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PubMed1977

[Treatment and follow-up of retinal tears associated with avulsed overlying retinal vessels (author's transl)].

The present clinical study is based on 17 cases of a specific clinical entity, which is characterised by a retinal break without retinal detachment, the tear being spanned by an avulsed patient retinal vessel invariably adjoining the operculum. The vessel was in the vitreous cavity and formed an arch above the break. All cases began with a sudden decrease or loss of visual acuity due to the rupture of the avulsed vessel and the occurrence of hemorrhages within the vitreous. These hemorrhages recurred in the course of the follow-up of the patients which lasted from 1-8 years. The recurrence of the bleeding was in most instances related to the mobility and the size of the vessel overlying the break. During treatment the cases were divided into two groups, group 1 comprising cases which were subjected only to light-coagulation, whereas in the cases of group 2 scleral buckling was performed in conjunction with cryopexy or light-coagulation. The comparatively best results were achieved in group 2. This condition is rare and amounted to only 1.5% of our total number of cases of retinal tears treated with light-coagulation during the last 8 years.

Aged↗
PubMed1998

Retinal arteriovenous malformation with fluctuating vision and ischemic central retinal vein occlusion and its sequelae: 25-year follow-up of a case.

A patient with a retinal arteriovenous malformation (AVM) had experienced episodic visual loss with spontaneous recovery for many years, followed by permanent visual loss secondary to central retinal vein occlusion. She subsequently progressed to development of retinal neovascularization extending onto the posterior vitreous face with recurrent vitreous hemorrhage requiring vitrectomy. A brief review of the literature is presented, and the cause of the fluctuations in vision and central retinal vein occlusion are discussed.

Adult↗
PubMed1982

Fine structure of the retinal epithelium and retinal tapetum lucidum of the goldeye Hiodon alosoides.

The fine structure of the retinal epithelium of the goldeye (Hiodon alosoides) has been investigated with electron microscopy in both the light- and dark-adapted condition. The retinal epithelial cells are extremely tall columnar cells. They form a single layer abutting on Bruch's membrane basally (sclerally) and interdigitating with bundles of photoreceptor cells apically (vitreally). The retinal epithelial cells and the photoreceptor bundles are arranged in a hexagonal fashion so that each epithelial cell normally contacts three photoreceptor bundles and three other epithelial cells. In the light-adapted state, melanosomes are sparsely but evenly distributed throughout the cell body except for the apices, which contain more melanosomes. In dark-adaptation, melanosomes become very concentrated in the cell apex between photoreceptor bundles, with some accumulation of melanosomes also noted basally. The predominant feature of these epithelial cells is the presence of numerous reflective bodies which act as a retinal tapetum lucidum. During light-adaptation these reflective bodies are scattered throughout the cell but in dark-adaptation they accumulate centrally. In the body of the epithelial cell these reflective particles are diffusely arranged, whereas they are regularly arranged where epithelial cells ensheath photoreceptor bundles. Circadian changes are also noted in the morphology of the myeloid bodies and mitochondria and in the location of the epithelial cell nucleus. Wandering phagocytes are present at the retinal epithelial-photoreceptor interface. Bruch's membrane is thick and trilaminate and the choriocapillaris endothelium is thin and sparsely fenestrated.

Animals↗
PubMed2004

Retinal replacement--the development of microelectronic retinal prostheses--experience with subretinal implants and new aspects.

BACKGROUND: Progress in the field of microelectronics has led to the development of visual prostheses for the treatment of blinding diseases. Different concepts of retinal replacement are currently under investigation. The aim of the retinal prostheses is to replace the function of lost photoreceptors in degenerative diseases, such as retinitis pigmentosa. METHODS: Within the field of visual prosthetic developments mainly two retinal based concepts are under investigation. One of the concepts is the epiretinal implant which acquires images of an external camera and after preprocessing by a computer reading this visual information into the human visual system. In the subretinal prosthesis design concept an array of stimulation electrodes is placed in the subretinal space. True to the concept the image falling on the retina and its light impulses are converted into electrical currents by microphotodiodes and the retina is stimulated with these locally. To test the feasibility of the concepts the biocompatibility and to determine basic stimulation parameters a lot of animal experiments and first human experiments were carried out. RESULTS: Currently the research conducted by teams in Germany, the USA and Japan into epiretinal and subretinal implants has reached the stage where clinical trials can now be performed. Individual pilot studies were carried out for both the epiretinal and the subretinal implant by different research groups. DISCUSSION: The results achieved by the researchers indicate that cortical action potentials can be triggered by electric retinal stimulation with both concepts. The experimental work has highlighted a whole range of obstacles, not all of which have yet been fully resolved. These findings offer hope that coarse restoration of vision may be feasible by electrical stimulation.

Animals↗
PubMed2004

AAV-mediated intravitreal gene therapy reduces lysosomal storage in the retinal pigmented epithelium and improves retinal function in adult MPS VII mice.

The beta-glucuronidase-deficient mucopolysaccharidosis type VII (MPS VII) mouse accumulates partially degraded glycosaminoglycans in many cell types, including retinal pigmented epithelial (RPE) cells in the eye. This lysosomal storage in RPE cells leads to progressive retinal degeneration and reduced function as measured by flash electroretinography (ERG). The impact of AAV-mediated intraocular gene therapy on pathology and retinal function was examined in normal and MPS VII mice treated at 4 weeks of age, when lysosomal storage is evident but functional impairment is minimal in affected animals. At 16 weeks, an age at which untreated MPS VII mice have advanced histologic lesions and significantly reduced ERG amplitudes, treated eyes had nearly normal levels of beta-glucuronidase activity, preservation of cells in the outer nuclear layer of the retina, and decreased lysosomal storage within the RPE. The AAV-treated MPS VII mice also had significantly increased dark-adapted ERG amplitudes compared to untreated MPS VII mice. Although retinal function was improved, the efficacy of the treatment depended heavily on parameters related to the injection procedure, such as the injection volume, injection site, and vector dose. These data suggest that intraocular AAV-mediated therapy may be efficacious for treating the retinal disease associated with certain lysosomal storage diseases.

Animals↗
PubMed1997

Optical rotation of the second harmonic radiation from retinal in bacteriorhodopsin monomers in Langmuir-Blodgett film: evidence for nonplanar retinal structure.

We observed optical rotation of the plane of polarization of the second harmonic (SH) radiation at 532 nm (in resonance with the retinal absorption) generated in reflection geometry in Langmuir-Blodgett film of bacteriorhodopsin (bR). The analysis of the experimental data showed that this effect arises from the nonvanishing contribution of the antisymmetrical part of the hyperpolarizability tensor. This requires that the dipole moment of the resonant electronic transition, the change of the dipole moment upon electronic excitation, and the long axis of the retinal not be coplanar. Such conditions are satisfied only if the retinal has a nonplanar geometry, a conclusion that could lend support to the heterogeneity model of the origin of the biphasic band shape of the linear CD spectrum of the retinal in bR. On the basis of our theoretical analysis, we were able to estimate the angle between the induced dipole moment and the plan that contains the long axis of the chromophore and the transition dipole moment of the retinal absorption.

Bacteriorhodopsins↗
PubMed2000

Unequal retinal and extra-retinal motion signals produce different perceived slants of moving surfaces.

Eye movements introduce retinal motion to the image and so affect motion cues to depth. For instance, the slant of a plane moving at right-angles to the observer is specified by translation and a component of relative motion such as shear. To a close approximation, the translation disappears from the image when the eye tracks the surface accurately with a pursuit eye movement. However, both translation and relative-motion components are needed to estimate slant accurately and unambiguously. During pursuit, therefore, an extra-retinal estimate of translation must be used by the observer to estimate surface slant. Extra-retinal and retinal estimates of translation speed are known to differ: a classic Aubert-Fleischl phenomenon was found for our stimuli. The decrease in perceived speed during pursuit predicts a corresponding increase in perceived slant when the eye tracks the surface. This was confirmed by comparing perceived slant in pursuit and eye-stationary conditions using slant-matching and slant-estimation techniques. Moreover, the increase in perceived slant could be quantified solely on the basis of the perceived-speed data. We found no evidence that relative-motion estimates change between the two eye-movement conditions. A final experiment showed that perceived slant decreases when a fixed retinal shear is viewed with increasing pursuit speed, as predicted by the model. The implication of the results for recovering metric depth estimates from motion-based cues is discussed.

Depth Perception↗
PubMed1994

Retinal photoreceptor count, retinal surface area, and optic disc size in normal human eyes.

PURPOSE: The optic disc area of normal human eyes shows an interindividual variability of 1:7. This study evaluated whether the variation in the optic nerve head size is correlated with a variability in the retinal photoreceptor count and the retinal surface area. METHODS: Forty-six normal human donor eyes with an axial length of less than 26 mm were examined. The corneoscleral button, lens, and vitreous body were removed. The remaining cup of the eye was cut into orange slice-like pieces. Up to 25 retinal biopsies were taken from areas arranged in increasing distance from and concentric to the fovea. The photoreceptor outer segments were sonographically removed. The photoreceptor inner segments were counted on photographs taken from the outer side of the retina. RESULTS: The count of the rods (mean +/- standard deviation: 57,447,000 +/- 10,481,000), the count of the cones (3,246,000 +/- 618,000), the optic disc size, and the retinal surface area (1204 +/- 184 mm2) were significantly (P < 0.05) and positively correlated with each other. CONCLUSIONS: The results indicate that eyes with large optic nerve heads as compared with eyes with small optic discs may have a higher count of rods and cones and a larger retinal surface area. It corresponds with the positive correlation between the optic nerve fiber count and the optic disc size. Taking into account a loss of photoreceptors in glaucoma as recently reported, it may point toward a higher anatomic reserve capacity in glaucomatous eyes with large optic discs than in eyes with small optic nerve heads.

Adolescent↗
PubMed1999

Abnormalities of retinal metabolism in diabetes or experimental galactosemia. VI. Comparison of retinal and cerebral cortex metabolism, and effects of antioxidant therapy.

Metabolic abnormalities observed in retina and in cerebral cortex were compared in diabetic rats and experimentally galactosemic rats. Diabetes or experimental galactosemia of 2 months duration significantly increased oxidative stress in retina, as shown by elevation of retinal thiobarbituric acid reactive substances (TBARS) and subnormal activities of antioxidant defense enzymes, but had no such effect in the cerebral cortex. Activities of sodium potassium adenosine triphosphatase [(Na,K)-ATPase] and calcium ATPase became subnormal in retina as well as in cerebral cortex. In contrast, protein kinase C (PKC) activity was elevated in retina but not in cerebral cortex in the same hyperglycemic rats. Dietary supplementation with an antioxidant mixture (containing ascorbic acid, Trolox, alpha-tocopherol acetate, N-acetyl cysteine, beta-carotene, and selenium) prevented the diabetes-induced and galactosemia-induced elevation of retinal oxidative stress, the elevation of retinal PKC activity and the decrease of retinal ATPases. In cerebral cortex, administration of the antioxidant diet also prevented the diabetes-induced decreases in (Na,K)-ATPase and calcium ATPases, but had no effect on TBARS and activities of PKC and antioxidant-defense enzymes. The results indicate that retina and cerebral cortex differ distinctly in their response to elevation of tissue hexose, and that cerebral cortex is more resistant than retina to diabetes-induced oxidative stress. The greater resistance to oxidative stress in cerebral cortex, as compared to retina, is consistent with the resistance of cerebral cortex to microvascular disease in diabetes, and with a hypothesis that oxidative stress contributes to microvascular disease in diabetes. Dietary supplementation with these antioxidants offers a means to inhibit multiple hyperglycemia-induced retinal metabolic abnormalities.

Animals↗
PubMed2002

A multi-layer model of retinal oxygen supply and consumption helps explain the muted rise in inner retinal PO(2) during systemic hyperoxia.

A multi-layer mathematical model of oxygen supply and consumption in the rat retina is described. The model takes advantage of the highly layered structure of the retina and the compartmentalisation of the available oxygen sources. The retina is divided into eight layers, each with a distinct oxygen consumption or supply rate. When applied to the available data from intraretinal oxygen measurements in the rat under normal physiological conditions, a close fit between the model and the data was achieved (r(2)=0.98+0.005, n=6). The model was then used to investigate recent evidence of oxygen regulating mechanisms in the rat retina during systemic hyperoxia. Fitting our model to the experimental data (r(2)=0.988+0.004, n=25) allowed the relative oxygen delivery or consumption of the key retinal layers to be determined. Two factors combine to produce the relative stability of inner retinal oxygen levels in hyperoxia. The retinal layer containing the outer plexiform layer/deep retinal capillaries, switches from a net source to a net consumer of oxygen, and the oxygen consumption of the outer region of the inner plexiform layer increases significantly. The model provides a useful tool for examining oxygen consumption and supply in all retinal layers, including for the first time, those layers within the normally perfused inner retina.

Animals↗
PubMed1989

Chemically induced retinal degeneration in the rdgB (retinal degeneration B) mutant of Drosophila.

Chemicals which affect different steps of the phototransduction cascade were used to identify the site of action of the rdgB gene product of Drosophila. In the rdgB mutant, the photoreceptor cells degenerate after several days of exposure to light, whereas raising the flies in the dark largely prevents the degeneration. In the rdgBKS222 mutant, which was used in the present studies, the light-induced degeneration is characterized by (1) selective degeneration of the peripheral but not the central photoreceptor cells; (2) random distribution of degenerated cells among ommatidia; and (3) the degeneration is specific to the rdgB but not the wild-type photoreceptor cells. In the present study, we show that application of specific chemical agents to the eyes of rdgBKS222 flies in the dark mimics the effects of light and causes retinal degeneration indistinguishable from light. The agents used in these studies are the metabolically stable GTP analogs GTP gamma S and Gpp(NH)p as well as fluoride ions, which are known to activate the transducing guanine nucleotide binding protein (G-protein of fly photoreceptors). It is unlikely that the chemically induced retinal degeneration is mediated by effects on energy metabolism, since application of the metabolic inhibitors CN- and 2-deoxy-D-glucose did not increase the extent of retinal degeneration over that observed in control flies treated with Ringer solution. The GDP analog GDP beta S, which inhibits G-protein activity, greatly reduced the extent of retinal degeneration in the dark, over that observed in control flies treated with Ringer solution. These results suggest that activation of the G-protein precedes the step in the transduction cascade that leads to retinal degeneration and provides a powerful tool to investigate the molecular mechanism of light-induced degeneration in the rdgB mutant.

Animals↗
PubMed2001

ABCR, the ATP-binding cassette transporter responsible for Stargardt macular dystrophy, is an efficient target of all-trans-retinal-mediated photooxidative damage in vitro. Implications for retinal disease.

A large body of experimental and clinical data have documented the damaging effects of light exposure on photoreceptor cells although the identities of the biologically relevant molecular targets of photodamage are still uncertain. Several lines of evidence point to retinoids or retinoid derivatives as chromophores that can mediate light damage. We report here that ABCR, a photoreceptor-specific transporter involved in the recycling of all-trans-retinal, is unusually sensitive to photooxidation damage mediated by all-trans-retinal in vitro. Partial loss of ABCR function is responsible for Stargardt macular dystrophy, which is associated with accumulation of A2E, a diretinoid adduct within the retinal pigment epithelium. Photodamage to ABCR causes it to aggregate in SDS gels and results in the loss of retinal-stimulated ATPase activity. Peripherin/RDS and ROM-1, two structural proteins that colocalize with ABCR at the outer segment disc rim, are also significantly more susceptible to all-trans-retinal-mediated photodamage than are the major proteins from the rod outer segment. These observations imply that there may be specific protein targets of photodamage within the outer segment, and they may be especially relevant to assessing the risk of light exposure in those individuals who already have diminished ABCR activity due to mutation in one or both copies of the ABCR gene.

ATP-Binding Cassette Transporters↗
PubMed1994

Retinal cholinergic system: characterization of rat retinal acetyltransferases using specific inhibitors of choline- and carnitine-acetyltransferases.

Choline acetyltransferase catalyzes the synthesis of acetylcholine from choline and acetylcoenzyme A (ACoA) in both nervous and non-nervous tissues. Carnitine acetyltransferase occurs in several tissues and transfers acetyl groups from ACoA to carnitine forming acetylcarnitine and exhibits weak choline acetyltransferase activity. Several haloacetylcholines and haloacetylcarnitines were synthesized to develop selective inhibitors of choline acetyltransferase and carnitine acetyltransferase. Acetylcholine is a transmitter for some presynaptic neurons and/or amacrine cells in retina. Selective inhibitors of choline acetyltransferase and carnitine acetyltransferase were used in the evaluation of choline acetyltransferase and carnitine acetyltransferase activities in the rat retina. Choline acetyltransferase and carnitine acetyltransferase activities were assayed by transferring of [14C]acetyl group from [14C]ACoA to choline or carnitine and estimating [14C]-acetylcholine or [14C]acetylcarnitine. This study gave the following results: (a) Bromoacetylcholine (BrACh) was a selective inhibitor of purified choline acetyltransferase (I50, 2.2 microM); (b) (R)-bromoacetylcarnitine [(R)-BrACa] was more potent for inhibiting purified carnitine acetyltransferase (I50, 4 microM) than purified choline acetyltransferase (I50, 46 microM); (c) Rat retinal sonicate gave choline acetyltransferase activity of 98 +/- 6 nmol of ACh formed/mg/10 min. When the carnitine acetyltransferase was completely inhibited by (R)-BrACa, the activity for choline acetyltransferase decreased to 47 +/- 1 nmol, and this decrease was possibly due to the formation of some [14C]acetylcholine by carnitine acetyltransferase. The net retinal choline acetyltransferase activity was 51 nmol acetylcholine/mg protein/10 min; (d) Rat retinal sonicate contained carnitine acetyltransferase activity of 102 +/- 7 nmol acetylcarnitine formed/mg protein/10 min. This was not altered by inhibition of choline acetyltransferase with BrACh. This means that choline acetyltransferase did not use carnitine as a substrate. Choline acetyltransferase and carnitine acetyltransferase activities did not change after dialysis of retinal sonicates at 4 degrees C for 24 hrs. These observations suggest that BrACh and (R)-BrACa are useful for assessing the correct values for choline acetyltransferase and carnitine acetyltransferase activities in retinal tissues.

Acetylcarnitine↗
PubMed2002

Retinal thickness analysis(RTA): an objective method to assess and quantify the retinal thickness in healthy controls and in diabetics without diabetic retinopathy.

BACKGROUND: Since it has been shown that photocoagulation is indicated in patients with diabetic macular edema, quantitative and objective assessment of retinal thickness is of clinical importance. METHODS: A laser slit beam was projected on the retina and scanned across a 2 x 2 mm retinal area in 200 msec. Nine type 1 and 2 diabetic patients without funduscopically and photographically visible diabetic retinopathy and 10 healthy controls were scanned with the RTA. The intraindividual and interindividual variabilities of the RTA were determined. RESULTS: The intraindividual and interindividual variability was 5 microm and 15 microm, respectively. The mean value of the mean foveal thickness (MFT) and perifoveal retinal thickness (PFT) in the 10 healthy controls was 152 +/- 15 microm and 175 +/- 14 microm, respectively, and 181 +/- 26 microm and 191 +/- 27 microm, respectively, in the group of nine diabetics without signs of diabetic retinopathy. The MFT in the group of diabetic patients was significantly (P < 0.001) larger than in the control groups. CONCLUSION: Retinal thickness in diabetic patients without diabetic retinopathy was increased in all measurements in comparison with the findings in healthy subjects. Retinal thickness measurements with the RTA could possibly detect early signs of diabetic retinopathy before funduscopic and photographic signs are visible and may be helpful in guiding treatment.

Adult↗
PubMed2003

Lipopolysaccharide/interferon-gamma and not transforming growth factor beta inhibits retinal microglial migration from retinal explant.

BACKGROUND: /aims: The retina possesses a rich network of CD45(+) positive myeloid derived cells that both surround inner retinal vessels and lie within the retina (microglia). Microglia migrate and accumulate in response to neurodegeneration and inflammation. Although microglia express MHC class II, their role remains undefined. The aims of this study are to investigate changes in human microglia phenotype, migration, and activation status in response to pro-inflammatory and anti-inflammatory stimulation. METHODS: Donor eyes were obtained from the Bristol Eye Bank with consent and whole retina was removed. 5 mm retinal trephines were cultured in glucose enhanced RPMI on cell culture insert membranes for up to 72 hours. The effects of lipopolysaccharide/interferon-gamma (LPS/IFNgamma) and transforming growth factor beta inhibits (TGFbeta) stimulation, alone or in combination, on migration, phenotype, and activation status (iNOS expression) of microglia were studied using immunofluorescence and cytokine analysis by ELISA. RESULTS: CD45(+) MHC class II(+) retinal microglia were observed within retinal explants, and in culture microglia readily migrated, adhered to culture membrane, downregulated MHC class II expression, and produced interleukin 12 (IL-12) and tumour necrosis factor alpha (TNFalpha). Following LPS/IFNgamma stimulation microglia remained MHC class II(-) iNOS(-), and secreted IL-10. Migration was suppressed and this could be reversed by neutralising IL-10 activity. TGFbeta did not affect ability of microglia to migrate and was unable to reverse LPS/IFNgamma induced suppression. CONCLUSIONS: Microglia readily migrate from retinal explants and are subsequently MHC class II(-), iNOS(-), and generate IL-12. In response to LPS/IFNgamma microglia produce IL-10, which inhibits both their migration and activation. TGFbeta was unable to counter LPS/IFNgamma effects. The data infer that microglia respond coordinately, dependent upon initial cytokine stimulation, but paradoxically respond to classic myeloid activation signals.

Cell Adhesion↗
PubMedDate not supplied

Modulation of retinal dopaminergic cells by nitric oxide. A protective effect on NMDA-induced retinal injury.

Nitric oxide (NO) may play an important role in regulating retinal neuronal survival. While the precise impact of NO mechanisms on retinal neurons remains to be elucidated, it has been reported that low doses of NO may have a neuroprotective effect against N-methyl-D-aspartate (NMDA)-induced retinal neurotoxicity. Dopamine has also been recognized to have neuroprotective actions. Retinal dopaminergic cells can be detected by the immunohistochemical staining of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine synthesis. We observed that NMDA dramatically decreased in TH immunostaining at the junction between the inner nuclear layer and inner plexiform layer, and that this reduction in immunostaining was attenuated by the co-injection of NOC 18, an NO donor. Thus, the current review focused on the NO-dopamine interactions in the retinal neuroprotection.

Animals↗
PubMed1991

Modulation of calcium channels in human retinal glial cells by basic fibroblast growth factor: a possible role in retinal pathobiology.

The objective of this study was to begin to examine the cellular and biophysical effects on human retinal glial cells of basic fibroblast growth factor (bFGF), which is endogenous to the retina and likely to play a role in retinal pathobiology. Experiments were performed on cultured glial cells derived from the adult postmortem retina. A proliferative response to bFGF established a sensitivity of the retinal glia to this growth factor. The possibility that bFGF alters calcium currents was assessed using the whole-cell recording configuration of the patch-clamp technique to analyze inward currents carried by barium. Two types of voltage-gated calcium channels could be expressed by the glial cells. One, similar to the T-type current described in various kinds of cells, had a low threshold of activation, a transient response, and an insensitivity to the dihydropyridine nifedipine. The other type of inward current, which closely resembles the L-type calcium current found in other cells, had a high threshold, had a long-lasting response, and was inhibited by nifedipine. When continuous whole-cell recordings were made from retinal glial cells, the L-type calcium current increased significantly within 20 min after exposure of the cells to bFGF. The physiological significance of this modulatory effect remains uncertain, though the observation that nifedipine inhibits both the L-type calcium current and the bFGF-induced proliferation is consistent with the hypothesis that dihydropyridine-sensitive channels may play a role in modulating the mitogenic response of retinal glial cells to this growth factor.

Adult↗
PubMed1989

Serum-induced proliferation of retinal capillary endothelial cells is inhibited in the presence of retinal extract.

Both crude retinal extract and serum contain growth factors for retinal capillary endothelial cells (EC). This study, however, has shown that the combined presence of both crude retinal extract (bovine) and adult serum, induces profound inhibition of EC growth in vitro. EC grown under these conditions develop as sparse colonies of cells which appear to be inhibited from spreading on the fibronectin-coated surface. The extract/serum mixture is not toxic to the cells since it does not affect the viability and typical cobblestone morphology of established confluent cultures. Combinations of retinal extract with adult sera from various species exert the inhibitory effect but foetal or newborn serum is not affected by the extract. Growth inhibition is also found with crude bovine brain extract but cannot be ascribed to the presence of basic fibroblast growth factor (bFGF) or heparin in the extract, nor to a previously identified heat-labile (56 degrees C, 30 min) inhibitory factor in retinal extract. The inhibition is selective for endothelial cells in that mural cells (pericytes) remain unaffected. The nature and relevance of this inhibitory activity remains to be determined.

Animals↗