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PubMed2005

Carbonic anhydrase XIV identified as the membrane CA in mouse retina: strong expression in Müller cells and the RPE.

The presence of carbonic anhydrase (CA) activity in the neural retina has been known for several decades. CA-II, a soluble cytoplasmic isoform expressed by Müller cells and a subset of amacrine cells, was thought to be the sole source of CA activity in the neural retina. However, CA-II deficient mice retain CA activity in the neural retina, which implies that another isoform must be present in that tissue. Recently CA-XIV, an integral membrane protein, was cloned and characterized. We, therefore, sought to determine whether CA-XIV is expressed in the neural retina, and hence is responsible for the CA activity observed in CA-II null animals. Immunohistochemical analyses of histological sections from CA-II null, CA-XIV null, and control mice were performed to localize the CA-XIV isoform, as well as other known retinal markers. Immunoblotting and real-time RT-PCR analyses were also performed to test for CA-XIV expression in retina and other mouse tissues. We determined herein that CA-XIV, a approximately 45kDa membrane protein, is expressed in retina, as it is in kidney. In the retina, CA-XIV is expressed on the plasma membrane of Müller cells. CA-XIV is also found on both the apical and basal membranes of the retinal pigmented epithelium. The data presented here indicate that like CA-II, CA-XIV is highly expressed in the neural retina and, like CA-II, more specifically by the Müller cells. The cellular compartmentalization of the two isoforms in the Müller cell-one cytoplasmic and the other on the plasma membrane-suggest that the two enzymes have specific and unique functions. Future studies will be necessary to assign functions to CA-II and CA-XIV in the mouse neural retina.

Animals↗

PubMed2006

Development of the human retina in the absence of ganglion cells.

Retinal development was studied in eyes from fetal and neonatal human anencephalic (AnC) and normal age-matched infants to determine the time of retinal ganglion cell (GC) loss and its effect on the development of other retinal neurons. At fetal week (Fwk) 14, GC loss was evident in central retina and by Fwk 19-20 almost all GC were absent, although immunocytochemical labeling for GC markers brain 3, neurofilament M and parvalbumin detected a few GC in the AnC far periphery at older ages. The inner nuclear and inner plexiform (IPL) layers showed variable amounts of thinning but all normal bipolar (BP) and horizontal cell markers were still present. The amacrine (AM) labels calbindin and calretinin were markedly reduced. Lamination for these markers in the IPL was less organized than in normal retinas, with BP and AM markers extending into the degenerated GC layer. Cone and rod photoreceptors had normal morphology and topography in AnC retina and each expressed normal phototransduction and synaptic markers. The prospective fovea was identified in AnC neonatal retina by cone packing and the absence of immunolabeled rod photoreceptors. In one AnC neonatal retina, blood vessels and astrocytes extended across the inner retina in the putative fovea and there was no evidence of a pit. In another AnC neonatal retina, blood vessels and astrocytes formed a foveal avascular zone in the inner retina and a shallow pit was present within this zone. However, both foveas showed evidence for the onset of cone elongation and packing. These findings support the model of Springer and Hendrickson [2005; Vis. Neurosci. 22, 171] in which the foveal avascular zone is critical for pit formation, but suggest that mechanisms inherent to the outer retina may be involved in early stages of foveal cone packing.

Anencephaly↗

PubMed2006

Induced expression of hematopoietic- and neurologic-expressed sequence 1 in retinal pigment epithelial cells during newt retina regeneration.

Newts can regenerate their organs even as adults. For instance, when their neural retinas are completely removed by operation, the remaining retinal pigment epithelial (RPE) cells dedifferentiate to reconstruct neural retinas. To elucidate the molecular mechanisms of newt retina regeneration, we investigated genes upregulated in dedifferentiating RPE cells using differential display methods. We observed that a cDNA fragment of hematopoietic- and neurologic-expressed sequence 1 (Hn1) appeared to be induced within a few days of surgical removal of newt neural retina. Using an anti-HN1 antiserum against the recombinant HN1 protein, we carried out immunohistochemical analyses. The anti-HN1 antiserum recognized the plexiform layers and ganglion cell layer (GCL) but not the RPE cell layer in unoperated (normal) newt retinas. Using a glial fibrillary acidic protein antibody, Hn1 was shown to be possibly expressed in glial cells in normal neural retina. During retina regeneration, immunoreactivity for HN1 appeared in dedifferentiating RPE cells 10 days post-operation, and in retinal progenitor cells 18 days post-operation. Twenty seven days post-operation, HN1 immunoreactivity was localized in the plexiform layers and GCL as in the normal retina. Therefore, HN1 possibly plays an undefined role in dedifferentiating RPE cells and retinal progenitor cells during newt retina regeneration.

Amino Acid Sequence↗

PubMed2000

Retinas from albino rats are more susceptible to ischaemic damage than age-matched pigmented animals.

Age- and sex-matched pigmented (Lister Hooded) and albino (Wistar) rats were used in this study. The retinas of the animals were subjected to pressure-induced ischaemia (35 min, 120 mmHg) and reperfusion (3 days) in precisely the same way. The b-wave of the electroretinogram (ERG) in the pigmented animals recovered to normal levels while those of the albino rats were reduced by more than 80%. Moreover, the choline acetyltransferase (ChAT) immunoreactivity associated with a sub-set of amacrine cells was almost completely obliterated in the retinas from the albino rats but unaffected in the retinas of the pigmented rats. Also, in certain areas of the retina from albino rats there was a suggestion that the calretinin-immunoreactivity was affected. This was never seen in the retinas of the pigmented animals. The GABA-immunoreactivity in the retina of both albino and pigmented rats appeared to be unaffected by ischaemia/reperfusion. The data presented show that retinas from albino rats are more susceptible to ischaemia/reperfusion than retinas from pigmented animals. The results also show that reduction of the b-wave of the ERG and changes in the nature of the ChAT immunoreactivity represent sensitive markers to detect the effect of ischaemia/reperfusion to the retina.

Age Factors↗

PubMed2000

Diurnal metabolism of dopamine in dystrophic retinas of homozygous and heterozygous retinal degeneration slow (rds) mice.

Dopamine metabolism was studied in dystrophic retinal degeneration slow (rds) mice which carry a mutation in the rds/peripherin gene. RDS mutations in humans cause several forms of retinal degeneration. Dopamine synthesis and utilization were analyzed at various time points in the diurnal cycle in homozygous rds/rds retinas which lack photoreceptor outer segments and heterozygous rds/+ retinas which have short malformed outer segments. Homozygous retinas exhibited depressed dopamine synthesis and utilization while the heterozygous retina retained a considerable level of activity which was, nevertheless, significantly lower than that of normal retinas. By one year, heterozygous rds/+ retinas which had lost half of the photoreceptors still maintained significant levels of dopamine metabolism. Normal characteristics of dopamine metabolism such as a spike in dopamine utilization at light onset were observed in mutant retinas. However, light intensity-dependent changes in dopamine utilization were observed in normal but not rds/+ retinas. The findings of this study suggest that human patients with peripherin/rds mutations, or other mutations that result in abnormal outer segments that can still capture light, might maintain light-evoked dopamine metabolism and dopamine-dependent retinal functions during the progression of the disease, proportional to remaining levels of light capture capabilities. However, visual deficits due to reduced light-evoked dopamine metabolism and abnormal patterns of dopamine utilization could be expected in such diseased retinas.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2003

Genetic deletion of somatostatin receptor 1 alters somatostatinergic transmission in the mouse retina.

In the mammalian retina, sparse amacrine cells contain somatostatin-14 (SRIF) which acts at multiple levels of neuronal circuitry through distinct SRIF receptors (sst(1-5)). Among them, the sst1 receptor has been localised to SRIF-containing amacrine cells in the rat and rabbit retina. Little is known about sst1 receptor localisation and function in the mouse retina. We have addressed this question in the retina of mice with deletion of sst1 receptors (sst1 KO mice). In the retina of wild type (WT) mice, sst1 receptors are localised to SRIF-containing amacrine cells, whereas in the retina of sst1 KO mice, sst1 receptors are absent. sst1 receptor loss causes a significant increase in retinal levels of SRIF, whereas it does not affect SRIF messenger RNA indicating that sst1 receptors play a role in limiting retinal SRIF at the post-transcriptional level. As another consequence of sst1 receptor loss, levels of expression of sst2 receptors are significantly higher than in control retinas. Together, these findings provide the first demonstration of prominent compensatory regulation in the mouse retina as a consequence of a distinct SRIF receptor deletion. The fact that in the absence of the sst1 receptor, retinal SRIF increases in concomitance with an increase in sst2 receptors suggests that SRIF may regulate sst2 receptor expression and that this regulatory process is controlled upstream by the sst1 receptor. This finding can be important in the design of drugs affecting SRIF function, not only in the retina, but also elsewhere in the brain.

Animals↗

PubMed2000

Upregulation of CD44 expression in the retina during the rds degeneration.

In adult mouse retinas the standard form of the cell surface adhesion/receptor molecule CD44 is localized to Müller cell apical microvilli. In the rds (retinal degeneration slow) mouse, however, CD44 immunolabel is increased and distributed throughout the retina by 3 months postnatal. At present, it is unclear if this labeling pattern is due to the increased expression of standard CD44, the expression of variant CD44 isoforms, or an unmasking of CD44 antigenic sites. To further characterize this response, we have studied the expression of CD44 mRNA and protein in rds retinas of different ages. RT-PCR analysis demonstrated one product which represented the message for standard CD44 in adult BALB/c mouse retina and in all ages of rds retinas studied. Upon Southern blotting, this major product was detected along with two minor bands of larger size in all samples. Northern blot analysis demonstrated a major transcript of approximately 4.0 kb and a minor one of 3.0 kb in all BALB/c and rds retinas. By 3 months postnatal in rds retinas, the expression of CD44 message was increased by at least two-fold. Western blot analysis demonstrated the presence of only the standard form of CD44 protein in all BALB/c and rds retinas. An increased amount of this standard CD44 protein was observed in 2, 3, and 6 month rds retinas. Thus, this study demonstrates that the inherited retinal degeneration exhibited by the rds mouse does not cause an altered expression of retinal CD44 isoforms, but does lead to an upregulation in the expression of mRNA and protein for standard CD44.

Aging↗

PubMed1998

Serotonergic projections to the retina of rat and goldfish.

Serotonin amacrine cells have been described in the retina of vertebrates, except mouse and rat. Moreover, serotonin immunoreactive fibers have been reported in the optic nerve of rodents, frog and stingray. The purpose of this work was to study serotonin dorsal raphe nucleus projections to the retina, and to determine whether this pathway occurs in teleosts. The existence of specific connections was investigated in the rat and in the goldfish by the use of the neurotoxic substance 5,7-dihydroxytryptamine followed by monoamines determination in the retina by HPLC. The administration of 5,7-dihydroxytryptamine into the central or the lateral area of the rat dorsal raphe nucleus decreased serotonin levels in the raphe area and in the hippocampus, but only the bilateral injection into the dorsal raphe nucleus decreased it in the retina. In the goldfish, the injection of 5,7-dihydroxytryptamine into the optic tectum decreased serotonin concentration in situ and in the retina. The binding of [3H]paroxetine, a marker of serotonin transporter, was reduced in the retina of both species after the central treatment with the neurotoxic substance. In addition, the administration of the serotonin precursor 5-hydroxytryptophan into the optic tectum increased serotonin levels in the site of the injection and in the retina. The intraocular administration of 5,7-dihydroxytryptamine produced a big decrease in the content of retinal serotonin. This indoleamine and 5-hydroxyindoleacetic acid were detected in the optic nerves of rat and goldfish. The results indicate the existence of serotonergic retinopetal fibers in the rat and in the goldfish, a pathway that was not specifically demonstrated for the rat and was not previously proposed for the fish. The study of these serotonergic projections from the brain to the retina could be of interest in the understanding of the functional role of serotonin in the retina.

5,7-Dihydroxytryptamine↗

PubMed1998

Nitric oxide synthase activity and L-arginine metabolism in the retinas from streptozotocin-induced diabetic rats.

1. Nitric oxide synthase (NOS) activity was studied in the retinas from normal rats and in the retinas from two groups of streptozotocin-induced (8 days and 4 months) diabetic rats. In each animal group, the NOS activity was correlated to the concentration of amino acids related to L-arginine metabolism and to L-arginine uptake. 2. Retinas from both groups of streptozotocin-induced diabetes (8 days and 4 months) showed an increased NOS activity compared with the NOS activity in retinas from normal rats. In retinas lysate from normal rats, the NOS activity was most potently inhibited by NO-Arg (1 mM), whereas, in both groups of streptozotocin-induced diabetes, the NOS activity was most potently inhibited by the NOS inhibitor aminoguanidine (0.5 mM). 3. The basal levels of the amino acids related to L-arginine metabolism-namely, L-arginine, L-citrulline, L-ornithine and L-glutamine-in retinas from both groups of rats with streptozotocin-induced diabetes were decreased compared with the amino acid levels in retinas from normal rats. 4. The uptake of L-[3H]arginine in retinas from both groups of rats with streptozotocin-induced diabetes was increased compared with the uptake of of L-[3H]arginine in retinas from normal rats.

Animals↗

PubMed2002

Outer retinal anoxia during dark adaptation is not a general property of mammalian retinas.

The purpose of this study was to measure the intraretinal oxygen distribution across the retina under conditions, which maximise outer retinal oxygen consumption. In particular, we looked for evidence of increased oxygen delivery from the choroid and the deep retinal capillary layer, and whether or not this was sufficient to avoid the development of intraretinal anoxia. Under dark-adapted conditions the photoreceptors need additional energy, at least part of which is derived from increased oxidative metabolism. In earlier studies in the cat retina it was revealed that dark adaptation could render some regions of the outer retina anoxic. The present study of the in vivo oxygen distribution across the rat retina in light and dark found no evidence of outer retinal anoxia in the dark. This was despite a mean increase of 52.6+/-11.4% (n=7) in outer retinal oxygen consumption in the dark. The mean value for the minimum outer retinal PO(2) in the dark was 5.2+1.2 mmHg. Oxygen delivery from both the choroid and the deep retinal capillary layer increased in the dark (P<0.01, and P<0.001, respectively). It is argued that the ability of the deep capillary layer to compensate for changes in oxygen demand in the outer retina is an important element in the maintenance of homeostasis in the retina. This is in addition to the role of the deep capillary layer in supplying oxygen to the highly consuming plexiform layers within the inner retina. These findings in the rat retina also demonstrate that intraretinal anoxia in the dark, is not, as implied by earlier work in the cat, a general feature of mammalian retinas.

Animals↗

PubMedDate not supplied

Ontogeny of preproenkephalin mRNA expression in the rat retina.

Endogenous opioid systems (i.e. opioid peptides and opioid receptors) modulate developmental events in the neonatal mammalian retina. In the present study, the mRNA encoding preproenkephalin A (PPE), the prohormone for the opioid growth factor (OGF), [Met5]-enkephalin, was studied in the developing and the adult retinas of rats. Northern analysis indicated the presence of a 1.4-kb message in the developing and adult retinas corresponding to rat PPE mRNA. Quantitation showed that PPE message was present on postnatal day 1 at 5% of the adult level, and increased during development until the adult quantity was reached by postnatal day 27. In situ hybridization experiments first detected the presence of PPE mRNA in retinal tissues during late gestation. In late prenatal and neonatal retinas, PPE message was associated with areas of the developing retina containing proliferating neuroblasts and postmitotic cells. Later in development, message appeared to be located primarily within the inner retina, with abundant PPE mRNA associated with putative horizontal cells of the inner nuclear layer (INL). The adult retina showed a similar pattern of PPE gene expression in the cells of the INL. These findings document that the gene expression in the retina for PPE begins in the fetus, continues during retinal development, and coincides with the presence of a PPE mRNA derivative ([Met5]-enkephalin) that regulates DNA synthesis during retinal ontogeny. Our results are also the first to show the presence of PPE message in the adult mammalian retina, suggesting transcription of an opioid gene in the mature visual system.

Animals↗

PubMedDate not supplied

NADPH diaphorase activity in mammalian retinas is modulated by the state of visual adaptation.

NADPH diaphorase histochemistry is commonly used to identify cells containing nitric oxide synthase (NOS), the enzyme catalyzing the production of nitric oxide from L-arginine. NADPH diaphorase activity and NOS immunostaining was demonstrated in different cells of the vertebrate retina; photoreceptors, horizontal cells, amacrine cells, ganglion cells, and Müller cells. However, the physiological role of nitric oxide (NO) in the retina has yet to be elucidated. In this study, we tested the assumption that NADPH diaphorase activity in the retinas of rabbits and rats depended on the state of visual adaptation. In the rabbit, light adaptation enhanced NADPH diaphorase activity in amacrine cells and practically eliminated it in horizontal cells. Dark adaptation induced the opposite effects; the NADPH diaphorase activity was reduced in amacrine cells and enhanced in horizontal cells. Retinas from eyes that were injected intravitreally with L-glutamate exhibited a pattern of NADPH diaphorase activity that was similar to that seen in dark-adapted retinas. In rats, the NADPH diaphorase activity of amacrine and horizontal cells exhibited adaptation dependency similar to that of the rabbit retina. But, the most pronounced effect of dark adaptation in the rat's retina was an enhancement of NADPH diaphorase activity in Müller cells, especially of the endfoot region. Assuming that NADPH diaphorase activity is a marker for NOS, these findings suggest that NO production in the mammalian retina is modulated by the level of ambient illumination and support the notion that NO plays a physiological role in the retina.

Adaptation, Ocular↗

PubMedDate not supplied

Distribution of tubulin, kinesin, and dynein in light- and dark-adapted octopus retinas.

Cephalopod retinas exhibit several responses to light and dark adaptation, including rhabdom size changes, photopigment movements, and pigment granule migration. Light- and dark-directed rearrangements of microfilament and microtubule cytoskeletal transport pathways could drive these changes. Recently, we localized actin-binding proteins in light-/dark-adapted octopus rhabdoms and suggested that actin cytoskeletal rearrangements bring about the formation and degradation of rhabdomere microvilli subsets. To determine if the microtubule cytoskeleton and associated motor proteins control the other light/dark changes, we used immunoblotting and immunocytochemical procedures to map the distribution of tubulin, kinesin, and dynein in dorsal and ventral halves of light- and dark-adapted octopus retinas. Immunoblots detected alpha- and beta-tubulin, dynein intermediate chain, and kinesin heavy chain in extracts of whole retinas. Epifluorescence and confocal microscopy showed that the tubulin proteins were distributed throughout the retina with more immunoreactivity in retinas exposed to light. Kinesin localization was heavy in the pigment layer of light- and dark-adapted ventral retinas but was less prominent in the dorsal region. Dynein distribution also varied in dorsal and ventral retinas with more immunoreactivity in light- and dark-adapted ventral retinas and confocal microscopy emphasized the granular nature of this labeling. We suggest that light may regulate the distribution of microtubule cytoskeletal proteins in the octopus retina and that position, dorsal versus ventral, also influences the distribution of motor proteins. The microtubule cytoskeleton is most likely involved in pigment granule migration in the light and dark and with the movement of transport vesicles from the photoreceptor inner segments to the rhabdoms.

Animals↗

PubMedDate not supplied

Endocannabinoids in the intact retina: 3 H-anandamide uptake, fatty acid amide hydrolase immunoreactivity and hydrolysis of anandamide.

There is much evidence for an endocannabinoid system in the retina. However, neither the distribution of endocannabinoid uptake, the regulation of endocannabinoid levels, nor the role of endocannabinoid metabolism have been investigated in the retina. Here we focused on one endocannabinoid, anandamide (AEA), and its major hydrolyzing enzyme, fatty acid amide hydrolase (FAAH), in the goldfish retina. Immunoblots of FAAH immunoreactivity (IR) in goldfish retina, brain and rat retina, and brain homogenates showed a single band at 61 kDa that was blocked by preadsorption with peptide antigen. Specific FAAH IR (blocked by preadsorption) was most prominent over Müller cells and cone inner segments. Weaker label was observed over some amacrine cells, rare cell bodies in the ganglion cell layer, and in four lamina in the inner plexiform layer. FAAH activity assays showed that goldfish-retinal and brain homogenates hydrolyzed AEA at rates comparable to rat brain homogenate, and the hydrolysis was inhibited by methyl arachidonyl fluorophosphonate (MAFP) and N-(4 hydroxyphenyl)-arachidonamide (AM404), with IC(50)s of 21 nM and 1.5 microM, respectively. Cellular 3H-AEA uptake in the intact retina was determined by in vitro autoradiography. Silver-grain accumulation at 20 degrees C was most prominent over cone photoreceptors and Müller cells. Uptake was significantly reduced when retinas were incubated at 4 degrees C, or preincubated with 100 nM MAFP or 10 microM AM404. There was no differential effect of blocking conditions on the distribution of silver grains over cones or Müller cells. The codistribution of FAAH IR and 3H-AEA uptake in cones and Müller cells suggests that the bulk clearance of AEA in the retina occurs as a consequence of a concentration gradient created by FAAH activity. We conclude that endocannabinoids are present in the goldfish retina and underlay the electrophysiological effects of cannabinoid ligands previously shown on goldfish cones and bipolar cells.

Amidohydrolases↗

PubMedDate not supplied

The topography of rod and cone photoreceptors in the retina of the ground squirrel.

The distributions of rod and cone photoreceptors have been determined in the retina of the California ground squirrel, Spermophilus beecheyi. Retinas were fixed by perfusion and the rods and cones were detected with indirect immunofluorescence using opsin antibodies. Local densities were determined at 2-mm intervals across the entire retina, from which total numbers of each receptor type were estimated and isodensity distributions were constructed. The ground squirrel retina contains 7.5 million cones and 1.27 million rods. The peak density for the cones (49,550/mm2) is found in a horizontal strip of central retina 2 mm ventral to the elongated optic nerve head, falling gradually to half this value in the dorsal and ventral retinal periphery. Of the cones, there are 14 M cones for every S cone. S cone density is relatively flat across most of the retina, reaching a peak (4500/mm2) at the temporal end of the visual streak. There is one exception to this, however: S cone density climbs dramatically at the extreme dorso-nasal retinal margin (20,000/mm2), where the local ratio of S to M cones equals 1. Rod density is lowest in the visual streak, where the rods comprise less than 5% of the local photoreceptor population, increasing conspicuously in the ventral retina, where the rods achieve 30% of the local photoreceptor population (13,000/mm2). The functional importance of the change in S to M cone ratio at the dorsal circumference of the retina is compromised by the extremely limited portion of the visual field subserved by this retinal region. The significance for vision, if any, remains to be determined. By contrast, the change in rod/cone ratio between the dorsal and ventral halves of the retina indicates a conspicuous asymmetry in the ground squirrel's visual system, suggesting a specialization for maximizing visual sensitivity under dim levels of illumination in the superior visual field.

Animals↗

PubMedDate not supplied

Nitric oxide modulates cGMP levels in neurons of the inner and outer retina in opposite ways.

In the mammalian retina, neuronal nitric oxide synthase (NOS) is mainly localized in subpopulations of amacrine cells. One function of nitric oxide (NO) is to stimulate soluble guanylate cyclases which in turn synthesize cGMP. We used an antibody specific for cGMP to demonstrate cGMP-like immunoreactivity (cG-IR) in bovine, rat, and rabbit retinae and investigated the effects on cGMP levels of both exogenously applied NO and of endogenously released NO. We found that cGMP levels in inner and outer retina were controlled in opposite ways. In the presence of the NO-donors SNP, SIN-1 or SNAP, cG-IR was prominent in neurons of the inner retina, mainly in cone bipolar cells, some amacrine and ganglion cells. Retinae incubated in IBMX showed weak cG-IR in bipolar cells. Glutamate increased cG-IR in the inner retina, presumably by stimulating endogenous NO release, whereas NOS inhibitors or GABA and glycine decreased cG-IR in bipolar cells by reducing NO release. In somata, inner segments and spherules of rod photoreceptors the situation was reversed. cG-IR was undetectable in the presence of NO-donors or glutamate, was moderate in IBMX-treated retinae, but increased strongly in the presence of NOS inhibitors or GABA/glycine. We conclude that NO is released endogenously in the retina. In the presence of NO, cGMP levels are increased in neurons of the inner retina, but are decreased in rods.

Animals↗

PubMedDate not supplied

Interactions between enkephalin and GABA in avian retina.

In addition to conventional neurotransmitters such as acetylcholine, dopamine, glycine and gamma-aminobutyric acid (GABA), a number of peptide-immunoreactive substances have recently been localized in the vertebrate retina. The functional roles of these retinal peptides and their interactions with conventional neurotransmitters are largely unknown. We have previously shown that exogenous opiates affect both the release of GABA and the firing patterns of ganglion cells in the goldfish retina, and we have now begun a systematic characterization of the opioid pathways in the chicken retina, because, among vertebrate retinas, avian retinas contain the highest concentration of enkephalins. Monoclonal antibodies specific for enkephalin have been used to demonstrate that a subpopulation of enkephalin-containing amacrine cells exists in the chicken retina. This retina also synthesizes Met-enkephalin and releases it on cell depolarization. The enkephalin-induced inhibition of GABA release in goldfish retina led us to examine whether similar interactions occur in chicken, and if so, whether enkephalins and GABA coexist in the same amacrine cells. Our results, presented here, indicate that exogenous enkephalins do indeed inhibit GABA release in the chicken retina. Surprisingly, we found that although some amacrine cells contain both enkephalin and GABA, others contain only one or the other.

Animals↗

PubMed1997

Glucose metabolism of the inner retina in pigs in darkness and light.

In the pig eye, oxygen and glucose consumption in the outer retina are reduced in light compared to the consumption in the dark and most of the glucose consumed is metabolized to lactate both in light and in the dark. In the present study, in order to characterize the metabolism of glucose in the inner retina. Blood was collected from an artery and from a plexus on the optic nerve draining blood from the retina. Arteriovenous concentration differences for glucose, lactate and oxygen were determined. Observations were made in dark-adapted eyes and then after light adaptation. The consumption of oxygen and glucose and the lactate formation in the inner retina were calculated on the basis of these observations and recent data for retinal blood flow. In dark-adapted eyes, approx. 69% of the glucose was oxidized and approx. 20% was used in lactate formation. After 5-10 min of exposure to constant light, the levels of oxygen consumption and lactate formation were no different from those in darkness. The results indicate that lactate formation is a normal property of the pig inner retina, but that it is much less pronounced than in the outer part. The metabolism of the inner retina in constant light is similar to that in darkness. A comparison with data for the outer retina indicates that oxygen consumption in the inner retina in constant light is approx. 47% of that in the whole retina, while for glucose consumption and lactate production, the corresponding figures are approx. 12 and 8%, respectively.

Animals↗