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J R Wolff

Publications and source records attributed to J R Wolff.

At least 127 records · Page 7Linked to original sources

"Seamless" endothelial cells of blood capillaries.

The distribution and number of seamless endothelial cells (SE) were studied in various organs and tissues of rats, rabbits and humans (1) by light microscopy after silver impregnation of the endothelial cell boundaries, (2) by electron microscopy, and (3) in three-dimensional reconstructions of duodenal villi and renal glomeruli. Since SE are situated mostly at branching points, the number of SE is roughly correlated to the number of branchings in the capillary system concerned. SE make up about 50% of all endothelial cells in the renal glomerulum and duodenal villi, and about 30% in the cerebral cortex. However, they rarely occur in bradytrophic tissues. SE have been found exclusively in net capillaries (true capillaries). They seem to be absent in most arterio-venous capillaries (capillary parts of thoroughfare channels), in the capillaries of endocrine glands, as well as in the sinusoidal systems of heart muscle, liver, spleen and bone marrow. It is concluded that SE are developed when tube formation is confined to a single endothelial cell. SE are intercalated most frequently in those capillaries that develop lastly in the terminal vascular bed. The seamless segments are canalized by fusion of intraendothelial vacuoles with pre-existing vascular walls. The existence of SE, confirming the dual structural design of capillary systems, may be used as a detector for net capillaries.

Adipose Tissue↗

Entorhinal lesions result in shrinkage of the outer molecular layer of rat dentate gyrus leading subsequently to an apparent increase of glutamate decarboxylase and cytochrome oxidase activities.

In intact dentate gyrus, glutamate decarboxylase immunoreactivity (GAD) and cytochrome oxidase activity (CyO) showed different distributions patterns. Entorhinal lesions caused increases of GAD and CyO in the outer molecular layer (OML) of the ipsilateral side. Submicroscopical localization of these enzymes did not change, except for CyO labeling more astrocytic mitochondria. The increase in numerical density of GAD puncta correlated quantitatively with shrinkage of OML, whereas in the whole molecular layer the number of GAD puncta remained unchanged. Hence, the localized increase of enzyme activities and lysosomes is apparently related to shrinkage of OML, but does not indicate plasticity of GABAergic neurons.

Afferent Pathways↗

Is there a non-synaptic component in the K+-stimulated release of GABA in the developing rat cortex?

Postnatal development of the K+-stimulated release of [3H]GABA in rat cortex slices was compared to the density of Gray type 2 synapses (which correlate with GABAergic synapses in rat cortex). The [3H]GABA release system develops earlier than the inhibitory synapses which suggests that, at least in the young cortical tissue, a large part of the release mechanism is associated with other than synaptic structures.

Aging↗

Axonal sprouts of the hypoglossal nerve implanted in the superior cervical ganglion of adult rats establish synaptic contacts under long-lasting GABA effect. An experimental degeneration study.

Experimental degeneration was used in this study to determine if the hypoglossal nerve implanted already in the superior cervical ganglion of adult rat under GABA treatment has established morphologically-identifiable synapses with the dendrites of principal ganglion cells. The implanted hypoglossal nerve trunk was cut in a re-operation, and the ganglionic samples were studied by electron microscopy after 0, 6, 12, 24 and 48 h survival times. First signs of degenerative changes were found in the myelinated and non-myelinated axons alike, 6 h after axotomy. The fine-structural signs of degeneration resembled those of the preganglionic nerve fibres. Degenerating nerve terminals establishing synaptic contacts with the dendrites of the principal ganglion cells were also seen, indicating that the axonal sprouts of the implanted hypoglossal nerve established synaptic contacts with the ganglion cells. It remained, however, to be elucidated whether or not these synapses of the hypoglossal nerve are functionally active contacts while the preganglionic innervation is also present within the ganglion.

Animals↗

Morphological changes induced by sodium bromide in murine neuroblastoma cells in vitro.

Sodium bromide was applied in vitro to mouse neuroblastoma cells of different ages for short and long periods (2 h to 10 days). The changes observed light-and-electron microscopically were similar to those described earlier after GABA treatment. Coated vesicles proliferated and originated by pinching off from the Golgi complex and from the rough endoplasmic reticulum. Numerous coated vesicles were continuous with the plasma membrane, especially near zones in which electron-dense material aggregated at the inner aspect of the plasmalemma. Small invaginations, similar in ultrastructure to coated vesicles, were also formed. It is unclear whether the coated vesicles or the dense plasmalemma invaginations contribute to the "undercoating" by fusing with the adjacent electron-dense plasma membrane. There was a distinct increase in the number and area of specialized contacts (intermediate junctions and zonulae adhaerentes) between cells and their processes. A floccular or filamentous electron-dense substance varying in amount and appearance was occasionally seen between the contacting membranes. Varicosities of terminal swellings of cell processes contained vesicles of variable size, shape and density, and also profiles of the smooth endoplasmic reticulum. Under the influence of sodium bromide, similar to the effect of GABA, mitochondria appeared within the varicosities, and primitive contacts (intermediate junctions) were formed between the terminal swellings and potential postsynaptic elements, which were absent in controls. Additionally, dense-core vesicles proliferated and aggregated at the cell periphery. They were often arranged linearly below the plasma membranes of perikarya and processes, and surrounded by a highly electron-dense substance. The similarity of the present findings to those obtained after GABA treatment and their relation to synaptogenesis are discussed.

Animals↗

Distribution patterns and individual variations of callosal connections in the albino rat.

After complete callosotomy the distribution of degeneration products was re-investigated in adult albino rats. Three to seven days post operation, coronal, horizontal and "flattened" sections were impregnated according to the new methods of Gallyas et al. (1980) which stain degenerating axons and terminals, respectively. The regional distribution patterns of callosal terminals were directly visualized with dark field illumination at low magnification. With this technique the distribution pattern of axons and terminals could be compared between different cortical regions and individuals. Callosal terminals tend to accumulate in patches or bands along the borders of cortical regions and areas. The concentration of callosal terminals was especially high at the common corners of more than two cortical areas. The callosal system shows a rather constant distribution pattern which is composed of column shaped subunits. Considerable individual variations were recognized concerning the number, position, shape, density and contiguity of the columnar units either occupied by callosal connections or empty. Although the laminar distribution of callosal terminals shows some similarities in different areas of the cortex, there is no common laminar pattern characteristic either for the whole neocortex or for any cortical region. The comparison between consecutive sections stained either for degenerating fibers or degenerating axon terminals revealed that the callosal axons do not determine directly the arrangement and packing density of callosal synapses. Whatever determines the position and amount of callosal synapses this influence seems to be exerted via translation into the columnar organization.

Animals↗

Axosomatic synapses in the visual cortex of adult rat. A comparison between GABA-accumulating and other neurons.

Differences in axosomatic synapses between GABA-accumulating [G(+)N] or non-accumulating [G(-)N] neurons have been investigated in the visual cortex of adult rat. The neurons were classified and localized in light microscopic autoradiograms after [3H]GABA injections. The cells resectioned for electron microscopic identification of type 1 synapses (T1S) and type 2 synapses (T2S). A total of 167 neurons [45 G(+)N, 122 G(-)N] situated in laminae II-VI were evaluated. The two groups of neurons were not uniform populations. G(-)N included both pyramidal and non-pyramidal neurons, whereas no typical pyramidal neurons were found among G(+)N. A total of 691 synaptic contacts was evaluated for these groups of somata. The density of synapses was higher on G(+)N than on G(-)N. This was mainly due to a difference in the number of T1S. On G(-)N the frequency distributions of both types of synapses represented Poisson distributions, indicating that there were stochastic variations around mean values. In contrast, on G(+)N the distribution was exponential which suggests that G(+)N include several subpopulations with different densities of T1S. On all cortical neurons the average density of T2S was 509-60 T2S per 1000 microns2 of soma surface, which resembles the density in the neuropil. In contrast, T1S varied from zero to a mean of 12 per 1000 microns2 on G(-)N and to a mean of 51 per 1000 microns2 on G(+)N, i.e. the density of T1S, unlike T2S, is much smaller on neuronal somata than in the surrounding neuropil. It is suggested that the formation of axosomatic T1S, but not of T2S, is suppressed to a variable degree on almost all cortical neurons. Only on pyramidal neurons does the suppression of T1S seem to be complete.

Animals↗

Effect of GABA-administration on murine neuroblastoma cells in culture. I. Increased membrane dynamics and formation of specialized contacts.

(Gamma aminobutyric acid) GABA was applied to cultures of mouse neuroblastoma cells of different ages at concentrations ranging from 10(-4) to 10(-6) M. The cultures were exposed to GABA either in short term experiments for 2 h to 2 days or for longer periods by adding the substance twice within 10 days at 5-day intervals. The following effects were observed: (1) There was a strong proliferation of coated vesicles, appearing to derive from the Golgi complex and the rough endoplasmic reticulum (RER), and also showing all intermediate stages of fusion and pinching off from the plasma membranes. (2) In numerous areas, electron-dense material aggregated at the inner aspect of the plasma membrane and around small invaginations of the plasmalemma. (3) The number and area of specialized contacts increased between cells and their processes. (4) Similar to cultures free of GABA, varicosities and terminal swellings of the cells and their processes were filled with small round vesicle, 40--60 nm in diameter, or with smooth, very large, empty-appearing vesicular inclusions, or with flat pleiomorphic vesicles. In addition, mitochondria and some formations of the smooth endoplasmic reticulum (SER) appeared, and primitive contacts (symmetrical densities) were formed. (5) Dense-cored vesicles were found peripherally and linearly arranged, surrounded by an electron-dense substance. (6) Electron-dense material of unknown origin was seen between cells or their processes near the peripherally arranged dense-cored vesicles. Exogenous GABA may play a specific role in the early stages of synaptogenesis, since it showed a positive effect on the neuroblastoma cells, which in the absence of GABA are only capable of forming primitive or immature presynaptic elements. The significance of the peripheral accumulation of dense-cored vesicles, accompanied by an amorphous, electron-dense substance occurring both intra- and extracellularly is discussed.

Animals↗

The temporo-spatial course of degeneration after cutting cortico-cortical connections in adult rats.

Adult albino rats received callosotomies or lesions in the paracingular cortex. Between 12 h and 3 months after injury the structure and topography of the degeneration products were studied by light- and electron-microscopy. The degeneration process was quantified by television-image analysis applied to sections prepared according to a new technique that stains reliably degenerating terminals and lysosomes (Gallyas et al. 1980). All types of cortico-cortical connections show a multiphasic degeneration process: During a precursor stage a small number of dense bodies and mitochondrial granules are stained. These and the few early degenerating axon terminals are much more diffusely distributed than the large number of terminals that degenerate during the following period. The terminal degeneration shows a biphasic time course. One maximum appears at 2-7 days post operation, which corresponds to the well known direct consequence of axotomy. The second peak at 10-20 days post operation could be caused by transneuronal reorganization of the cortical connectivity. Terminal degeneration always begins along the borders between cortical regions and areas, but it may change its laminar and columnar distribution pattern during the second phase. The degeneration products that are phagocytosed by astrocytes seem to be removed by intracellular transport to their perivascular endfeet. The degeneration process ends with fiber degeneration which, especially in laminae I and VI, may form a separate peak after 20 days or more.

Animals↗

Prenatal and postnatal development of GABA-accumulating cells in the occipital neocortex of rat.

The development of the 3H-GABA-accumulating cells in the neocortex has been followed by light microscopical autoradiography, and after resectioning of the original autoradiograms, by electron microscopy. The validity of the methods used are discussed. The study has been limited to the primary visual cortex and its precursors of rat, from embryonic day (E) 15 to adult. GABA-accumulating cells were found from E 16 onwards in the occipital cortex, which is one to two days after cells arrive in the pallial anlage and one day before the first synapses have been found. Until E 18, the prevalent positions of labeled cells were in lamina I and below the cortical plate. Later, labeled cells also occurred as strands within the cortical plate. During the perinatal period, more and more GABA-accumulating neurons and glial cells began to differentiate and show a characteristic distribution at the periphery of unlabeled cell clusters. From postnatal day 11, no apparent change in density or position of labeled neurons took place. At prenatal stages, two main types of labeled cells were found: 1) Comparatively large cells with rounded nuclei and rough endoplasmic reticulum consisting of narrow, electron-lucent cisterns. These cells were tentatively identified as preneurons. 2) Smaller, polymorphous cells with irregular nuclei and rough endoplasmic reticulum with wide cisterns filled with a dense matrix. These cells are probably precursors of glial cells. Both labeled neurons and glial cells were identified at postnatal stages. In young and adult rats, only neurons to be characterized as nonpyramidal neurons were labeled. Synapses were not found on the perikarya of labeled cells until E 21. Also, in postnatal preparations, labeled neurons showed few axo-somatic synapses. These data were correlated with other events of the structural and functional development of the neocortex. The delay between the appearance of GABA accumulating cells and synaptogenesis indicates that apart from being an inhibitory neurotransmitter, GABA might play a specific morphogenetic role in synaptogenesis. This could even be its primary function during early developmental stages.

Animals↗