Biomedical subjects

Andreas Reichenbach

Publications and source records attributed to Andreas Reichenbach.

At least 73 records · Page 4Linked to original sources

PubMed2004

In vitro cultured islet-derived progenitor cells of human origin express human albumin in severe combined immunodeficiency mouse liver in vivo.

Studies in rodents suggest the presence of a hepatopancreatic stem cell in adult pancreas that may give rise to liver cells in vivo. The aim of the present study was to determine the ability of human islet-derived cells to adopt a hepatic phenotype in vivo. Cultured human islet-derived progenitor cells that did not express albumin in vitro were stained with the red fluorescent dye PKH26 and injected into the liver of severe combined immunodeficiency mice. After 3 or 12 weeks, red fluorescent cells were detected in 11 of 15 livers and were mostly single cells that were well integrated into the liver tissue. Human albumin was found in 8 of 11 animals by immunohistochemistry, and human albumin mRNA was detected in 4 of 10 host livers. The mechanism underlying this phenomenon seems to be transdifferentiation, because human and mouse albumin were found to be expressed in distinct cells in the host liver.

Albumins↗

PubMed2003

Targeted inactivation of dystrophin gene product Dp71: phenotypic impact in mouse retina.

The abnormal retinal neurotransmission observed in Duchenne muscular dystrophy (DMD) patients and in some genotypes of mice lacking dystrophin has been attributed to altered expression of short products of the dystrophin gene. We have investigated the potential role of Dp71, the most abundant C-terminal dystrophin gene product, in retinal electrophysiology. Comparison of the scotopic electroretinograms (ERG) between Dp71-null mice and wild-type (wt) littermates revealed a normal ERG in Dp71-null mice with no significant changes of the b-wave amplitude and kinetics. Analysis of DMD gene products, utrophin and dystrophin-associated proteins (DAPs), showed that Dp71 and utrophin were localized around the blood vessels, in the ganglion cell layer (GCL), and the inner limiting membrane (ILM). Dp71 deficiency was accompanied by an increased level of utrophin and decreased level of beta-dystroglycan localized in the ILM, without any apparent effect on the other DAPs. Dp71 deficiency was also associated with an impaired clustering of two Müller glial cell proteins-the inwardly rectifying potassium channel Kir4.1 and the water pore aquaporin 4 (AQP4). Immunostaining of both proteins decreased around blood vessels and in the ILM of Dp71-null mice, suggesting that Dp71 plays a role in the clustering and/or stabilization of the two proteins. AQP4 and Kir4.1 may also be involved in the regulation of the ischemic process. We found that a transient ischemia resulted in a greater damage in the GCL of mice lacking Dp71 than in wt mice. This finding points at a crucial role played by Dp71 in retinal function.

Animals↗

PubMed2003

Recovery from hepatic retinopathy after liver transplantation.

BACKGROUND: In chronic liver disease the neuroglial cells may be affected by neurotoxic metabolites which, in turn, could be expected to affect neuronal functions. The aim of this study was to evaluate the electroretinograms (ERG) from patients before and after liver transplantation, in order to study possible functional changes of the retina. METHODS: Twelve patients with liver cirrhosis underwent routine ophthalmological examination and ERG before and after successful liver transplantation. Laboratory parameters, including ammonia, aspartate aminotransferase (AST), bilirubin, and cholinesterase, were compared. Patients were grouped according to the Child classification: three patients were Child A, six were Child B, three were Child C. RESULTS: Most obvious ERG abnormalities were found in patients with cirrhosis Child C. Before transplantation 7 of 21 ERG parameters were out of the normal range, but in the follow-up examination after transplantation only one parameter was not within the normal range. Significant ( P<0.05) postoperative improvements were found for the latencies of scotopic, mesopic and photopic b-waves and mesopic a-waves and for the photopic implicit time. Patients in the Child B group revealed less changes in the ERG. Before the transplantation only one parameter of the ERG was out of the normal range. All postoperative parameters were within the normal range. At 40+/-9 months after the liver transplantation a significant decrease in serum ammonia levels, AST and bilirubin and a significant increase in cholinesterase levels were observed. CONCLUSION: Patients with restored liver function after liver transplantation showed significantly improved ERG parameters. Our data suggest a recovery of the cells involved in hepatic retinopathy, including the Müller (glial) cells.

Adult↗

PubMed2003

Differentiation of cones in cultured rabbit retina: effects of retinal pigment epithelial cell-conditioned medium.

This study was aimed at investigating the postnatal differentiation of cone photoreceptors in the rabbit retina in an organotypic explant culture system. Both short wavelength (S) and middle wavelength (M) cone opsins were expressed in culture but M cones appeared only in retinal explants from the dorsal half of the eye. Stimulating the explants with retinal pigment epithelial cell (RPE) conditioned medium resulted in a suppression of opsin expression despite of an increase of the number of presumptive peanut agglutinin-labeled cones. These results suggest that at birth the immature cones are largely undetermined in terms of their final cone identity although some positional information ('dorsal' vs. 'ventral' retina) is present. Furthermore, factors from RPE may inhibit as well as stimulate different steps of cone cell differentiation.

Animals↗

PubMed2003

Upregulation of purinergic P2Y receptor-mediated calcium responses in glial cells during experimental detachment of the rabbit retina.

To investigate injury-induced alterations of purinergic P2Y receptor-mediated calcium responses in glial (Müller) cells of the rabbit retina, neural retinae were experimentally detached from the pigment epithelium. The ATP-evoked calcium responses were recorded in the endfeet of glial cells at the vitread surface of retinal wholemounts. In control retinae, approximately 7% of the glial cells investigated showed ATP-evoked calcium responses. Within 24 h of detachment, significantly more retinal glial cells (42%) showed calcium responses, and glial ATP responsiveness increased further in retinae which were detached for 48 (44%) or for 72 h (64%). The results indicate that in the detached retina, glial cells upregulate their responsiveness to extracellular ATP within 24 h of injury. Thus, P2Y receptor-mediated signalling may be involved in the early steps of glial response to retinal injury.

Animals↗

PubMed2003

The retinal anatomy and function of the myelin mutant taiep rat.

PURPOSE: To study the histology and the physiological function of the retina in the neurological myelin mutant, taiep rats during the postnatal developmental period (P20-P360). METHODS: Electroretinography (ERG) was applied to evaluate intensity dependence and spectral sensitivity of the responses to light. Retinal histology, morphometry, and immunocytochemistry were used to characterize the structure of the retina, with particular emphasis on the Müller (glial) cells. RESULTS: In the taiep rats of all ages studied, the scotopic ERG showed normal a- and b-wave amplitudes and latencies; likewise, the scotopic spectral sensitivity function was the same for control and taiep animals, with a maximal sensitivity (lambda(max)) at 500 nm. However, in adult taiep rats (P90 to P360) a secondary cornea-positive wave ('b(2)') was observed in response to high stimulus intensities, which never occurred in controls. This correlated with the observation that in the photopic ERG responses of the taiep rats, the b-wave was reduced in amplitude, and was followed by a rapid cornea-negative after-potential. After 1 year of life, in taiep rats the outer plexiform layer (OPL) became slightly thinner and the inner plexiform/ganglion cell layers (IPL/GCL) appeared to be swollen, and increased in thickness; in addition, the number of retinal neurons (particularly, of photoreceptor cells) slightly decreased. Increased GFAP immunoreactivity revealed a hypertrophy and reactivity of the Müller cells in 1-year-old taiep rats. CONCLUSIONS: The present results suggest the occurrence of a relatively mild and slowly progressing neural retinal alteration in taiep rats, which becomes histologically and functionally evident at the end of the first year of life, and mainly affects the circuit(s) of the photopic ON-response. It is speculated that this alteration is due to missing/altered signals from demyelinated optic nerve.

Adaptation, Ocular↗

PubMed2003

Graded sensitiveness of the various retinal neuron populations on the glyoxal-mediated formation of advanced glycation end products and ways of protection.

BACKGROUND: The accumulation of advanced glycation end products (AGEs) in retinal cells is known to be associated with the risk of diabetic retinopathy. To develop a model of AGE-related metabolic stress in retinal organ cultures, we investigated the accumulation of a typical glycoxidation product (N(epsilon)-[carboxymethyl] lysine [CML]) and its possible pro-apoptotic effects on different retinal cell populations. METHODS: Retinal organ cultures (rat) were kept for 9 h in the Ames medium containing 0 (control), 5, 25, 50, 150, 300 and 800 micro M glyoxal. The expression of bax, active caspase-3, and the accumulation of CML were studied by using immunohistochemistry after the paraffin embedding of retinal explants. Apoptosis was studied using the terminal deoxynucleotidyl transferase-mediated dUTP digoxigenin nick end labeling (TUNEL) test and electron microscopy. Alpha lipoic acid (alpha-LA), sodium metavanadate (NaVO(3)), N-acetylcysteine (NAC), aminoguanidine (AG), and nicotinamide (NA) were used to influence glyoxal effects in organ cultures. RESULTS: In cultured normal non-diabetic retinae, small amounts of CML and the apoptosis-promoting factors bax and active caspase-3 were present. CML, bax and active caspase-3 increased after incubation with glyoxal. Incubation with glyoxal (<300 micro M, 9 h) increased apoptotic events in all layers. At low glyoxal concentrations, we found a graded sensitiveness of the different layers: at 25 micro M 39.4% in GCL, 28.2% in INL, 11.9% in ONL. After 800 micro M glyoxal, approximately 50% of the cells in all layers of the retina were apoptotic. In the ONL, this ratio was reduced by NaVO(3) (17%), by AG (27%), by NA (24.8%), by NAC (25.2%), and by alpha-LA (33.5%). In the INL, AG (25.9%) produced the best result. In the GCL, NAC, NaVO(3) and AG reduced apoptosis. A-LA had no significant protective effect. CONCLUSION: The glyoxal-induced rapid formation of CML shows the ability of our retina model to simulate AGE-related effects in vitro. The dose-dependent expression of apoptosis-promotor molecules indicates that the apoptosis-inducing machinery starts in most retinal cells within 9 h. The neurotoxicity of glyoxal-induced AGE formation was shown by the significantly increased rate of cell death in the retina. The significant decrease of apoptotic events (P<0.01) indicates that antioxidants and AGE formation blocker can exert a differentiated cytoprotection for each of the retinal cell layers.

Acetylcysteine↗

PubMed2003

Age-related decrease of potassium currents in glial (Müller) cells of the human retina.

BACKGROUND: Age-dependent alterations have been investigated far less in retinal glial cells than in retinal neurons. We investigated age-dependent alterations of inwardly rectifying potassium (Kir) currents in Müller glial cells of the human retina. METHODS: Müller cells were isolated immediately post mortem from donors without a reported history of eye disease, and the amplitudes of Kir currents and of currents through high-voltage-activated (HVA) calcium channels were measured by whole-cell patch clamping. RESULTS: The amplitude of the Kir currents was lower in the cells from donors older than 50 years than in the cells of younger donors; the decrease was strongly correlated with the donor's age (p < 0.001). The current amplitude in the cells from donors older than 60 years was about 40% lower than the amplitude in the cells from donors younger than 50 years. The amplitude of the HVA currents was greater in the cells from donors older than 55 years than in the cells from younger donors; the increase, up to about 500%, was strongly age-dependent (p < 0.001). INTERPRETATION: The age-related decrease in Kir-current amplitude in Müller cells may reflect the neuron loss in the aged retina. Our findings also indicate that retinal glial cells have enhanced cytoplasmic calcium signals in the course of aging.

Adult↗

PubMed2003

Characterization of the acute immune response in the retina of Borna disease virus infected Lewis rats.

In Lewis rats infected intracerebrally with the highly neurotropic Borna disease virus (BDV), the retina is one of the most severely affected central nervous system (CNS) structures. While BDV-induced damage in the brain has been previously shown to be caused by a T-cell-dependent process, the immunopathological mechanisms leading to BDV-induced retinitis remain to be elucidated. RNA samples from retinae were subjected to RNase protection assays to detect transcripts of proinflammatory cytokines and chemokines known to be involved in the recruitment of T-cells and macrophages in the CNS. The observed expression profile of proinflammatory cytokines and chemokines, as well as the immunohistochemical detection of alpha beta TCR-positive, CD4- and CD8-positive T-cells in the BDV-infected retinae, is reminiscent of the situation observed in the brains of Lewis rats during the acute phase of Borna disease (BD). This suggests that similar immunopathological mechanisms are operating in retinae and brains of infected rats.

Acute Disease↗

PubMed2003

P2Y receptor-mediated stimulation of Müller glial cell DNA synthesis: dependence on EGF and PDGF receptor transactivation.

PURPOSE: To determine whether P2Y receptor-evoked proliferation of Müller glial cells depends on transactivation of receptor tyrosine kinases. METHODS: Primary cultures of Müller cells of the guinea pig were treated with test substances for 16 hours. The DNA synthesis rate was assessed by a bromodeoxyuridine (BrdU) immunoassay, and the phosphorylation states of the extracellular signal-regulated kinase (ERK1/2) and the p38 mitogen-activated protein kinase (p38 MAPK) were determined by Western blot analysis. RESULTS: In Müller cells, the mitogenic effect of P2Y receptor activation by extracellular adenosine triphosphate (ATP) depended on transactivation of both the platelet-derived growth factor (PDGF) and the epidermal growth factor (EGF) receptor tyrosine kinases, as suggested by the blocking effects of the tyrphostins AG1296 and AG1478 on the ATP-induced proliferation and phosphorylation of ERK1/2. Moreover, the PDGF-induced proliferation may depend on transactivation of the EGF receptor kinase. Antibodies against heparin-binding EGF (HB-EGF) or PDGF, as well as inhibition of matrix metalloproteinases (MMPs) blocked ATP-evoked proliferation. At least one metalloproteinase (MMP-9), was implicated in the signal transfer from P2Y to EGF receptors. In contrast, the mitogenic effect of fetal calf serum was independent of growth factor receptor activity. P2Y receptor activation stimulated Müller cell proliferation by activating the ERK1/2 and the phosphatidylinositol 3 (PI3) kinase signaling pathways, whereas the p38 MAPK pathway was not involved in mitogenic signaling. CONCLUSIONS: The present data suggest that P2Y-receptor-induced mitogenic signaling in Müller cells is mediated by transactivation of the PDGF and EGF receptor tyrosine kinases. The transactivation may be mediated by release of PDGF and MMP-dependent shedding of HB-EGF from the Müller cell matrix, respectively. The transactivation of the receptor tyrosine kinases may result in activation of ERK1/2 and PI3 kinase and an increase in the proliferation rate.

Adenosine Triphosphate↗

PubMed2003

Early glial cell reactivity in experimental retinal detachment: effect of suramin.

PURPOSE: In a rabbit model of retinal detachment, early Müller glial cell reactivity was monitored-specifically, changes in membrane features-to determine whether these changes involve an upregulation of purinergic P2 receptor-mediated responses and whether all or some of these alterations could be blocked by suramin or pyridoxal phosphate 6-azophenyl-2',4'-disulfonic acid (PPADS). In addition, the immune cell reactivity (microglial cells and blood-derived immune cells) was monitored. METHODS: A local retinal detachment was induced by subretinal injection of a sodium hyaluronate solution. Three, 24, 48, and 72 hours after surgery, Müller cells were acutely isolated, and patch-clamp records of the whole-cell potassium currents were made. The presence of P2 receptor-mediated responses was determined by measuring extracellular adenosine triphosphate (ATP)-induced membrane current increases, and by recording of ATP-induced calcium responses at the vitreal surface of retinal wholemounts. The density of isolectin B(4)-labeled immune cells was determined in the nerve fiber layer of retinal wholemounts. RESULTS: Within 24 hours of detachment, Müller cell reactivity was evident. The cells downregulated the density of their inwardly rectifying potassium currents to 60% and 47% of the control value at 48 hours and 72 hours of detachment, respectively. This downregulation was accompanied by an enhanced incidence of cells which showed calcium and current responses after ATP application (control: 14%; 24 hours of detachment: 42%; 72 hours of detachment: 80%). Müller cell hypertrophy was apparent at 48 and 72 hours of detachment. Application of suramin during surgery inhibited the downregulation of potassium currents, but not the elevated responsiveness to extracellular ATP; PPADS had no effect. Suramin also inhibited the inflammatory response that was induced by the surgical procedure and that was apparent by the increased number of immune cells. CONCLUSIONS: Reactive responses of Müller cells occur within 24 hours of detachment. Suramin inhibits several (but not all) reactive glial alterations and therefore may represent one candidate for further investigations in the search for drugs that limit detrimental effects of immune cell activation and Müller cell gliosis during retinal detachment.

Adenosine Triphosphate↗

PubMed2002

Patch-clamp recording of Müller glial cells after cryopreservation.

Human and other primate retinal Müller cells display dominating K(+) currents as well as other membrane conductances that may change in cases of retinal pathology. Because the use of human and primate tissue is limited by reasons of availability, a method for long-term storage of these cells is desirable. We describe a cryopreservation method in which isolated Müller cells are stored in liquid nitrogen. After thawing, the cells can be used for patch-clamp experiments immediately, without culturing. We show that the main electrophysiological properties are not altered by this method and that voltage- and ligand-gated currents can be recorded from cryopreserved cells even after 2-years storage.

Adenosine Triphosphate↗

PubMed2002

ATP-evoked calcium responses of radial glial (Müller) cells in the postnatal rabbit retina.

Here we show that rabbit Müller cell differentiation from radial glial progenitor cells is accompanied by a decreasing capability to respond to specific stimuli (depolarization and extracellular adenosine 5'-triphosphate [ATP]) with an elevation of intracellular calcium. Intracellular free calcium was recorded in retinal wholemounts from young (postnatal days [P] 2 to 31) and adult rabbits. Images were taken from the nerve fiber/ganglion cell layers where the endfeet of radial glial/ Müller cells can be identified after selective uptake of calcium-sensitive dyes. The area of responding endfeet was determined as the percentage of the total area occupied by Müller cell endfeet, as an estimate of the percentage of responding cells. In response to depolarization (50 mM potassium), an increase of intracellular free calcium occurred in 19% of cells from young postnatal retinae (P2-31) but only in 2% from adults. This depolarization-induced calcium rise was caused both by a calcium influx from extracellular space and by an intracellular calcium release. The latter response was inhibited by the P2 receptor blocker pyridoxal phosphate 6-azophenyl-2',4'-disulfonic acid (PPADS), indicating that extracellular calcium-independent ATP release into the extracellular space occurs during retinal depolarization. When extracellular ATP (200 microM) was applied, calcium responses were recorded in 83% of cells from young postnatal retinae (P2-6); in the course of further development, both the percentage of responding cells (7% in retinae from adult rabbits) and the amplitude of the calcium responses decreased. It is concluded that during the differentiation of immature radial glia into mature Müller cells, stimulus-evoked intracellular calcium signaling mechanisms change.

Adenosine↗

PubMed2002

Diversity of Kir channel subunit mRNA expressed by retinal glial cells of the guinea-pig.

One of the main functions of Müller glial cells is the performance of retinal K+ homeostasis which is thought to be primarily mediated by K+ fluxes through inwardly rectifying K+ (Kir) channels expressed in Müller cell membranes. Until now, there is limited knowledge about the types of Kir channel subunits expressed by Müller cells. Using RT-PCR, we investigated the expression of mRNA encoding different Kir channel subunits in the retina of the guinea pig. In order to verify expression by Müller cells, primary cultures of guinea pig Müller cells were also investigated. Both retinae and cultured Müller cells express mRNA for a diversity of Kir channel subtypes which include members of at least four channel subfamilies: Kir2.1, Kir2.2, Kir2.4, Kir3.1, Kir 3.2, Kir4.1, Kir6.1, and Kir6.2. mRNAs for the following Kir channel subtypes were not detected in Müller cells: Kir1.1, Kir2.3, Kir3.3, Kir3.4, Kir4.2, and Kir5.1. It is concluded that the spatial buffering of extracellular K+ by Müller cells may be mediated by cooperation of different subtypes of Kir channels, and that the distinct Kir channel types involved in this function may change depending on the physiological or metabolic state of the retina.

Animals↗

PubMed2002

Bergmann glial cells form distinct morphological structures to interact with cerebellar neurons.

It is well established that Bergmann glial cells closely interact with neuronal elements in the molecular layer of the cerebellum. We reconstructed dye-labeled Bergmann glial cells from electron microscopic serial sections and identified their contact sites with neurons as "glial microdomains" (Grosche et al. [1999] Nature Neurosci. 2:139-143). In the present paper we describe these structures in more detail, and show that 1) immature Bergmann fibers up to postnatal day 7 are smooth and lack appendages but contain several large mitochondria at sites where the first indications of growing side branches are observed; 2) Bergmann fibers from cerebella at postnatal day 30 form two types of outgrowths, short simple thorns and longer complex appendages; 3) each of the latter (i.e., a glial microdomain) is in contact with only a few synapses and nonsynaptic neuronal excrescences; 4) every given region of the neuropil is occupied by (at least) two interdigitating glial microdomains; 5) the synaptic clefts are entirely surrounded by glial protrusions, whereas the extrasynaptic surfaces and small axons are only partially covered; and 6) many small neuronal excrescenses without vesicles are completely ensheathed by glial caps, representing novel glial-neuronal structures of unknown function (glial thimbles). Computational modelling of the microdomains indicates that each is electrotonically independent of the stem process from which it arises, as well as of neighbouring domains. We assume that the glial microdomain is a morphological unit to compartmentalize ensembles of synapses, serving to synchronize local synaptic activity.

Aging↗

PubMed2002

SURI and Kir6.1 subunits of K(ATP)-channels are co-localized in retinal glial (Müller) cells.

ATP-sensitive potassium channels (K(ATP)), unlike other inwardly rectifying potassium (Kir) channels, require two structurally diverse subunits to form functional channels: one member of the Kir6 channel family (Kir6.1 or Kir6.2), and one sulfonylurea receptor (SUR) of the ATP-binding cassette superfamily (SURI, SUR2A or SUR2B). We have previously shown that two pore-forming subunits of K(ATP)-channels are differently distributed in frog retina. Kir6.1 is localized in Miller (glial) cells, whereas Kir6.2 is found in neurons. Using immunocytochemistry, the present study reveals that in adult frog retina, SURI is restricted to Müller (glial) cells whereas SUR2A and SUR2B are found in neurons. These data suggest that functional K(ATP) channels in Müller cells may be formed by Kir6.1/SURI, and in neurons by Kir6.2/SUR2A and/or Kir6.2/SUR2B.

ATP-Binding Cassette Transporters↗

PubMed2002

Activation of P2Y receptors stimulates potassium and cation currents in acutely isolated human Müller (glial) cells.

The ability of various neurotransmitters/neuroactive substances to induce fast, transient rises of Ca(2+)-activated K(+) currents (I(BK)) caused by release of Ca(2+) from intracellular stores was investigated in Müller glial cells of the human retina. Müller cells were enzymatically isolated from retinas of healthy donors or of patients with proliferative vitreoretinopathy, and the transmembrane ionic currents were recorded using the whole-cell and the cell-attached patch-clamp techniques. The results of the screening experiments indicate that human Müller cells express, in addition to GABA(A) and perhaps glutamatergic and cholinergic receptors, predominantly P2 receptors. ATP and other nucleotides exerted two effects on membrane currents: repetitive transient increases of the I(BK) amplitude and, in a subpopulation of cells investigated, the appearance of a transient cation conductance at negative potentials. ATP and UTP increased dose-dependently the I(BK) amplitude with half-maximal effects at 0.33 and 0.50 microM, respectively. Since several different P2 receptor agonists increased the I(BK), it is assumed that human Müller cells express a mixture of different types of P2Y receptors. In cell-attached patches, extracellular application of ATP or UTP transiently increased the open probability of single putative BK channels. The increase of I(BK) and the appearance of the cation conductance in whole-cell records were abolished when intracellular Ca(2+) was buffered by a high-EGTA pipette solution or when IP(3) was included in the pipette solution. The expression of agonist-evoked transient cation currents was found to be stronger in cells from patients as compared to cells from healthy donors. It is concluded that human Müller glial cells express P2Y receptors that, via IP(3) formation, cause intracellular Ca(2+) release. The increased intracellular Ca(2+) concentration stimulates the activity of BK channels and may induce opening of cation channels. Both the ATP-induced activity of BK channels and the increased expression of Ca(2+)-gated cation channels may be important in respect to proliferative Müller cell gliosis.

Adenosine Triphosphate↗

PubMed2002

Electrophysiological characterization of retinal Müller glial cells from mouse during postnatal development: comparison with rabbit cells.

The electrophysiology of murine Müller cells, and of their precursors, during postnatal development was investigated by using the whole-cell patch-clamp technique. Membrane potential, membrane capacitance, and expression of voltage-gated Na+ currents increased during the first 3 postnatal weeks. During the same period, the membrane resistance decreased due to an upregulation of both inward and outward K+ currents. Glutamate transporter-mediated currents increased during the first postnatal weeks, as well. In Müller (precursor) cells from rabbits, these transporter currents already achieved adult levels at postnatal day 6, the earliest stage studied. Together with the developmental time course of K+ currents, this indicates a delay in the maturation of murine Müller cells, as compared with cells from rabbit.

Aging↗