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At least 631 records · Page 35Linked to original sources
PubMed2006

Intraocular injection of folate antagonist methotrexate induces neuronal differentiation of embryonic stem cells transplanted in the adult mouse retina.

Transplanted embryonic stem (ES) cells can be integrated into the retinas of adult mice as well-differentiated neuronal cells. However, the integrated ES cells also have a tumorigenic effect just because they have the ability for multipotential differentiation to various types of tissues. Thus, control of neoplastic potentials of ES cells is very important for the treatment of degenerative or injured diseases. Mouse ES cells carrying the sequence for the green fluorescent protein (GFP) gene were transplanted into adult mouse retinas by intravitreal injections 20 h after intravitreal N-methyl-d-aspartate (NMDA) administration. One week after the ES cell injection, folate antagonist methotrexate (MTX) was injected intravitreally. Eyes were retrieved 4 weeks after ES cell transplantation for histologic analyses. Conventional histological analysis was performed by hematoxylin and eosin staining with the use of paraffin-embedded sections. Neuronal differentiation and teratogenic potential of ES cells were demonstrated by immunohistochemistry. The proliferative activity of transplanted cells was detected by mitotic index, proliferating cell nuclear antigen index and AgNOR count. The incorporation of transplanted ES cells in MTX-treated and non-treated retinas at 4 weeks after transplantation was observed in 8/16 eyes (50%) and 8/16 eyes (50%), respectively. Transplanted ES cells in MTX-treated retina showed increased neuronal differentiation and decreased expression of teratogenic markers, compared with ES cells in non-treated retina. The proliferative activity of transplanted ES cells in MTX-treated retina was lower than that in non-treated retina. These results suggest that intravitreal MTX treatment following transplantation can induce neuronal differentiation in the transplanted ES cells and decrease their proliferative activity.

Alkaline Phosphatase↗
PubMed2005

Pituitary adenylate cyclase-activating polypeptide (PACAP) can act as determinant of the tyrosine hydroxylase phenotype of dopaminergic cells during retina development.

In the chick retina, dopaminergic cells are generated between embryonic days 3 and 7 (E3/E7). However, the expression of tyrosine hydroxylase (TH), the first enzyme in the catecholamine synthetic pathway, is only detected after E11/E12. During the interval comprising E7 to E12, signals conveyed by cAMP are important to determine the TH phenotype. The present study shows that pituitary adenylyl cyclase-activating polypeptide (PACAP), via cAMP, is a major endogenous component in defining the TH phenotype of retina dopaminergic cells during development. PACAP type 1 receptor and its mRNA were detected in retinas since E6. PACAP was also immunodetected in cells localized in the inner nuclear layer of retinas since E8. This peptide promoted greater than 10-fold increase in cAMP accumulation of retinas obtained from embryos since E8, an effect that was blocked by PACAP6-38 (PAC1 receptor antagonist). In cultured retina cells from E8 and E9, maintained for 6 days in vitro with 10 nM PACAP (for 5 days), the number of dopaminergic cells expressing tyrosine hydroxylase increased 2.4-fold. The cAMP analog, 8-Br-cAMP and 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inhibitor) also increased the number of tyrosine hydroxylase-positive cells by 4- to 6-fold. IBMX plus PACAP treatment resulted in 17-fold increase in the number of cells positive for tyrosine hydroxylase. Under this condition the amount of tyrosine hydroxylase expression, as detected by western blot analysis, was also increased. The protein kinase-A inhibitor, rp-cAMPS, significantly reduced the effect of PACAP. Our data show that this peptide is an important factor influencing the definition of the tyrosine hydroxylase phenotype of retina dopaminergic cells within a narrow window of development.

1-Methyl-3-isobutylxanthine↗
PubMed2005

Heterogeneous populations of microglia/macrophages in the retina and their activation after retinal ischemia and reperfusion injury.

Activation of Microglia/macrophages has been observed in ischemia-reperfusion injury of the brain. This study was undertaken to investigate the different subpopulations of microglia/macrophages in the normal rat retina and their activation after retinal ischemia. Retinal ischemia was induced by elevation of intraocular pressure to 120 mmHg for 60 min. Microglia/macrophages were identified on frozen retinal sections by four antibodies, namely OX42, 5D4, OX6 and ED1. In the normal retina, there were heterogeneous populations of resident microglia/macrophages as characterized by their differences in morphology, antigen expression and distribution. OX42+ cells had delicate processes and were located in the inner layers of the retina, while 5D4+ cells were highly ramified and mostly scattered in the inner plexiform layer (IPL) and the outer plexiform layer. Few amoeboid ED1+ cells were also seen in the ganglion cell layer and IPL. OX6+ (MHC-II antigen presenting) cells were not detected in the normal retinas. Double labeling with OX42 and 5D4 antibodies on normal retinal sections showed few microglia exhibited positive labeling with both OX42 and 5D4, while the majority of the microglia were labeled with either OX42 or 5D4 antibodies. After retinal ischemia single labeling with these antibodies showed increased number of these antigen-expressing cells, disappearance of normal cellular processes, and rounding or amoeboid like appearance of the cell bodies. At 1 day after ischemia, there was a significant infiltration of round OX42+, ED1+ and OX6+ cells with loss of the cellular processes in the inner retina. From 3 to 14 days, all subpopulations of microglia/macrophages differentiated cellular processes and became dendritic again. Double labeling on retinas after 1 day of recovery showed OX42+ cells were co-labeled with ED1+ or OX6+ cells, but not with 5D4+ cells. Scattered amoeboid OX42+, 5D4+, and ED1+ cells were noted in the subretinal space 3-14 days after ischemia. In summary, there were heterogeneous populations of resident microglia/macrophages in the normal inner retina and they were activated early after ischemia-reperfusion injury and exhibited different antigenic expression which were further altered in the recovery phase.

Animals↗
PubMed2005

High resolution imaging of fluorescein patterns in RCS rat retinae and their direct correlation with histology.

To assess the progressive changes in the retinal vascular bed of dystrophic and non-dystrophic Royal College of Surgeons (RCS) rats, retinae, were visualised correlating in vivo fundus fluorescein angiography (FA) with histology. FA was performed in rats aged 5 weeks to 2 years, using a Zeiss confocal scanning laser ophthalmoscope (cSLO). After the final imaging session, a subset of retinae were prepared for flat-mount histology and the vascular bed was visualised using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) staining. While non-dystrophic rat retinae showed no substantive changes in vascular patterns with age and no demonstrable fluorescein leakage up to at least 1 year, dystrophic rat retinae showed abnormal vascular formations, demonstrable on FA and NADPH-d staining, which could be correlated in single retinae. Hyperfluorescent spots and late angiographic leakage were evident beginning at 10 weeks and progressed in severity with time: they were coincident in distribution with abnormal histological vascular complexes. The ability to monitor the same retina serially makes this approach a valuable tool for studying the dynamics of vascular change in the diseased retina, not only during the course of degeneration but also when assessing efficacy of potential therapeutic approaches.

Animals↗
PubMed2006

Effect of light exposure on the accumulation and depletion of retinyl ester in the chicken retina.

A previous study has shown that in the cone-rich chicken retina, 11-cis retinyl ester increases with light exposure and decreases in subsequent dark adaptation. The purpose of this research is to study how light exposure (intensity and duration) determine the rate of accumulation and utilization as well as the size of this 11-cis retinyl ester pool in the chicken retina. Chickens were dark-adapted overnight before exposure to different light intensities and durations. Animals were sampled at regular time intervals. 11-cis retinal and 11-cis retinyl ester were extracted from the retina and analyzed by HPLC. An increase in light intensity from 1,000 and 2,000 Lux (for a 20 min exposure) increased the amount of 11-cis retinyl ester from 0.38 to 0.75 nmol/mg. An increase in the duration of light exposure from 10 to 20 min (at 2,000 Lux) also increased the amount of 11-cis retinyl ester in the chicken retina (from 0.37 to 0.75 nmol/mg). This 11-cis retinyl ester pool in the chicken retina was rapidly reduced to baseline level ( approximately 0.20 nmol/mg) upon dark adaptation. The rate of accumulation of 11-cis retinyl ester was dependent on light intensity and duration of exposure and the maximum rate was approximately 0.03 nmol/mg/min. In comparison, dark adaptation was associated with a significantly higher rate of 11-cis retinyl ester depletion (approximately 0.05), indicating that light exposure and dark adaptation were associated with different biochemical steps of retinoid storage and utilization. Results from this study are the first to show that the size of the 11-cis retinyl ester pool, as well as the rate of its accumulation and depletion in the cone-rich chicken retina, are determined by the intensity and duration of light exposure. These data support the suggestion that a light-driven cone cycle exists in the chicken retina.

Adaptation, Ocular↗
PubMed2006

Analysis of apoptotic and survival mediators in the early post-natal and mature retina.

Apoptosis, a cellular process critical to retinal neurogenesis, has been implicated in several neurodegenerative disorders. As the retina matures the suppression of apoptosis occurs and the emphasis shifts towards survival. To identify the cellular changes that bring about this critical shift in the balance, we performed an expression analysis of pro- and anti-apoptotic mediators in the immature, post-natal day 6 (P6) and the post-mitotic adult P60 mouse retina. Laser capture microdissection (LCM) of the P6 and the P60 retina, followed by reverse transcriptase-polymerase chain reaction (RT-PCR) was employed to elucidate changes in the mRNA expression of Apaf-1, caspase-3 and caspase-9 in the individual retinal layers in the young and mature tissue. RT-PCR and Western blotting of whole P6 and P60 retinal preparations was carried out to determine changes in other caspases and key survival mediators at the mRNA and protein level, respectively. Our results demonstrate that each neuronal cell layer in the adult retina down-regulates the gene expression of Apaf-1 and caspase-3, and to a lesser extent, caspase-9. The protein expression levels of other executioner and initiator caspases are also reduced in the adult tissue. Interestingly, XIAP, a potent caspase inhibitor, increases in expression in the adult retina. Additionally, we demonstrate age-dependent increased expression and activation status of the components of the MAPK transduction cascade. Conversely, we observe decreased PI3-K and AKT expression and decreased activity of AKT (pAKT) in the adult retina. Furthermore, results from RNAi experiments demonstrate an additional mechanism of PI3-K regulation in photoreceptor cells. Our findings suggest that a survival strategy adopted by the post-mitotic retina involves a down-regulation of key pro-apoptotic factors concomitant with changes in expression and activation status of certain pro-survival mediators.

Animals↗
PubMed2006

Age-related changes in sympathetic neurotransmission in rat retina and choroid.

While age-related night vision loss and age-related macular degeneration are well characterized, less is known about the normal aging process in the retina and choroid. The purpose of this study was to ascertain whether dopamine beta-hydroxylase (DBH), beta1- and beta2-adrenergic receptor gene and protein expression are altered in the retina and choroid with age. The retina and choroid were dissected from F344xBNF1 hybrid rats aged 8, 22, and 32 months. Real-time PCR and Western blot analysis were conducted to determine steady-state mRNA and protein expression. Immunohistochemistry (IHC) was conducted to localize DBH protein expression in the retina. DBH protein expression was substantially decreased with age in the retina, particularly in the outer nuclear layer, with no changes in DBH expression noted in the choroid. There was a significant increase in beta1-adrenergic receptor protein expression in retinal samples at 22 months, while beta2-adrenergic receptor protein expression was not affected by age. Decreased expression of DBH with age in the retina could lead to reduced production of norepinephrine, potentially resulting in an increase of beta1-adrenergic receptor expression due to denervation supersensitivity. Gene expression for DBH, beta1- and beta2-adrenergic receptors were observed to peak at 22 months and return to baseline levels by 32 months of age in the choroid. Our findings suggest that the retina may be more sensitive to age-related loss of sympathetic neurotransmission than the choroid, which may partially explain normal age-related vision loss in the elderly.

Aging↗
PubMed2007

The selective retention of lutein, meso-zeaxanthin and zeaxanthin in the retina of chicks fed a xanthophyll-free diet.

Lutein and zeaxanthin are pigmented oxygenated carotenoids, or xanthophylls, derived from plants and concentrated in the retina of primates and birds. We investigated the transport, distribution and depletion of lutein and zeaxanthin in the plasma and tissues of newly hatched chicks fed xanthophyll-free diets. One-day-old Leghorn chicks were randomly divided into two groups. A control group was fed a diet containing lutein and zeaxanthin (5.2 and 1.7 mg/kg diet, respectively) for 28 days. An experimental group was fed a diet containing no lutein and zeaxanthin for 28 days. Plasma and tissues were analyzed for lutein and zeaxanthin at 28 days (control) and on days 1, 14 and 28 (experimental). At hatching, lutein and zeaxanthin were the predominant carotenoids present in the blood and tissues. As indicated by their similar mass contents, there was complete transfer of these carotenoids from egg yolk to chick. Lutein and zeaxanthin concentrations in the plasma and tissues of chicks fed the xanthophyll-free diet decreased rapidly to almost zero (with a depletion time of seven days [t(1/2)]). In contrast, the retina retained its initial concentrations of lutein and zeaxanthin similar to the control group. meso-Zeaxanthin and cis-zeaxanthin were identified only in the retina. The retina concentrated zeaxanthin over lutein. Lutein and zeaxanthin were selectively retained in the retinas of chicks fed a xanthophyll-free diet. In contrast, the plasma and other tissues lost up to 90% of their original content of xanthophylls. These data emphasize the relative stability of lutein and zeaxanthin in the cone-rich retina where they are present as esters in oil droplets. The tissue depletion suggests the need for a regular dietary intake of lutein and zeaxanthin because of rapid depletion in the body. It is clear that these xanthophylls may have an essential role in the cone-rich retina of the chick as evidenced by their selective retention.

Animals↗
PubMed2007

Constant illumination causes spatially discrete dopamine depletion in the normal and degenerate retina.

A fully competent retinal dopamine system underpins normal visual function. Although this system is known to be compromised both prior to and during retinal degeneration, the spatial dynamics of dopamine turnover within the degenerate retina are at present unknown. Here, using immunohistochemistry for dopamine in combination with quantitative optical density measurements, we reveal a global decline in retinal dopamine levels in the light adapted RCS dystrophic rat, which is restricted to plexiform layers in the dark. Pharmacological blockade of dopamine production with the drug alpha-methyl-p-tyrosine (AMPT) allows the direct visualisation of dopamine depletion in normal and degenerate retina in response to constant illumination. In normal retinae this effect is spatially discrete, being undetectable in perikarya and specific to amacrine cell fibres in sublamina 1 of the inner plexiform layer. A similar response was observed in the retinae of dystrophic rats but with a reduction in amplitude of approximately 50%. It is suggested that the pattern of dopamine depletion observed in rat retina may reflect an AMPT-resistant pool of perikaryal dopamine and/or a reduction in extrasynaptic release of this neurotransmitter in response to illumination in vivo. We conclude that the visualisation of dopamine depletion reported here represents a release of this neurotransmitter in the response to light. Turnover of dopamine in the dystrophic retina is discussed in the context of surviving photoreceptors, including the intrinsically photosensitive melanopsin ganglion cells of the inner retina.

Animals↗
PubMed2006

A novel organotypic culture model of the postnatal mouse retina allows the study of glutamate-mediated excitotoxicity.

A novel organotypic culture method of mouse retina explants is being introduced and characterized to evaluate its usefulness in studying glutamate excitotoxicity. Retinal whole-mounts were dissected from eyes of C57BL/6 mice aged P10-14 and transferred to poly-D-lysine/laminin coated round coverslips. After 7 days in vitro, retina explants were treated with varying concentrations of L-glutamate and cell death was accessed with TUNEL histochemistry. Neurofilament-68 kDa immunoreactivity was used to identify retinal ganglion cells (RGC) with immunohistochemistry. Additional cell markers were used to further characterize the cytoarchitecture of the organotypic retina cultures. Retina explants attached very well to the coated coverslips allowing for experimental manipulation and pharmacological access to the tissue. Hematoxylin-Eosin (HE) staining of vertical cryostat sections of retina explants demonstrated well preserved intact cytoarchitecture under organotypic culture conditions and PKCalpha, Calbindin, GABA, Rhodopsin, GFAP and neurofilament immunoreactivities identifying rod bipolar, horizontal, amacrine, photoreceptor, glial, and retinal ganglion cells, respectively, were not different from freshly isolated mouse retina. Dose dependent glutamate toxicity and accompanying RGC apoptotic cell death were determined by TUNEL histochemistry. In contrast to previously published methods using slice or floating whole-mount cultures, the ex vivo culture system presented here combines accessibility to experimental manipulation, and adherence of whole-mount cultures to a substrate with a significant preservation of retinal cell types, numbers and morphology. The described retina explant culture on glass coverslips allows for effective pharmacological manipulation including the study of neuronal cell death and RGC physiology.

Animals↗
PubMed2004

Neurofilament subunits undergo more rapid translocation within retinas than in optic axons.

Axonal transport of neurofilaments (NFs) has long been considered to be regulated by phosphorylation, although recent studies have challenged this hypothesis. Our prior analyses of axonal transport in optic axons demonstrated two distinct NF transport rates that spatially and temporally correlated with changes in NF phosphorylation. In our prior studies, we focused on subunits already within axons. Re-examination of these data using additional approaches and examining additional earlier time points have allowed us to calculate rates at which subunits transport out of retinas and into optic axons. NF subunits were radiolabeled by intravitreal injection of 35S-methionine. NF axonal transport was monitored by following the location of the front of radiolabeled subunits immunoprecipitated from retinas and segments of optic axons, which demonstrated four distinct transport rates. Subunits within retinas exhibited the fastest rate, and underwent a 50% slowing upon exiting the retina and entering optic axons. While this slowing could be due to a regional caliber increase and/or regional increase in NF phosphorylation within the first segment, prior studies indicated that inhibition of phosphatase activities increased NF phosphorylation within retinas and slowed NF subunit exit from retinas to a degree similar to that normally observed within the first segment of axons, suggesting that regional phosphorylation played a major role in slowing of NF transport following their exit from the retina. These findings provide additional support for the notion that phosphorylation regulates NF axonal transport.

Animals↗
PubMed2004

Methamphetamine exacerbates the toxic effect of kainic acid in the adult rat retina.

The recreational use of the psychoactive drug, methamphetamine has increased markedly over the last three decades. It has long been known that this drug has detrimental effects upon the mammalian brain monoaminergic system, but the long- or short-term effects on the retina, a neurological extension of the central nervous system, have received little attention. The aim of this study was, therefore, to determine whether intraocular injection of methamphetamine (MA) is toxic to the healthy adult rat retina and to analyse its effects on the compromised retina after an injection of the ionotropic glutamate receptor agonist, kainate, which is known to cause retinal neuropathology. The equivalent of 1 mM (in the vitreous humour) MA and/or kainate (40 microM) were injected intravitreally. Flash electroretinograms (ERGs) were recorded before and 2 and 4 days after treatment. Five days after treatment, animals were killed and the retinas analysed either for the immunohistochemical localisation of various antigens or for electrophoresis/Western blotting. Some animals were kept for 19 days after treatment and the retinas analysed for tyrosine hydroxylase immunoreactivity. No differences could be found between vehicle- and MA-treated retinas with respect to the nature or localisation of either tyrosine hydroxylase immunoreactivity after 5 or 19 days or other antigens after 5 days. Moreover, the normal ERG and GFAP and calretinin protein antigens were unaffected by MA. Kainate treatment, however, caused a change in the ERGs after 2 and 4 days, an alteration in every antigen localised by immunohistochemistry and an increase in the retinal levels of calretinin and GFAP proteins. Significantly, the changes seen in the b-wave amplitude and implicit time of the ERG after 4 days and the increased level of GFAP protein after 5 days following kainate treatment were enhanced when MA was co-injected. Intravitreal injection of methamphetamine had no detectable detrimental effect on the normal adult rat retina but exacerbated the damaging effects of kainic acid. Such data suggest that a neurotoxic effect of MA may be more obviously illustrated when the tissue is already compromised as occurs in, for example, ischemia.

Animals↗
PubMed2006

Norepinephrine acts as D1-dopaminergic agonist in the embryonic avian retina: late expression of beta1-adrenergic receptor shifts norepinephrine specificity in the adult tissue.

Dopamine is the main catecholamine found in the chick retina whereas norepinephrine is only found in trace amounts. We compared the effectiveness of dopamine and norepinephrine in promoting cyclic AMP accumulation in retinas at embryonic day 13 (E13) and from post-hatched chicken (P15). Dopamine (EC(50)=10microM) and norepinephrine (EC(50)=30microM), but not the beta(1)-adrenergic agonist isoproterenol, stimulated over seven-fold the production of cyclic AMP in E13 retina. The cyclic AMP accumulation induced by both catecholamines in embryonic tissue was entirely blocked by 2microM SCH23390, a D(1) receptor antagonist, but not by alprenolol (beta-adrenoceptor antagonist). In P15 retinas, 100microM isoproterenol stimulated five-fold the accumulation of cAMP. This effect was blocked by propanolol (10microM), but not by 2microM SCH23390. Embryonic and adult retina display beta(1) adrenergic receptor mRNA as detected by RT-PCR, but the beta(1) adrenergic receptor protein was detected only in post-hatched tissue. We conclude that norepinephrine cross-reacts with D(1) dopaminergic receptor with affinity similar to that of dopamine in the embryonic retina. In the mature retina, however, D(1) receptors become restricted to activation by dopamine. Moreover, as opposed to the embryonic tissue, norepinephrine seems to stimulate cAMP accumulation via beta(1)-like adrenergic receptors in the mature tissue.

Animals↗
PubMed2004

Neuronal susceptibility to damage: comparison of the retinas of young, old and old/caloric restricted rats before and after transient ischemia.

Compared to young rats, old age increases susceptibility and caloric restriction decreases susceptibility for the loss of retinal ganglion cells and displaced amacrine cells following retinal ischemia/reperfusion. In retinas of old animals before ischemia, reactive gliosis, including activation of Muller cells, microglia and astrocytes, is increased compared to retinas from young and old/caloric restricted animals. Post-ischemia, the existing reactive gliosis in retinas of old animals is not neuroprotective and the reactive gliosis is even further increased in old animals compared to young or old/caloric restricted animals. In retinas from old/caloric restricted animals, inducible heat shock protein-70 and brain-derived neurotrophic factor increased more markedly after ischemia/reperfusion compared to retinas from young and old animals. Thus, compared to retinas in young animals, neurons of old animals may be more susceptible to cell death by secondary glial mechanisms after retinal ischemia/reperfusion. Caloric restriction in old animals is neuroprotective against damage in the retina following ischemia, perhaps by suppressing glial activity and by the neuroprotective effects of inducible heat shock protein-70 and brain-derived neurotrophic factor.

Aging↗
PubMed2004

Neurokinin 1 receptor expression and substance P physiological actions are developmentally regulated in the rabbit retina.

We investigated the expression of the substance P (SP) receptor (the neurokinin 1 receptor, NK1 receptor) and SP functional effects in developing rabbit retinas. NK1 receptors in adult retinas were in a population of cone bipolar cells and in dopaminergic amacrine cells, as previously described. In contrast, at birth and at postnatal day (PND) 6, NK1 receptors were exclusively expressed by cholinergic amacrine and displaced amacrine cells. NK1 receptor expression in cholinergic cells was still observed at PND10 (eye opening), while at PND21 it was confined to cholinergic cells of the inner nuclear layer. Starting at PND10, NK1 receptors were also in bipolar cells and in dopaminergic amacrine cells. A fully mature NK1 receptor expression pattern was observed at PND35. Dopamine release was assessed in isolated retinas in the presence of SP, the NK1 receptor agonist GR73632 or the NK1 receptor antagonist GR82334. At PND35, extracellular dopamine was significantly increased by 10 microM SP or 0.01-100 microM GR73632, and it was decreased by 0.01-10 microM GR82334. No effects were detected in developing retinas up to PND21. Ca2+ imaging experiments were performed in single cholinergic cells identified by their "starburst" morphology in perinatal retinas. Intracellular Ca2+ levels were significantly increased by 1 microM SP or GR73632. This effect was reversibly inhibited by 1 microM GR82334. These data demonstrate that both NK1 receptor expression and SP physiological actions are developmentally regulated in the retina. SP neurotransmission in the immature retina may subserve developmental events, and SP is likely to represent an important developmental factor for the maturation of retinal neurons and circuitries.

Acetylcholine↗
PubMed2004

Expression of the neurokinin 1 receptor in the mouse retina.

Previous studies have revealed that the expression pattern of the neurokinin 1 receptor (the preferred receptor for substance P, SP) varies in different mammalian retinas. We investigated NK1 receptor expression in the mouse retina to provide background information for future studies in transgenic mice on SP functional roles in the retina. Mouse retinal sections were treated for single and double-label immunofluorescence. NK1 receptor immunoreactivity was in bipolar cells and in numerous amacrine cells. Double-label studies showed that NK1 receptor-expressing bipolar cells constituted a population of ON-type cone bipolar cells, since they were distinct from rod bipolar cells and contained glycine. They were nonrandomly distributed with highest density in central retina. These cells were similar and may correspond to the population of NK1 receptor-expressing bipolar cells of the rabbit retina. Different subsets of NK1 receptor-expressing amacrine cells were identified on the basis of the expression of selected neurotransmitter substances: i) about 23% of NK1 receptor-expressing amacrine cells also contained glycine; ii) the remaining 77% were likely to be GABAergic, although some inconsistency was observed in the GABA immunostaining obtained with two different GABA antibodies; iii) all dopaminergic amacrine cells also expressed NK1 receptors; iv) about one third of SP-containing amacrine cells also expressed NK1 receptors. These findings confirm and expand previous observations in rat and rabbit retinas. In particular, common to all three species is the expression of NK1 receptors in dopaminergic amacrine cells, indicating that SP neurotransmission may be a universal feature of the circuitry of the dopaminergic amacrine cell. Peculiar to the mouse retina is the presence of putative NK1 autoreceptors expressed by SP-containing amacrine cells.

Amacrine Cells↗
PubMed1986

Goldfish retina and tectum influence each other's growth activity during regrowth of the retinotectal projection.

Variations in retinal and tectal growth activity, during regrowth of the goldfish retinotectal projection, were monitored by measuring the rates of incorporation of [14C]leucine into soluble protein and tubulin-enriched fractions at different times after crushing the optic nerves. Other experiments tested for growth-modulating interactions between tectum and retina. Here we studied how the absence of one of these structures (i.e. tectal ablation or eye removal) affected the profile of biosynthetic activity in the other. Experiments were also conducted on groups of fish in which the tectum was reinnervated by a half-retina (either half-nasal (1/2 N) or half-temporal (1/2 T) retina). This was done to ascertain if growth interactions between retina and tectum display any position-dependent differences that may be relevant to retinotopic ordering during regeneration. Our studies have revealed that: the retina and tectum of 1/2 T and 1/2 N groups differ in their growth responses during regeneration of the visual pathway: the tectum may exert a stimulatory and at other times an inhibitory influence on retinal protein synthesis; and retina and tectum display a bimodal profile of biosynthetic activity during regeneration that coincides with two stages of increased cell division (primarily glia) which other workers have found occurs in the tectum and tract during regeneration of the retinotectal projection. Indeed it seems there may be a link between this glial proliferation and the neurotrophic and guiding influences which tectum and retina exert upon one another during regeneration.

Animals↗
PubMed2003

AII amacrine cells express the MT1 melatonin receptor in human and macaque retina.

AII amacrine cells are critical interneurons in the rod pathway of mammalian retina, active primarily in dim lighting conditions. Melatonin, a neuromodulator produced at night in the retina, is believed to induce retinal adaptation to dim lighting conditions in most vertebrate species examined to date, including humans. We hypothesized that melatonin may influence retinal light adaptation by acting on AII cells directly and thus investigated whether melatonin receptors were expressed in AII neurons. Postmortem nonpathological eyes from four human donors as well as two eyes from two Macaque Fasicularis monkeys were analyzed. Double immunocytochemistry was performed using an anti-MT(1) antibody and an antibody to calretinin, an AII marker. Analysis utilized confocal microscopy. A polyclonal anti-calretinin antibody labelled amacrine cells exhibiting the distinct AII morphology, in both human and macaque retina. MT(1) immunoreactivity in macaque retina was similar to human staining, in that horizontal, amacrine and ganglion cell bodies were stained, as were inner segments of photoreceptors. In human retina 86% of calretinin positive cells expressed the MT(1) receptor peripherally, whereas centrally, 78% colocalization was observed. In the macaque retina, 100% of AII amacrine cells expressed MT(1) immunoreactivity both centrally and peripherally. That virtually all AII neurons express the MT(1) receptor in both human and macaque retina, may provide the first evidence demonstrating a role for melatonin in AII regulation, furthering the hypothesis of melatonin function in retinal light adaptation.

Amacrine Cells↗