Basic methods of EMG quantification.
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Electromyography↗
Biomedical subjects
H de Weerd
Publications and source records attributed to H de Weerd.
Tanycytes in the medial habenular nucleus of the rat.
Tanycytes with foot processes contacting capillary basal membranes were identified in the rat medial habenular nucleus. They constitute a relatively small but constant population of cells among the conventional ependymal cells. In contrast to tanycytes in most circumventricular organs, habenular tanycytes possess cilia. Superimposed upon the cells are nerve fibers belonging to the serotonergic supraependymal axon plexus. Their ultrastructure differs in many respects from that of hypothalamic tanycytes.
Animals↗
Membrane specializations and their relation to HRP transport in the medial habenular nucleus of the rat.
In the medial habenular nucleus of the rat, ependymal and endothelial membrane specializations were studied with TEM and freeze-fracturing. They comprise ependymal adherent junctions - not manifest in freeze-fracture replicas-, gap junctions, and membrane-associated orthogonal particle complexes ("assemblies") - not identifiable in thin-sectioned material. Ependymal tight junctions being absent, no brain-liquor barrier exists. The capillary endothelium is provided with tight junctions only. Intraventricularly injected HRP was transported in large amounts through the ependyma, mainly through the intercellular spaces and additionally by way of massive pinocytosis through the cytoplasm of particular ependymal cells only, and finally through the parenchymal intercellular compartments towards habenular capillaries. Following intravenous injection of HRP, considerable transport of the enzyme took place by means of transendothelial pinocytosis, followed by some pinocytotic transport through diverse parenchymal elements and markedly profuse incorporation and lysis within pericytes. The habenular blood-brain barrier appeared to be considerably leaky with respect to HRP.
Animals↗
A specificity for cellular fibronectin in its effect on cultured chondroblasts.
Chick cellular fibronectin has previously been shown to alter the phenotypic properties of cultured chick-embryo vertebral chondroblasts. Over the course of several days, adhesion and spreading on plastic substrata in the presence of serum was stimulated, the morphology of the cells was changed, the synthesis of cartilage-specific type-IV proteoglycan was inhibited, and the synthesis of type-I collagen and fibronectin was induced or stimulated. In the present study, chick plasma fibronectin was isolated and observed to mimic the effect of cellular fibronectin on cell adhesion and spreading. Both kinetic and dose-response relationships were similar between the two isoproteins. In contrast, chick plasma fibronectin, at up to tenfold higher concentrations by weight, did not alter cell morphology or synthesis of type-IV proteoglycan. Control experiments showed that plasma fibronectin could not neutralize cellular fibronectin and that plasma fibronectin did not simply conceal an effect on type-IV proteoglycan production by shifting the balance released into the culture medium. The results suggest that the effect of cellular fibronectin on the differentiated properties of chondroblasts relies on some unique feature not possessed by plasma fibronectin, and thus is not solely dependent on its own ability to stimulate adhesion and spreading.
Animals↗
Supraependymal cell clusters in the rat hypothalamus.
The fine structure of supraependymal cell clusters of the median eminence was studied with TEM. The cluster cells were identified on the basis of ultrastructure and histochemical determination of glial fibrillar acidic protein (GFA). The phagocytic properties were also studied by means of intraventricular injections of HRP. Neurons, neuroglia cells and degenerating ependyma- and glial cells were found. The extrusion of degenerating infundibular elements into the ventricle is a constant phenomenon but its precise localization and intensity are variable. The close proximity of the clusters to capillary loops is stressed. Because of the broken ependyma at the neck of the cluster, the permeability of the infundibular lining for HRP is increased. Clusters may be seen as sites lacking a brain--CSF barrier.
Animals↗
The fine structure of the ependymal surface of the recessus infundibularis in the rat.
The surface of the recessus infundibularis of the third ventricle has been studied with the scanning and transmission technique in normal and experimental material. Surface specializations such as microvilli, craters and areas of discontinuous lining are described. Supraependymal cells and fibres have been found; some of these cells form wide-meshed networks. The supraependymal fibres may be regular or varicose; the former seem to perforate the ependyma. With the transmission electron microscope the supraependymal cells are divided into three categories; nerve cells, lymphocytes and "dense cells". Two fibre populations are distinguished: thin profiles (nerve fibres) and thick profiles (nerve terminals). Axosomatic and axoaxonic synapses are described. Synapses between supraependymal fibres and ependyma cells have also been found.
Animals↗
Microvascular changes in aged rat forebrain. Effects of chronic nimodipine treatment.
In the present study the effects of long-term treatment with the 1,4-dihydropyridine calcium antagonist nimodipine on ultrastructural alterations of the microvascular morphology were examined in the frontoparietal cortex, entorhinal cortex and CA1 of the hippocampus in the aged rat. Qualitative observations of cerebral microvasculature of aged (30 months) Wistar rats revealed the presence of microvascular fibrosis, membranous inclusions within the basement membrane and basement membrane thickenings. In several cortical regions the percentage of aberrant microvessels was significantly reduced in the nimodipine-treated rats. The observed microvascular anomalies were classified into five distinct categories of which microvascular fibrosis type II, defined as collagen deposits up to 1 micron within the microvascular basement membrane, showed the strongest reduction in the nimodipine-treated cases. The decrement of the percentage of aberrant microvessels and the relative occurrence of several classes of microvascular deviations showed some variation in the various brain regions examined and was most pronounced in frontoparietal cortex layer III. These results may provide a morphological basis for the improved motor and cognitive performance in aged rats after long-term oral nimodipine administration.
Aging↗