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B J McLaughlin

Publications and source records attributed to B J McLaughlin.

At least 73 records · Page 4Linked to original sources
PubMed1984

Lectin cytochemistry and freeze-fracture study of phagocytosis in the rat retina.

Lectin cytochemistry and freeze-fracture intramembrane morphology have been studied in adult rat retinas during various stages of the phagocytic cycle. Animals were perfused with aldehydes at various times during the first 6 hours of light and the retinas were removed. Chopped sections of tissue were stained with one of two lectin-peroxidase conjugates: ricinis communis agglutinin (RCA), which is specific for n-acetylgalactosamine and galactose, or wheat germ agglutinin (WGA), which is specific for n-acetylglucosamine and sialic acid. Other sections were frozen and prepared for freeze fracture. During the first hour of light onset, numerous phagosomes are already present in the retinal pigment epithelial (RPE) cytoplasm. The engulfment stages of phagocytosis whereby the RPE microvilli wrap around and enclose shed rod outer segment (ROS) tips are rarely observed at this time. Newly formed phagosomes are present in the apical RPE cytoplasm while older and more osmiophilic phagosomes are located deeper within the RPE cytoplasm. Between 2 and 4 hours of light onset fewer phagosomes are present in the RPE cytoplasm, but it is common to observe many ROS tips in various stages of microvillous engulfment. By 6 hours phagosomes are rarely present but some engulfed ROS tips continue to be observed. Both RCA and WGA stain RPE microvilli and plasma membranes of photoreceptor outer segments. WGA, in addition, labels some intradisc membranes of intact and also shed outer segments that are being engulfed but does not label disc membranes in phagosomes. At all times, phagosomes are rimmed by both lectin stains, but their internal contents are never stained. Lysosomes and multivesicular and residual bodies are labeled by both lectins. Freeze-fractured retinas show that as the ROS tips are engulfed, particle-free areas are present on disc P-face (cytoplasmic) membranes. Many newly formed phagosomes also display particle-free membrane areas and older phagosome membranes are completely devoid of particles. These observations show that the changes in WGA staining and intramembrane particle distribution on disc membranes occur in retinas during phagocytosis and suggest that some membrane component that is present for the initial phagocytic interaction may be rapidly degraded thereafter.

Animals↗
PubMed1984

Acid phosphatase localization in normal and dystrophic retinal pigment epithelium.

In this study acid phosphatase (ACPase) was localized in the retinal pigment epithelium (RPE) of normal and Royal College of Surgeons (RCS) rats pink-eyed and pigmented with inherited retinal dystrophy to determine differences in staining during the post-engulfment stages of phagocytosis using two substrates, Na-beta-glycerophosphate and cytidine-5'-monophosphate. Staining was similar using either substrate and in the normal RPE the Golgi system, lysosomes and phagosomes were ACPase-positive. In the dystrophic RPE, which has a diminished capacity to phagocytose photoreceptor rod outer segments, ACPase staining was localized on melanosomes in the pigmented dystrophic and on the apical microvillous membranes in the pink-eyed dystrophic, but was not localized on phagosomes in either the pink-eyed or pigmented dystrophic RPE. Since only a few phagosomes were seen at any given time in dystrophic RPE in vivo, a tissue explant system was used to examine the number of latex beads phagocytosed by normal and RCS RPE, as well as the number of phagosomes containing both beads and ACPase activity in the normal and mutant RPE. Our findings indicate that in the dystrophic, fewer phagosomes are ACPase-positive than in the normal, and that some enzyme may be inappropriately shunted to either the apical microvilli or to melanosomes instead of to phagolysosomes.

Acid Phosphatase↗
PubMed1984

Lectin-ferritin binding on dystrophic and normal retinal pigment epithelial membranes.

Phagocytosis in the rat retina is a process which involves uptake of shed photoreceptor outer segments by the overlying retinal pigment epithelium (RPE). In rats with inherited retinal degeneration, there is a defect in phagocytosis. One aspect of this phagocytic defect may be an alteration in glycoconjugate-containing membrane components on RPE membranes which mediate this phagocytic interaction. Lectin binding sites have been studied in order to localize the distribution of glycoconjugates on pigment epithelial microvilli in normal and dystrophic retinas and to determine if there are differences in the dystrophic retinas which would provide a clue about the defect. The following ferritin-conjugated lectins were used in this study: Concanavalin A (Con A-fe) or lens culinaris haemagglutinin (LcH-fe) for mannosyl-containing glycoconjugates; and wheat germ agglutinin (WGA-fe) for n-acetylglucosamine and sialic acid-containing glycoconjugates. Control tissue was incubated in the lectin in the presence of its competitor sugar. The number of ferritin particles or lectin-ferritin binding sites per micrometre of microvillous membrane was quantified from electron micrographs using a computer and a digitizing tablet. The number of WGA-fe binding sites on normal RPE microvillous membranes (56.0/micron) was statistically equivalent to the dystrophic membranes (48.8/micron). The number of Con A-fe binding sites on normal (27.3/m) and dystrophic RPE (26.7/micron) was also the same. A dramatic difference in LcH-fe binding sites was demonstrated on normal (1.5/micron) as compared to dystrophic RPE (19.1/micron). Our results indicate that more mannosyl residues are accessible on dystrophic microvillous membranes and, based on what is currently known about LcH binding, that these residues belong to glycoconjugates having fucosyl-containing carbohydrate cores. The data also suggest that in normal animals without a phagocytic defect such fucosyl-containing glycoconjugates are not as accessible and may be masked by other sugar residues in the oligosaccharide chain.

Animals↗
PubMed1984

Redistribution of Na-K-ATPase in the dystrophic rat retinal pigment epithelium.

Our previous studies have shown that a breakdown in tight junctions in the dystrophic retinal pigment epithelium (RPE) of Royal College of Surgeons' rats is accompanied by changes in intramembrane structure which suggest a redistribution of intramembrane particles. We have now investigated, using the p-nitrophenyl phosphate technique, the possibility that a specific membrane protein, Na-K-ATPase, is redistributed as tight junctions break down in the dystrophic RPE. In the normal RPE, Na-K-ATPase activity is restricted to the apical membrane. Junctional membranes and membranes around phagosomes are free of enzyme activity, suggesting a segregation of the transport enzyme from the junctional and phagocytic membrane. In the dystrophic RPE, prior to changes in tight junctions, enzyme activity is restricted to the apical membrane. During the initial stages of junctional breakdown, junctional membranes and membranes around cytoplasmic inclusions are also labelled. As the breakdown progresses, Na-K-ATPase activity is often present laterally and basolaterally and is sometimes absent apically. Enzyme activity is seen basally only where RPE cells have detached from Bruch's membrane and are superimposed over each other. These changes suggest that Na-K-ATPase redistributes during junctional breakdown, but that attachments between the RPE and Bruch's membrane may restrict the redistribution. The apparent reduction of enzyme activity apically suggests that active transport across the dystrophic RPE may be reduced as the tight junctions break down.

Animals↗
PubMed1984

Phagocytosis of lectin-coated beads by dystrophic and normal retinal pigment epithelium.

In the dystrophic pigmented Royal College of Surgeons (RCS) rat, the retinal pigment epithelium (RPE) has a diminished capacity to phagocytose shed photoreceptor outer segments (ROS). An alteration in phagocytic recognition or ligand-receptor interactions between the RPE and ROS's could contribute to this defect. To this end, we have examined whether or not RPE lectin receptors are implicated in phagocytosis in the normal and dystrophic rat RPE by comparing differences in phagocytic uptake of lectin-coated beads. To test this, the following lectins were bound either indirectly to sugar-coated latex beads or directly to activated beads: Concanavalin A (conA), specific for mannose; Ulex europeus (ULEX), specific for fucose; Lens culinaris (LcH), specific for mannose; and wheat germ agglutinin (WGA), specific for N-acetyl glucosamine and sialic acid. The distribution of the lectin binding around beads was visualized and confirmed using lectin-Ferritin conjugates. Lectin-coated beads were fed to normal and dystrophic pigmented RPE tissue explants to determine differences in phagocytic uptake. We found that whether beads were directly or indirectly coated, similar results were obtained, but that there were differences in uptake of two types of lectin-coated beads by dystrophic as compared with normal animals. The dystrophic RPE phagocytosed greater numbers of conA-mannose beads (6.9/cell) than the normal RPE (3.6/cell). LcH-mannose beads were also phagocytosed by dystrophic (2.7/cell) but not by the normal (0/cell). A similar number of ULEX-fucose beads were taken up by dystrophic (3.8/cell) and normal (3.4/cell) RPE and neither took up WGA-N-acetyl glucosamine beads (0/cell). These results showing that the dystrophic RPE takes up greater numbers of conA and LcH-coated beads than the normal RPE suggest that a ligand-receptor interaction involving mannose may contribute to this difference in phagocytic uptake.

Animals↗
PubMed1984

A quantitative study of intramembrane changes during cell junctional breakdown in the dystrophic rat retinal pigment epithelium.

Previous electron microscope freeze-fracture and tracer studies have revealed that intercellular junctions in the retinal pigment epithelium (RPE) of Royal College of Surgeons (RCS) rats with inherited retinal dystrophy [5] break down between three and six postnatal weeks [6, 7]. In this study quantitative computer techniques were used to analyze the freeze-fracture changes in the dystrophic RPE. The following parameters were measured: length of tight junctional strands/micron2; number of tight junctional strand anastomoses/micron2; number of gap junctional aggregates/micron2; area of gap junctional aggregates/micron2; and density of background intramembrane particles/micron2. At three postnatal weeks, the dystrophic junctional complex membrane is similar to normal, but at 10 weeks and later there are dramatic decreases in tight junctional strand length/micron2 and number of anastomoses/micron2, as well as in the number/micron2 and area of gap junctions/micron2, while the density of background particles/micron2 is dramatically increased. Correlational analysis revealed that changes in gap and tight junctions were significantly related to each other and to the increase in background particle density. The diameter of background particles within the normal and post-breakdown dystrophic junctions was measured in order to see whether the dispersal of gap and tight junctional particles (8-10 nm) into the surrounding membrane contributes to the increased particle density. These measures showed that background particles in all size ranges were more numerous in the dystrophic RPE, but that the largest increase was in the smallest diameter particles (6-7 nm). Thus, while gap and tight junctional sized particles contribute to the increase, particles from other sources may also be involved. Particle density of apical and basal membranes in the normal and in the 10 week and older dystrophic RPE was analyzed to study the effects of tight junctional breakdown on the distribution of intramembrane particles. These measures showed that particle density was greater basally than apically in the normal RPE and that particle density in both membranes decreased slightly in the dystrophic RPE, but that their ratio remained unchanged. It has been shown previously that even a single intact tight junctional strand is sufficient to maintain differences in particle density between apical and basal surfaces [14, 15] and in the majority of abnormal dystrophic junctional complexes at least one tight junctional strand remains intact.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Surface-replica topography of retinal pigment epithelium during phagocytosis.

The initial step in retinal phagocytosis may be mediated by complementary recognition molecules on the pigment epithelial microvilli and outer segment membrane surfaces. These molecules may display a surface morphology which is related topographically to phagocytic events. In order to explore this, we have developed a method for replicating the membrane surfaces of rat pigment epithelial explants during phagocytosis of latex beads. The explants are fixed in a mixed aldehyde and osmium fixative and the basal surface glued to a coverslip. After dehydration and critical point drying, the tissue is replicated with platinum and carbon in a freeze-fracture apparatus using either rotary or unidirectional coating and the replicas are examined by transmission electron microscopy. The membrane surfaces of the pigment epithelial cells and their microvilli are studded with numerous surface particles varying in size from 20 to 50 nm that are closely packed and give a cobblestone appearance to the membrane topography. During the early stages of phagocytosis, microvillous processes appear to spread over the beads and form branched processes as they contact bead surfaces. During bead engulfment the microvilli have shortened into flattened sheets with interdigitating processes overlapping the beads. These uptake sites resemble Venus' fly-traps, which as they close over the beads create craters in the membrane surfaces of the pigment epithelium. The crater-like uptake sites appear to flatten out in the later stages and form flattened membrane domains which are surrounded by crenulated membrane that displays an irregular particulate morphology.

Animals↗
PubMed1983

Permeability of retinal pigment epithelial cell junctions in the dystrophic rat retina.

We have studied permeability of retinal pigment epithelial (RPE) cell junctions in Royal College of Surgeons rats with inherited retinal degeneration, and their genetic controls, using the horseradish peroxidase and lanthanum nitrate electron microscope tracer techniques. We find that early in the dystrophic process, at two postnatal weeks in the pink-eyed retina and three postnatal weeks in the black-eyed retina, RPE cell tight junctions form a barrier to extracellular tracer. However, at three postnatal weeks in the pink-eyed retina, at about the same time that degenerating photoreceptor nuclei begin to appear, RPE cell tight junctions become permeable. The permeability increase occurs later in the black-eyed strain, but by six postnatal weeks junctions are permeable in both strains. By 72 postnatal days, when most photoreceptor nuclei have disappeared, many RPE cells are abnormal in shape, with an elongated and flattened appearance, and some appear to have lost their junctions entirely. In the horseradish peroxidase experiments, many pinocytotic vesicles filled with reaction product were observed in the dystrophic RPE after the junctional breakdown. This suggests that an increase in transcellular transport may also occur in the dystrophic RPE.

Aging↗
PubMed1983

The use of sugar-coated beads to study phagocytosis in normal and dystrophic retina.

In this study, a technique is described for coupling the sugars to carboxylated latex beads for use in phagocytic studies of dystrophic and normal retinal pigment epithelium. The presence and distribution of the sugars, mannose and fucose, on the bead surfaces are visualized by transmission electron microscopy using the lectin-Ferritin conjugates. Concanavalin A-Ferritin (Con A-Fe) and Ulex-europeus-Ferritin (Ulex-Fe), respectively. Both lectin-Ferritin conjugates label the surfaces of the sugar coated beads. Control experiments to determine the extent of nonspecific lectin-Ferritin binding using Con A-Fe with fucose-coated beads, Ulex-Fe with mannose-coated beads, or beads without coupling reagent show little to no labeling. Lectin-Ferritin conjugates are also incubated with the appropriate sugar-coated beads and their competing sugars and little to no labeling is observed. Our data shows that when sugar-coated beads are presented to retinal pigment epithelial explants, differences in phagocytic uptake are observed. Uncoated beads are avidly taken up by normal and dystrophic tissue, but fucose-coated beads are not taken up by either. Twice as many mannose beads are phagocytized by the normal as compared to dystrophic tissue. It remains to be established whether these differences in bead uptake indicate a difference in ligand-receptor interactions between normal and dystrophic retinal pigment epithelium.

Animals↗
PubMed1983

Tracer uptake by photoreceptor synaptic terminals. I. Dark-mediated effects.

This electron microscope study examines the sites of uptake and subsequent redistribution of the extracellularly applied tracer, horseradish peroxidase (HRP), in photoreceptor synaptic terminals during dark adaptation. First, chicks are sacrificed by perfusion fixation at various intervals after the addition of tracer to in situ eyecups. It is demonstrated that when terminals contain only one tracer-labeled organelle, this may be either a synaptic or a coated vesicle. At later times vacuoles in terminals become labeled. Some of these are seen as involutions of terminal membrane and some are observed in the cell body. Therefore, it seems likely that some involutions of terminal membrane pinch off and are transported retrogradely. Second, chicks are given intraocular injections of HRP at various intervals in a 12-hr dark period and sacrificed 1 hr later. Terminals of chicks sacrificed at 1 hr into the dark period contain predominantly tracer-labeled synaptic vesicles and vacuoles, whereas terminals of chicks sacrificed at 3 hr into the dark period contain tracer-labeled coated vesicles also. Diverticular membrane, thought to be the result of synaptic vesicle fusion and coalescence with the presynaptic membrane, waxes during the first hour of darkness and then wanes over a period of several hours (N. Cooper and B. McLaughlin, 1982, J. Ultrastruc. Res. 79, 58-73). These observations, together with those presented here, suggest that not all synaptic vesicles coalesce to form the diverticular membrane and that during the waxing stage, some synaptic vesicles are recycled rapidly without passing through a coated vesicle intermediate stage. This is discussed in the context of current models of localized synaptic vesicle membrane recycling.

Animals↗
PubMed1983

Synaptic membrane domains in photoreceptors of chick retina: a thin-section and a freeze-fracture study.

In this freeze-fracture study of synaptic terminals of chick photoreceptors, three regions of synaptic terminal plasmalemma can be distinguished on the basis of intramembrane characteristics. The first region is the synaptic vesicle fusion region in which rows of P-face depressions and E-face mounds are observed. In the absence of exocytotic figures this zone is relatively free of P-face particles and E-face pits. Adjacent to this, a second region is seen, rich in P-face particles and complementary E-face pits. This second region waxes and wanes in size during dark and light stimulation (Cooper and McLaughlin, 1982) and may correspond to similar expansions and contractions of synaptic plasmalemma induced by less physiological modes of stimulation, as observed in other synaptic terminals (Ceccarelli et al., 1979b; Model et al., 1975; Boyne and McLeod, 1979). During the waxing period, P-face particles and E-face pits are present in this membrane, and its expansion gives rise to diverticula of the synaptic terminal. During the waning period when the diverticula begin to disappear, aggregates of P-face particles and complementary patches of E-face pits are seen in the diverticular membrane. The third region, the nonsynaptic plasmalemma enclosing the terminal, contains a high density of P-face particles but does not contain E-face pits. Serial sections of vacuoles within the cytoplasm demonstrate that some vacuoles retain connections with this nonsynaptic plasmalemma. Vacuoles that are connected in this way are depleted of intramembrane particles. Such regions appear to represent separate domains within the photoreceptor terminal and are discussed in the context of membrane addition and retrieval.

Animals↗
PubMed1981

Freeze-fracture study of photoreceptor outer segments and pigment epithelium in dystrophic and normal retinas.

The intramembrane organization of outer segment (OS) membranes and pigment epithelial (PE) microvilli has been studied in rats (10-17 postnatal days) with inherited retinal degeneration (RCS) and in normal retinas from genetically controlled rats (RCS-rdy+). The OS plasma membranes of both dystrophic and normal retinas are characterized by large particles surrounding circular, particle-free zones on the P-faces (cytoplasmic leaflets) and a sparse distribution of particles on the E-faces (external leaflets). No regional differences in particle distribution are observed in either basal or distal plasma membrane regions. Outer segment disc membranes are characterized by large, densely packed P-face particles and ridged E-faces with very few particles. Small, particle-free patches of membrane are present in the basal disc P-faces of both normal and dystrophic retinas, which Andrews and Cohen ("79) have described as characteristic of newly added disc membrane. In dystrophic retinas, larger, particle-free domains are observed in the distal disc membranes (P-faces) and accumulating membranous debris. In older retinas, which have accumulated more debris, the particle-free domains occupy vast areas of the membrane faces and it is not possible to identify these membranes as belonging to either discs of plasma membranes. No comparable areas of particle-free membrane are observed in the distal discs and OS plasma membranes of normal retinas. Pigment epithelial microvillus membranes are characterized by an intermixture of large and medium-sized particles surrounding irregular particle-free areas, but no differences between normal and dystrophic PE membranes are observed. The changes in particle distribution observed in the dystrophic retinas suggests that the intramembrane molecular composition of older disc membranes has become altered or rearranged as the OS membranes accumulate as debris.

Aging↗
PubMed1981

A freeze-fracture study of photoreceptor presynaptic membranes during ribbon synapse formation.

The outer plexiform layer (OPL) of the developing chick retina from 11 embryonic days to 11/2 weeks posthatching has been studied by freeze-fracture to characterize changes in the membrane structure of photoreceptor terminals during synaptogenesis. At early stages, the undifferentiated photoreceptor synaptic base is characterized by a sparse distribution of intramembrane articles on the inner leaflet (P-face). Later, as the synaptic base begins to differentiate by extending filopodia into the OPL, numerous small aggregates of large particles appear between and on filopodial surfaces. Many of the aggregates occupy crater-like expressions, which are seen in cross-fractures through the underlying cytoplasm to be associated with vesicular invaginations of the presynaptic membrane. Corresponding thin sections through these regions at this time reveal immature arciform densities and coated vesicles fusing with the presynaptic membrane adjacent to these densities. At later stages, many of the particle aggregates on the photoreceptor membrane appear to have coalesced into longer arrays overlying ridges surrounded by numerous vesicle fusion sites. These intramembrane changes correlate with the formation of the mature arciform density-synaptic ribbon specialization in the photoreceptor presynaptic terminal and with physiological maturation of the chick retina.

Animals↗
PubMed1981

Gap junctions in the outer plexiform layer of te chick retina: thin section and freeze-fracture studies.

Previous studies have established that gap junctions between presumptive retinal neurons of the chick retina disappear during the course of embryogenesis. The present study examines the 2-3-week-old chick retina to determine if gap junctions are present in the outer plexiform layer of the more mature animal as would be in accordance with evidence from morphological and physiological studies on a variety of other vertebrates. Thin section and freeze-fracture techniques are used in a complementary manner to demonstrate that gap junctions are present between horizontal cell processes in the distal regions of the outer plexiform layer. These junctions appear to be between axon terminals and between spines that project from axon terminals to rods and double cones. Gap junctions are also observed between photoreceptors. They are seen on the synaptic terminals of all classes of cones and are located between the cone synaptic terminals and cone basal processes. Gap junctions are also seen between unidentified photoreceptor basal processes within the neuropil of both distal and proximal parts of the outer plexiform layer. Gap junctions are also present between cone synaptic terminals and deeply invaginated, vesicle-containing processes the origin of which remains to be determined.

Animals↗
PubMed1980

The localization of lectin binding sites during photoreceptor synaptogenesis in the chick retina.

Carbohydrate-containing macromolecules have been localized in the outer plexiform layer of the embryonic and hatchling chick retina by horseradish peroxidase-conjugated wheat germ agglutinin (WGA) and Ricinus communis agglutinin (RCA) lectins. Both WGA and RCA binding sites are present along developing photoreceptor synaptic membranes in the embryonic retina and the plasma membranes of developing neurites and glia. After photoreceptor synapse formation, RCA staining is restricted to non-synaptic membranes, but WGA staining is present on the pre- and post-synaptic membranes of receptor ribbon synapses in addition to non-synaptic membranes. These differing results between the accessibility of RCA and WGA binding sites on mature synaptic membranes in the chick retina suggests that RCA receptors on synaptic membranes are somehow masked after synapse formation and maturation, but that WGA receptors remain accessible. The effects of enzymatic digestion on WGA and RCA binding has been studied after prior treatment with neuraminidase. RCA staining of developing synaptic and non-synaptic membranes in the embryo remains the same after treatment with the enzyme, but in the hatchling RCA staining of non-synaptic membranes is enhanced, which suggests that galactosyl residues are relatively exposed on immature membranes but inaccessible to the lectin on mature membranes until neuraminidase acts to expose them by removing the terminal sialic acid residues. WGA staining on developing synaptic and non-synaptic membranes in the embryo is greatly diminished after neuraminidase pretreatment which suggests that a considerable amount of staining at this time is due to sialic acid in addition to N-acetylglucosamine. In the hatchling, photoreceptor synaptic membranes are no longer labeled with WGA and non-synaptic membrane staining is reduced after neuraminidase digestion, which suggests that after synapse formation synaptic membrane WGA labeling is primarily to sialyl residues, whereas most of the non-synaptic labeling is to N-acetylglucosamine residues.

Age Factors↗
PubMed1980

Fine structural analysis of membrane changes during reaggregation culture of chick optic tectum.

Thin section and freeze-fracture electron microscopy have been used to characterize the changes in membrane morphology of reaggregating cultures of chick optic tectum. The cells are rounded and freely dispersed at 0 hr after dissociation. Between 2 and 6 hr the cells become closely apposed on all sides by other cells and form small aggregates. At this time punta adhaerentia junctions and focal densities are seen along the membranes of neighboring cells. Between 1 and 5 days in vitro (DIV) neurites containing growth cone regions are present. At 5 DIV the first synaptic contacts are observed. Between 7 and 14 DIV, the number of synaptic contacts increase and fewer growth cone regions are observed. As early as 7 DIV profiles are observed which strongly resemble both astrocytic and oligodendroglial cell somata and processes. Freeze-fracture analysis of aggregates at 0--4 hr reveals a sparse particle distribution on the P and E faces of apposed cells. By 1 DIV small clusters of loosely packed, large sized particles are seen on the P face of apposed cell membranes which may represent junctional contacts. Apparent coated vesicle fusion sites are common on the P face at 1--2 DIV. By 7 DIV. By 7 DIV, E face particle arrays are seen on cell bodies and neurites which correspond to specializations characteristic of excitatory synaptic junctions. By 8--10 DIV particle arrays are seen on the P face of post-synaptic membrane which may represent inhibitory synaptic contacts. Other types of particle specializations seen in freeze-fracture replicas include: specializations characteristic of gap junctions between cells and orthogonal assemblies of particles thought to be characteristic of astrocytes.

Animals↗
PubMed1980

Fine structural studies of synaptogenesis in the superficial layers of the chick optic tectum.

Synaptogenesis in the superficial layers of the rostral pole of the optic tectum has been studied in the chick from embryonic day six (E6) to seven days post-hatching. Symmetrical membrane densities of puncta adhaerentia are observed prior to the detection of synapses and throughout development. Immature synaptic contacts are observed by E7. These early synapses are primarily axodendritic; however, somatodendritic, dendrodendritic, axosomatic and axoglial synapses are also observed. The majority of these synapses have asymmetrical membrane densities and the presynaptic terminals contain clear, spherical, synaptic vesicles. Synaptic terminals containing pleomorphic vesicles and making symmetrical synaptic contacts are not commonly observed until the third week of embryonic development, and may represent the onset of inhibitory function within the tectum. Comparison of the number of synapses per unit area in control versus experimental tecta, after unilateral eye enucleations of E3, indicates that the presynaptic terminals of some synapses present at E8 are of retinal origin. It is suggested that the development of retinotectal synapses follows a rostrocaudal gradient in the tectum and corresponds to the intrinsic tectal pattern of cytoarchitectonic differentiation.

Aging↗