, when it was just before regrowing optic axons after injury. A cDNA clone for goldfish purpurin for which expression was upregulated during the early stage of optic nerve regeneration was isolated from the retina cDNA library. Purpurin was discovered as a secretory retinol-binding protein in developing chicken retinas. Levels of purpurin mRNA and protein transiently increased and rapidly decreased 2-5 d and 10 d after axotomy, respectively. Purpurin mRNA was localized to the photoreceptor cells, whereas the protein was diffusely found in all of the retinal layers. A recombinant purpurin alone did not affect any change of neurite outgrowth in explant culture of the control retina, whereas a concomitant addition of the recombinant purpurin and retinol first induced a drastic enhancement of neurite outgrowth. Furthermore, the action of retinol-bound purpurin was effective only in the control (untreated) retinas but not in those primed (treated) with a previous optic nerve transection. Thus, purpurin with retinol is the first candidate molecule of priming neurite outgrowth in the early stage of optic nerve regeneration in fish.

Amino Acid Sequence↗
PubMed2005

Glucagon-expressing neurons within the retina regulate the proliferation of neural progenitors in the circumferential marginal zone of the avian eye.

Glucagon-expressing retinal amacrine cells have been implicated in regulating postnatal ocular growth. Furthermore, experimentally accelerated rates of ocular growth increase the number of neurons added to the peripheral edge of the retina. Accordingly, we assayed whether glucagon-expressing neurons within the retina regulate the proliferation of progenitors in the circumferential marginal zone (CMZ) of the postnatal chicken eye. We found that glucagon-containing neurites are heavily clustered within the CMZ at the peripheral edge of the retina. Many of these neurites originate from a cell type that is distinct from other types of retinal neurons, which we termed large glucagon-expressing neurons (LGENs). The LGENs are immunoreactive for glucagon and glucagon-like peptide 1 (GLP1), have a unipolar morphology, produce an axon that projects into the CMZ, and are found only in ventral regions of the retina. In dorsal regions of the retina, a smaller version of the LGENs densely ramifies neurites in the CMZ. Intraocular injections of glucagon or GLP1 suppressed the proliferation of progenitors in the CMZ, whereas a glucagon-receptor antagonist promoted proliferation. In addition, we found that glucagon, GLP1, and glucagon antagonist influenced the number of progenitors in the CMZ. We conclude that the LGENs may convey visual information to the CMZ to control the addition of new cells to the edge of the retina. We propose that glucagon/GLP1 released from LGENs acts in opposition to insulin (or insulin-like growth factor) to regulate precisely the proliferation of retinal progenitors in the CMZ.

Animals↗
PubMed2001

Pineal organ-like organization of the retina in megachiroptean bats.

Phylogenetically originated from photoreceptive structures, the pineal organ adapts the organism to circadian and circannual light periodicity of the environment, while the retina develops to a light-based locator. Bats have a nocturnal life and an echolocator orientation presumably modifying the task of photoreception. Looking for morphological basis of the special functions, in the present work we compared the fine structure and immunocytochemistry of the retina and pineal organ in micro- and megacrochiroptean bats. We found that there is a high similarity between the retina and pineal organ in megachiropterans when compared to other species investigated so far. Besides of photoreceptor derived pinealocytes, the pineal organ of both micro- and megachiropterans contain intrapineal neurons and/or ganglionic cells as well as glial cells. Like spherules and pedicles of retinal photoreceptors, axon-type processes of pinealocytes form synaptic ribbon containig terminals. Similar to retinal photoreceptors and neurons, pinealocytes and pineal neurons contain immunoreactive glutamate and aspartate. In addition, excitatory amino acids accumulate in the pineal neurohormonal endings and might have a role in the hormonal (serotonin?) release of the organ. Concerning the structure of the retina the highest similarity to the organization of the pineal organ was found in the megachiroptean fruit eating bats Cynopterus sphinx and Rusettus niloticus. The retina of these species forms folds and crypts in its photoreceptor layer. This organization is similar to the folds of the pineal wall successively developed during evolution. Since a folded photoreceptor layer is not viable for a photolocator screen in decoding two-dimensional images, we suppose that this peculiar organization of the megachiropteran retina is connected to a "pineal-like" photometer task of the eye needed by these species active at night.

Animals↗
PubMed2003

Increased expression of glutamate binding protein mRNA in rat retina after ischemia-reperfusion injury.

We investigated the distribution and expression of glutamate-binding protein (GBP) in the rat retinas after ischemia-reperfusion injury. Ischemia-reperfusion injury was induced in rats by clamping of the optic nerve for one hour. The distribution of GBP immunoreactivity was determined at 6, 24, 72, and 168 hours after reperfusion. Also, RT-PCR was performed to detect the change of GBP mRNA expression in the reperfused retinas. In untreated control retinas, GBP immunoreactivity was observed in the cells of ganglion cell layer, inner plexiform layer, and inner nuclear layer. At 6, 24, and 72 hours after reperfusion, GBP immunoreactivity was seen not only in the GCL, IPL, and INL, but also in the outer plexiform layer and photoreceptor outer segment. At 168 hours after reperfusion, GBP immunoreactivity in the OPL was decreased. Moreover, we found increased GBP mRNA expression at 24 hours after reperfusion. In this study, we demonstrated that ischemia-reperfusion induced increase of GBP immunoreactivity in the inner retina and increase of GBP mRNA expression in the rat retinas. Our results suggest that NMDA receptor-like complex may play some role in the ischemic cell death of the inner retina.

Animals↗
PubMed1994

Neuropeptide Y-immunoreactive neurons in the retina of two Australian lizards.

Wholemounts and sectioned retina from adults of two lizard species, Pogona vitticeps and Varanus gouldii, were studied by immunohistochemistry for neuropeptide Y (NPY)-like immunoreactivity. In both species the morphology of two classes of amacrine cells (types A and B) were described. Cell somata were located mostly in the inner nuclear layer (INL) but were occasionally displaced into the ganglion cell layer (GCL). In the Pogona retina, type A cells had large somata and dendritic arbor that branched in sublamina (S) 1 and 2/3 of the inner plexiform layer (IPL). Type B amacrine cells had smaller somata and dendritic arbor branching mostly in S5 of the IPL. In the Varanus retina, the levels of dendritic branching of types A and B amacrine cells in the IPL were similar to those in Pogona although branching in the middle of the IPL occurred at S3. NPY-immunoreactive cells with small somata and narrow to medium sized dendritic fields were predominant. Unclassified cells also displayed NPY-like immunoreactivity; however, their dendritic morphology could not be determined due to the faint and inconsistent staining. In transverse retinal sections three bands of NPY-like immunoreactivity were evident in the IPL of both species, to which the unclassified cells also contributed. In both species type A cells were most numerous. Total NPY-immunoreactive cells were estimated to be 8,600 in Pogona and 32,860 in Varanus. In both species types A and B cells were non-uniformly distributed across the retina. The most apparent non-uniformity in distribution was observed in type A cells in Varanus. Peak cell density was found across the horizontal meridian of the retina from where cell density decreased towards the dorsal and ventral retinal margins. The results of this study provide evidence for the presence of NPY-immunoreactive amacrine cells in the lizard retina of which two types were morphologically characterized. Cross-species comparisons were also made among NPY-immunoreactive amacrine cells, and their possible function/s discussed.

Animals↗
PubMed2002

Morphologic features of degeneration and cell death in the neurosensory retina in dogs with primary angle-closure glaucoma.

OBJECTIVE: To investigate cellular death in the neurosensory portion of the retina during the first 7 days after onset of clinical signs of overt primary angleclosure glaucoma (PACG) in dogs. SAMPLE POPULATION: 14 globes from dogs with PACG and 2 normotensive globes from dogs with PACG in the opposite eye. PROCEDURES: Retinas were examined via light microscopy and terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick end-labeling. RESULTS: Necrosis of ganglion cells and segmental degeneration of the nerve fiber layer rapidly progressed to scattered full-thickness retinal attenuation and disorganization. Apoptosis was detectable within 1 day after onset of PACG and was prominent by 3 days. Necrosis of ganglion cells was significantly greater in retinas affected for < or = 1 day, compared with retinas affected for > 1 day. In contrast, apoptosis in the ganglion cell layer was significantly greater in retinas affected for > 1 day, compared with retinas affected for < or = 1 day. End-stage retinal atrophy was seen by day 7. CONCLUSIONS AND CLINICAL RELEVANCE: The presence of necrotic ganglion cells within 1 day after onset of clinical signs suggests a narrow window of opportunity to initiate effective therapy in overt PACG. Photoreceptor death is an important and striking aspect of neurosensory retinal degeneration after acute onset of PACG.

Animals↗
PubMed1992

Immunity and immune privilege elicited by autoantigens expressed on syngeneic neonatal neural retina grafts.

Achieving the long-term goal of successful engraftment of retinal tissues into eyes blinded by endogenous retinal failure will depend, at least in part, on controlling the immune response to antigens expressed on retinal grafts. Since histoincompatible tissues will have to be used for such transplants, methods to control immune rejection directed at transplantation alloantigens must be devised. In addition, it has recently been observed in mice that developing neural retinal tissues express retina-specific antigens that have the potential to contribute to graft failure. To examine the potential risk of this contribution, syngeneic neonatal neural retinas were implanted into the anterior chamber, vitreous cavity, and subconjunctival space of adult BALB/c mice. During two weeks post-implantation, the fate of these grafts was observed clinically and histologically, and the retina-specific immune responses of the recipients were evaluated. Whereas grafts placed intraocularly thrived, carried out their inherent developmental potential, and were healthy and intact at the end of the observation interval. Grafts placed extraocularly expressed their differentiation program poorly. These grafts underwent rapid decline and attrition, although the process was not accompanied by significant inflammation. Recipients of subconjunctival, but not AC or VC, implants developed retina-specific delayed hypersensitivity. Alternatively, mice bearing AC and VC implants of neonatal neural retina developed retina-specific anterior chamber associated immune deviation. It is concluded that retinal autoantigens are expressed on developing neural retinal tissues and these antigens are highly immunogenic when retinal grafts are placed at conventional body sites. When similar grafts are placed in immune privileged compartments of the normal eye, they enjoy significant survival. Circumstantial evidence indicates that intraocular retinal grafts are protected and maintained in part by the emergence of systemic retinal auto-antigen-specific immune suppression.

Animals↗
PubMed1996

Immunocytochemical localization of retinoid-binding protein in the dogfish retina.

PURPOSE: The cellular localization of retinoid-binding proteins has been extensively studied in the mammalian retina. Less is known about the distribution and identity of retinoid-binding proteins in lower vertebrate retinas. To understand their cellular functions, we have examined the distribution of specific retinoid-binding proteins in the neural retina and RPE of an elasmobranch, the dogfish. METHODS: Retinoid-binding proteins were localized in cryostat sections of dogfish eyes by the indirect immunofluorescence technique. We used well-characterized antibodies that have been previously employed for immunostaining. Immunoblotting was carried out to identify the antigen. RESULTS: The studies show that the cellular retinaldehyde-binding protein is present in the RPE and retinal Müller cells, and the interphotoreceptor retinoid-binding protein is found in the interstitial space between pigment epithelium and retina. CONCLUSIONS: The distribution of retinoid-binding proteins in dogfish retina is similar to that found in the mammalian retina which suggests that the sites of action of the retinoid-binding proteins are highly conserved in vertebrates.

Animals↗
PubMed1993

Histopathologic and ultrastructural findings of photocoagulation lesions produced by transpupillary diode laser in the rabbit retina.

Transpupillary retinal photocoagulations were performed on ten eyes of five pigmented rabbits using a diode laser (Nidek Co., LTD, Aichi, Japan) emitting infrared radiation at 800 nm wavelength. A histological and an ultrastructural study on the treated eyes were done at 1, 3, 5, and 7 days after retinal photocoagulations. The purpose of this study was to observe the sequential changes in the retina and the choroid following transpupillary diode laser retinal photocoagulations at the parameters of laser power which produced a grayish white retinal discoloration with distinct white center. It seemed that the lesion was grade 3 retinal photocoagulation by Tso et al's classification. It appeared that the parameters necessary to produce grade 3 photocoagulation lesions were 160 mW power, and 0.2 second duration at 200 microns size. In general, with an agreement to other reports, histologic study of the diode laser lesions showed that the outer retina was damaged more severely than the inner retina. However, on day 1 after laser treatment, the alterations were more profound in the inner retina than in the outer retina and an occasional swelling of the axons in the nerve fiber layer was observed on the ultrastructural study. The results observed have not been found in other previous studies and suggest that the inner retina might be injured directly by 800 nm wavelength diode laser radiations. Thus we could conclude that 800 nm wavelength diode radiation might be absorbed by melanin pigment and also by other chromophores contained in inner retinal tissues. Further studies must follow to verify the laser-tissue interactions in diode laser retinal photocoagulations.

Animals↗
PubMed2002

Spatiotemporal features of early neuronogenesis differ in wild-type and albino mouse retina.

In albino mammals, lack of pigment in the retinal pigment epithelium is associated with retinal defects, including poor visual acuity from a photoreceptor deficit in the central retina and poor depth perception from a decrease in ipsilaterally projecting retinal fibers. Possible contributors to these abnormalities are reported delays in neuronogenesis (Ilia and Jeffery, 1996) and retinal maturation (Webster and Rowe, 1991). To further determine possible perturbations in neuronogenesis and/or differentiation, we used cell-specific markers and refined birth dating methods to examine these events during retinal ganglion cell (RGC) genesis in albino and pigmented mice from embryonic day 11 (E11) to E18. Our data indicate that relative to pigmented mice, more ganglion cells are born in the early stages of neuronogenesis in the albino retina, although the initiation of RGC genesis in the albino is unchanged. The cellular organization of the albino retina is perturbed as early as E12. In addition, cell cycle kinetics and output along the nasotemporal axis differ in retinas of albino and pigmented mice, both absolutely, with the temporal aspect of the retina expanded in albino, and relative to the position of the optic nerve head. Finally, blocking melanin synthesis in pigmented eyecups in culture leads to an increase in RGC differentiation, consistent with a role for melanin formation in regulating RGC neuronogenesis. These results point to spatiotemporal defects in neuronal production in the albino retina, which could perturb expression of genes that specify cell fate, number, and/or projection phenotype.

Albinism↗
PubMed1999

c-jun Is dispensable for developmental cell death and axogenesis in the retina.

Although a number of studies have implicated c-Jun in neuronal death and axonal regeneration, it is unknown whether Jun function is essential for either response. One approach to resolve this issue is to analyze knock-out mice. However, c-jun-null mice die at midgestation, precluding critical investigation. Therefore, a xenograft paradigm was used in which retinas from embryonic day 12.5 (E12.5) c-jun nullizygous or wild-type mice were transplanted onto the superior colliculus of newborn rats. The rats were allowed to develop, and the grafts were assayed at various times for cell death and axon growth. Histologically, grafts of both genotypes developed in identical manners and had morphological characteristics of retinas. A functional c-jun allele was not essential for axogenesis, because ganglion cells in retinal grafts from c-jun nullizygous mice developed axons that projected into the colliculus. Programmed cell death (PCD) was also evident in the age-appropriate regions of the retina in both wild-type and c-jun-null grafts. Furthermore, there were no discernible differences in the number or location of dying cells in the two genotypes. That c-jun was not essential for PCD was supported by two additional findings. First, a c-jun-lacZ reporter gene was expressed in many cells in developing and grafted retinas, although only a few of these cells were destined to die. Second, in E12.5 c-jun-null embryos there were normal levels of PCD in the trigeminal ganglion. Together, these data indicate that c-Jun is not essential for axon growth in the retina or for PCD in the retina and trigeminal ganglion.

Alleles↗
PubMed1999

Light and choroidal PO2 modulation of intraretinal oxygen levels in an avascular retina.

PURPOSE: To determine the influence that choroidal oxygen level and outer retinal oxygen demand have on oxygen availability to the inner retina when the choroid is the only source of retinal oxygenation. This condition prevails in avascular retinas and in vascularized retinas suffering vascular occlusion. METHODS: Oxygen-sensitive microelectrodes were used to measure the oxygen tension as a function of depth in the naturally avascular retina of anesthetized and mechanically ventilated guinea pigs (n = 6). Choroidal PO2 was manipulated by varying the ventilation gas mixture, and outer retinal oxygen consumption was modulated by light-dark adaptation. Individual PO2 profiles were fitted to a multilayer mathematical model of PO2 distribution, and pairs of profiles at different choroidal PO2 levels, or under light and dark conditions, were fitted to an intraretinal PO2 difference model. Both models reflect the purely choroidal supply of retinal oxygenation. RESULTS: An increase in choroidal PO2 produced an equivalent increase in all retinal layers. Light induced a decreased oxygen consumption in the region of the inner segments of the photoreceptors, which resulted in a significant increase in PO2 in this layer, flowing on unattenuated to all inner retinal layers. The intraretinal PO2 distribution and the light- and ventilatory-induced changes in PO2 were consistent with theoretical predictions of the mathematical models. CONCLUSIONS: The present experimental studies confirm that when the choroid is the only source of retinal oxygenation, the full effect of increased choroidal oxygen level or reduced uptake in the outer retina passes through to the inner retinal layers if the oxygen utilization by the inner retina remains constant.

Animals↗
PubMed1999

Effects of photodynamic therapy using verteporfin on experimental choroidal neovascularization and normal retina and choroid up to 7 weeks after treatment.

PURPOSE: To study the long-term effects of photodynamic therapy (PDT), using liposomal benzoporphyrin derivative (BPD) or Verteporfin, on experimental choroidal neovascularization (CNV) and on normal retina and choroid (with no CNV) in the cynomolgus monkey eye. METHODS: Photodynamic therapy was performed in 8 cynomolgus monkey eyes with experimental CNV induced by laser injury. The effect of PDT on normal retina and choroid (with no CNV) was studied in 9 monkey eyes. Liposomal BPD was administered intravenously (0.375 mg/kg) either as a bolus, as a slow infusion over 32 minutes, or as a fast infusion over 10 minutes. Photodynamic therapy was performed using light at a wavelength of 689 or 692 nm, with an irradiance of 600 mW/cm2 and fluence of 150 J/cm2. Follow-up studies, including fundus photography and FA, were performed at 24 hours after PDT and then weekly. Indocyanine green and BPD angiography were performed in selected cases. Tissues were examined with light and electron microscopy at the end of follow-up. RESULTS: Twenty-three of the 32 areas of CNV treated with PDT showed absence of angiographic leakage at 24 hours. Twenty-eight areas of CNV were followed for 4 weeks; 22 of 28 showed absence of angiographic leakage at 2 weeks; and 20 of 28 at 4 weeks of follow-up. Forty spots on the normal retina and choroid were treated with PDT and were followed for 4 to 7 weeks. These spots showed pigment-laden cells in the outer retina, variably pigmented retinal pigment epithelium (RPE) in the treated area, intact neurosensory retina, and reperfusion of the choriocapillaris. CONCLUSIONS: Photodynamic therapy leads to absence of angiographic leakage for at least 4 weeks in experimental CNV in the monkey model. In the normal monkey eye the RPE and choriocapillaris show generalized recovery with preservation of the neurosensory retina 7 weeks after PDT.

Animals↗
PubMed2000

Localization and developmental expression patterns of the neuronal K-Cl cotransporter (KCC2) in the rat retina.

The processing of signals by integrative neurons in the retina and CNS relies strongly on inhibitory synaptic inputs, principally from GABAergic and glycinergic neurons that serve primarily to hyperpolarize postsynaptic neurons. Recent evidence indicates that the neuron-specific K-Cl cotransporter 2 (KCC2) is the major chloride extrusion system permitting hyperpolarizing inhibitory responses. It has been hypothesized that depolarizing GABA responses observed in immature neurons are converted to hyperpolarizing responses in large part by the expression of KCC2 during the second week of postnatal development. The cell-specific localization and developmental expression of KCC2 protein have been examined in relatively few neural tissues and have never been studied in retina, of which much is known physiologically and morphologically about inhibitory synaptic circuits. We examined the localization of KCC2 in adult rat retina with immunohistochemical techniques and determined the time course of its postnatal expression. KCC2 expression was localized in horizontal cells, bipolar cells, amacrine cells, and, most likely, ganglion cells, all of which are known to express GABA receptor subtypes. Developmentally, KCC2 expression in the retina increased gradually from postnatal day 1 (P1) until P14 in the inner retina, whereas expression was delayed in the outer plexiform layer until P7 but reached its adult level by P14. These data support the hypothesis that the function of KCC2 is intimately involved in GABAergic synaptic processing. Furthermore, the delayed temporal expression of KCC2 in the outer plexiform layer indicates that GABAergic function may be differentially regulated in retina during postnatal development and that GABA may produce depolarizing responses in the outer plexiform layer at times when it generates hyperpolarizing responses in the inner plexiform layer.

Aging↗
PubMed2000

Localization of tubby-like protein 1 in developing and adult human retinas.

PURPOSE: To localize tubby-like protein 1 (TULP1) in developing and adult human retinas. METHODS: TULP1 was localized by immunofluorescence microscopy in human retinas, aged 8.4 fetal weeks to adult. TULP1-positive cells were identified by double labeling with antibodies specific for cones, rods, and astrocytes. RESULTS: In adult retinas, anti-TULP1 labels cone and rod inner segments, somata, and synapses; outer segments are TULP1-negative. A few inner nuclear and ganglion cells are weakly TULP1-positive. In fetal retinas, cells at the outer retinal border are TULP1-positive at 8.4 weeks. At 11 weeks, the differentiating central cones are strongly TULP1-reactive and some are positive for blue cone opsin. At 15.4 weeks, all central cones are strongly positive for TULP1 and many are reactive for red/green cone opsin. At 17.4 weeks, central rods are weakly TULP-reactive. In peripheral retina at 15.4 weeks to 1 month after birth, displaced cones in the nerve fiber layer are positive for TULP1, recoverin, and blue cone opsin. Some ganglion cells are weakly reactive for TULP1 at 11 weeks and later, but astrocytes and the optic nerve are TULP1-negative at all ages examined. CONCLUSIONS: The finding of TULP1 labeling of cones before they are reactive for blue or red/green cone opsin suggests an important role for TULP1 in development. TULP1 expression in both developing and mature cones and rods is consistent with a primary photoreceptor defect in retinitis pigmentosa (RP) caused by TULP1 mutations. Weak TULP1-immunolabeling of some inner retinal neurons in developing and adult retinas suggests that optic disc changes in patients with RP who have TULP1 mutations may be primary as well as secondary to photoreceptor degeneration.

Adult↗
PubMed2000

Expression of somatostatin subtype 1 receptor in the rabbit retina.

PURPOSE: To detect mRNAs for somatostatin (somatotropin release-inhibiting factor [SRIF]) receptor subtypes 1 to 5 (sst(1) through sst(5)) in rabbit retinas by reverse transcription-polymerase chain reaction (RT-PCR) and to investigate the distribution of sst(1) by single- and double-label immunocytochemistry. METHODS: Semiquantitative RT-PCR using sst-specific primers from mouse sequences was performed. sst(1) was localized using a polyclonal antiserum directed to human sst(1) in cryostat sections of retinas from either normal or optic nerve-transected animals. Immunolabeled cell sizes and densities were measured in wholemounted retinas using computer-assisted image analysis. Double-label immunofluorescence was performed using the sst(1) antiserum in conjunction with monoclonal antibodies directed to SRIF, tyrosine hydroxylase (TH), parvalbumin (PV), or gamma-aminobutyric acid (GABA). RESULTS: With RT-PCR it was found that all five sst mRNAs were expressed in the rabbit retina, with highest levels of sst(1) mRNA. sst(1) immunolabeling was localized to amacrine cells in the proximal inner nuclear layer (INL) of all retinal regions and to displaced amacrine cells in the ganglion cell layer (GCL) of the ventral retina. Some large sst(1)-immunoreactive (IR) somata were also present in the GCL. They were not observed after optic nerve transection. Double-label immunofluorescence showed sst(1) expression by all TH-IR amacrine cells and by other amacrine cells that were neither PV-IR nor GABA-IR. In addition, sst(1) was expressed by all SRIF-containing displaced amacrine cells. CONCLUSIONS: All five sst mRNAs are expressed in the rabbit retina. The localization of sst(1) suggests that it may mediate SRIF actions onto amacrine (including dopaminergic) and sparse ganglion cells. sst(1) expression in SRIF-IR cells suggests that this receptor may also act as an autoreceptor.

Animals↗
PubMed2000

Mice lacking specific nicotinic acetylcholine receptor subunits exhibit dramatically altered spontaneous activity patterns and reveal a limited role for retinal waves in forming ON and OFF circuits in the inner retina.

Before phototransduction, spontaneous activity in the developing mammalian retina is required for the appropriate patterning of retinothalamic connections, and there is growing evidence that this activity influences the development of circuits within the retina itself. We demonstrate here that the neural substrate that generates waves in the mouse retina develops through three distinct stages. First, between embryonic day 16 and birth [postnatal day 0 (P0)], we observed both large, propagating waves inhibited by nicotinic acetylcholine receptor (nAChR) antagonists and small clusters of cells displaying nonpropagating, correlated calcium increases that were independent of nAChR activation. Second, between P0 and P11, we observed only larger propagating waves that were abolished by toxins specific to alpha3 and beta2 subunit-containing nAChRs. Third, between P11 and P14 (eye opening) we observed propagating activity that was abolished by ionotropic glutamate receptor antagonists. The time course of this developmental shift was dramatically altered in retinas from mice lacking the beta2 nAChR subunit or the beta2 and beta4 subunits. These retinas exhibited a novel circuit at P0, no spontaneous correlated activity between P1 and P8, and the premature induction at P8 of an ionotropic glutamate receptor-based circuit. Retinas from postnatal mice lacking the alpha3 nAChR subunit exhibited spontaneous, correlated activity patterns that were similar to those observed in embryonic wild-type mice. In alpha3-/- and beta2-/- mice, the development and distribution of cholinergic neurons and processes and the density of retinal ganglion cells (RGCs) and the gross segregation of their dendrites into ON and OFF sublaminae were normal. However, the refinement of individual RGC dendrites is delayed. These results indicate that retinal waves mediated by nAChRs are involved in, but not required for, the development of neural circuits that define the ON and OFF sublamina of the inner plexiform layer.

Action Potentials↗
PubMed2000

Incorporation and differentiation of hippocampus-derived neural stem cells transplanted in injured adult rat retina.

PURPOSE: In a previous study it has been shown that adult rat hippocampus-derived neural stem cells can be successfully transplanted into neonatal retinas, where they differentiate into neurons and glia, but they cannot be transplanted into adult retinas. In the current study, the effect of mechanical injury to the adult retina on the survival and differentiation of the grafted hippocampal stem cells was determined. METHODS: Mechanical injury was induced in the adult rat retina by a hooked needle. A cell suspension (containing 90,000 neural stem cells) was slowly injected into the vitreous space. The specimens were processed for immunohistochemical studies at 1, 2, and 4 weeks after the transplantation. RESULTS: In the best case, incorporation of grafted stem cells was seen in 50% of the injured retinas. Most of these cells located from the ganglion cell layer through the inner nuclear layer close to the injury site. Immunohistochemically, at 1 week, more than half of the grafted cells expressed nestin. At 4 weeks, some grafted cells showed immunoreactivity for microtubule-associated protein (MAP) 2ab, MAP5, and glial fibrillary acidic protein (GFAP), suggesting progress in differentiation into cells of neuronal and astroglial lineages. However, they showed no immunoreactivity for HPC-1, calbindin, and rhodopsin, which suggests that they did not differentiate into mature retinal neurons. Immunoelectron microscopy revealed the formation of synapse-like structures between graft and host cells. CONCLUSIONS: By the manipulation of mechanical injury, the incorporation and subsequent differentiation of the grafted stem cells into neuronal and glial lineage, including the formation of synapse-like structures, can be achieved, even in the adult rat retina.

Animals↗