Biomedical subjects

C Kaur

Publications and source records attributed to C Kaur.

At least 73 records · Page 4Linked to original sources

PubMed1993

Uptake of tracer by the epiplexus cells via the choroid plexus epithelium following an intravenous or intraperitoneal injection of horseradish peroxidase in rats.

Rapid passage of horseradish peroxidase (HRP) from the blood circulation to the cerebrospinal fluid was demonstrated in postnatal rats. At 30 min-1 h after an intravenous (i.v.) injection of HRP, the extravasated tracer from the blood vessels entered the connective tissue of the choroid plexus to reach the epithelial intercellular spaces where it was retarded by the apical tight junctions. The HRP which accumulated in widened intercellular spaces was readily endocytosed by the epithelial cells, notably at their lateral surfaces. This was especially pronounced 3 h after the injection. The endocytosed HRP was either routed to lysosomes or discharged apically by exocytosis into the CSF via membrane-bound vesicles by the epithelial cells. After longer survival periods, i.e. 6 h after injection, the intercellular spaces were relatively clear of tracer. HRP-labelled vacuoles or vesicles had diminished with a concomitant increase in the number of lysosomes containing HRP reaction product. In the course of HRP injection, the epiplexus cells residing on the choroid epithelium progressively accumulated HRP by endocytosis so that in rats killed 6 h after injection, the cells were heavily loaded with HRP incorporated into massive lysosomes. The labelling pattern of epithelial and epiplexus cells in rats injected intraperitoneally followed that observed in those receiving i.v. injections. These results suggest that the epiplexus cells together with lysosomal activity by the choroid epithelial cells serve as a protective line of defence for the blood-CSF barrier which appears to be inefficient.

Animals↗

PubMed1993

Induced hydrocephalus in postnatal rats following an intracerebral injection of ricin.

A single injection of peroxidase-labelled Ricinus communis agglutinin (RCA-HRP) was given intracerebrally in 5-day old postnatal rats to determine its effects on neural tissues. The rats were sacrificed at various time intervals ranging from 1 hour to 8 weeks after the injection. 5 days after the injection, the lateral ventricle ipsilateral to the injection was progressively enlarged. The size of the ventricle continued to expand so that 10-15 days after the injection the ventricle on the contralateral side was also affected. In longer surviving rats, i.e 3-8 weeks after the injection, both the ventricles were extremely dilated resulting in the thinning of the cerebral cortex. Scanning electron microscopy of the dilated ventricles showed signs of disruption of the ependyma in some regions. A number of cells including macrophages, neurons, glioblasts, astrocytes and oligodendrocytes were present on the ependyma. Their identification was confirmed by scanning- and transmission electron microscopy. Transmission electron microscopy of the cerebral cortex subjacent to the dilated ventricles showed the presence of many degenerating neurons, 2-5 hours after the injection of RCA-HRP. The neurons displayed typical features of degeneration, i.e. displacement of nucleus, dilatation of cisternae of rough endoplasmic reticulum, and swelling and disintegration of mitochondria. In conclusion, following a single intracerebral injection of RCA-HRP, drastic neuronal degeneration was elicited near the site of injection and this resulted in the dilatation of the lateral ventricles similar to hydrocephalus.

Agglutinins↗

PubMed1993

Variation with age in the labelling of amoeboid microglial cells in rats following intraperitoneal or intravenous injection of a fluorescent dye.

Amoeboid microglial cells (AMC) in the corpus callosum were selectively labelled following a single intraperitoneal (i.p.) injection of the fluorescent dye, rhodamine isothiocyanate (RhIc) into postnatal rats. The frequency of RhIc-labelled cells varied with age, with the largest number occurring in 7-d-old animals. Thereafter, the labelled cells declined drastically in number and fluorescence and were barely detectable in 12-d-old injected rats. Labelled cells were absent in 13-d or older rats given an RhIc injection. When the injected RhIc was followed over a time course sequence, it was first detected in the cerebral blood vessels and their lining endothelia within 5 min after the injection. A variable number of AMC emitting a weaker fluorescence were closely adherent to the outer walls of the blood vessels. With time, the fluorescence in the AMC was progressively enhanced, but that in the blood vessels showed a concomitant reduction. In the rats that received an intravenous (i.v.) injection of RhIc, the labelling pattern of AMC, both in terms of its variation with age and in temporal sequence, paralleled that in rats given i.p. injections. In 12-d-old rats subjected to a stab wound coupled with an i.p. injection of RhIc, a considerable number of AMC not normally labelled at this age were activated. The cells exhibited an intense fluorescence and expressed MHC surface antigen immunoreactivity. It is concluded from this study that when injected i.p. or i.v., RhIc is readily circulated to the cerebral vessels, where it enters brain tissue by transendothelial transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1992

Ultrastructural and immunocytochemical studies of macrophages in an excitotoxin induced lesion in the rat brain.

An epidural application of kainic acid (KA) over the cerebral cortex in rat resulted in an extensive lesion in the ipsilateral cerebral cortex. This procedure elicited an accumulation of a large number of macrophages at the site of lesion covering a period of 4 weeks beginning 4 days after the KA application. The macrophages in the centre of lesion were characterized by abundant cytoplasm containing a variable number of lysosomes and phagosomes. Neurons at the same site were depleted during the period examined. They underwent degeneration following the KA treatment. With the monoclonal antibodies OX-42, OX-18 and OX-6, intense immunoreactivity was observed in these cells at the light and electron microscopic levels. Besides these antibodies, the cells were stained positively with the isolectin Griffonia simplicifolia (GSAI-B4). At the periphery of the lesion, many cells bearing the external morphology of microglia were also intensely stained with the GSAI-B4 and the monoclonal antibodies. It was concluded from this study that neuronal degeneration, caused by the excitotoxin KA, induced the accumulation of macrophages which exhibited CR3 receptors (marked by OX-42), MHC I antigen (marked by OX-18) and MHC Ia (marked by OX-6). The expression of these surface antigens may be related to their active phagocytic activity. The reaction with GSAI-B4 indicates the presence of specific lectin receptors on the macrophages which would serve a similar function. The present lectin histochemistry and immunohistochemical studies suggest that macrophages in the centre of the KA-induced lesion were derived from infiltrated monocytes while those at the periphery originated from the activation of local microglial cells.

Animals↗

PubMed1992

Activation and re-expression of surface antigen in microglia following an epidural application of kainic acid in the rat brain.

Following an epidural application of kainic acid over the sensorimotor cortex in rats, the ipsilateral hippocampus and the ventrobasal nuclear complex of the thalamus showed extensive neural degeneration. The neuronal death, either as a result of direct neurotoxic destruction or wallerian and retrograde degeneration, elicited a dramatic expression of immunoreactivity on numerous cells bearing the external morphology of microglia. Thus, with the monoclonal antibody OX-42, many amoeboid immunoreactive cells bearing stout processes were observed in the above-mentioned lesioned sites. The present electron microscopic immunocytochemical study confirmed that these OX-42 positive cells were activated microglia characterised by an abundant cytoplasm containing a variable number of lysosomes and phagosomes. The surfaces of these activated microglial cells were thrown into pseudopodial processes engaged in the phagocytosis of cellular debris. Immunoreactivity was also observed in these cells with the monoclonal antibodies OX-18 and OX-6, although in the latter the immunoreactive cells were fewer and less intensely stained. With OX-42, the corresponding areas on the contralateral side showed some widely scattered typical microglial cells bearing extremely fine processes. They were not stained with either OX-18 or OX-6. It was concluded from this study that neural degeneration induced the expression of CR3 receptors (marked by OX-42) and MHC encoded antigens (marked by OX-18 and OX-6) in microglia. The elevation of the former antigen was related to their active phagocytic activity. The latter, on the other hand, would facilitate the capability of interaction between the activated microglia and T lymphocytes in a possible immune response.

Animals↗

PubMed1992

Expression of major histocompatibility complex antigens and CR3 complement receptors in activated microglia following an injection of ricin into the sciatic nerve in rats.

The ventral horn motor neurons in the lower lumbar cord underwent rapid degeneration following an injection of Ricinus communis agglutinin-60 (RCA) into the sciatic nerve. The cell death which was most drastic between the fifth and seventh post-injection day elicited a significant increase in the number of microglia. The activated microglia were scattered throughout the neuropil but the dramatic feature was their close association with the somata of the degenerating neurons. Often several microglial cells were seen surrounding the soma of a degenerating neuron. Immunocytochemical study showed that both the interstitial as well as the perineuronal activated microglia were labelled with the monoclonal antibodies OX-18 and OX-42 for the detection of MHCI encoded antigen and type three complement receptors, respectively. Intense immunoreactivity was observed especially in the perineuronal microglia with OX-18. Electron microscopic study confirmed the identification of the activated microglia. Although the activated microglia closely apposed the neuronal soma, there was no sign of a direct endocytosis. The cytoplasm of the activated microglia, however, contained massive lipofuscin bodies in longer survival animals. Electron microscopic immunocytochemical study showed that the immunoreactivity of the activated microglia was localized along their plasma membrane facing the neuronal soma. Since the microglia cells on the contralateral side of the ventral horn were not marked by the antibodies used, it was postulated that the vigorous expression of MHCI antigen and CR3 receptors on the activated microglia was induced by the neuronal degeneration resulting from the application of the toxin ricin.

Animals↗

PubMed1991

Study of the transformation of amoeboid microglial cells into microglia labelled with the isolectin Griffonia simplicifolia in postnatal rats.

The transformation of amoeboid microglial cells into ramified microglial cells in the brain of postnatal rats has been studied by labeling the cells with the isolectin Griffonia simplicifolia (GSA1-B4). The latter served as a specific membrane marker of the cell type. Thus, at the light-microscopic level, the amoeboid microglial cells in 1- to 5-day-old rats were intensely stained with GSA1-B4. All the stained cells appeared round. In 10-day-old rats, while most of the stained cells were round, some had assumed an oval appearance. In older rats, i.e. 15-22 days, all the stained cells became flattened or fusiform with long cytoplasmic processes. The present electron-microscopic study confirmed the above features but also added the fact that the reaction for GSA1-B4 was localized at the plasma membrane in the amoeboid microglial cells in all the age groups studied. The reaction for the isolectin was also detected in some vacuoles in the cytoplasm of the round cells. It was concluded from this study that the round amoeboid microglial cells differentiate to become the ramified microglia with age. In the course of this transformation, they retained specific membrane receptors for the isolectin which distinguished them from other glial cell types.

Animals↗

PubMed1991

Expression of major histocompatibility complex and leukocyte common antigens in amoeboid microglia in postnatal rats.

The expression of major histocompatibility complex (MHC) antigen and leukocyte common antigen (LCA) was observed in the amoeboid microglial cells in postnatal rat brain. Considerable MHC class I surface antigen was detected at the plasma membrane and its tubular invaginations in the amoeboid microglia in the corpus callosum using the monoclonal antibody OX-18. In early postnatal (2 and 5 day) rats, the OX-18 positive cells were mostly round but a few possessed stout processes. With increasing age (9 and 15 days) the OX-18 positive amoeboid microglia assumed an oval or elongated form. By the time of weaning (21 days) and in older animals, the immunoreactivity was extremely weak and was detectable only on some branched microglia bearing fine processes. The presence of MHC class Ia antigens with OX-3 and OX-6 was hardly detectable except for a few weakly stained cells in the corpus callosum and cavum septum pellucidum in early postnatal rats. The expression of LCA was observed in amoeboid microglial using the monoclonal antibody OX-1 and this followed a similar temporal pattern to that with OX-18. The additional phenotypic features of amoeboid microglial cells in the present study support their monocytic origin. These cells are endowed with MHC class I antigens which may serve as the restriction elements for T lymphocytes, at least in the early postnatal brain.

Animals↗

PubMed1990

Response of intraventricular macrophages to crotoxin-coated microcarrier beads injected into the lateral ventricle of postnatal rats.

Crotoxin-coated microcarrier beads were injected into the lateral ventricles of 5 days old postnatal rats. The morphology of the cells attached to the beads at various time intervals was studied by scanning and transmission electron microscopy. Scanning electron microscopy showed that very few cells were associated with the surface of the beads 18 hours after the injection. After 2 days a large number of spherical cells showing blebs and filopodia were attached to the surface of the beads. One week after the injection, these cells became oval and, in longer survival periods between 2 weeks and 30 days after the injection, the cells developed a flattened or angular cell body bearing a number of radiating slender processes. Transmission electron microscopy of the re-embedded materials from animals killed 2 days after the injection showed many cells with an eccentric nucleus containing dense chromatin masses. Their abundant cytoplasm was endowed with a variable number of lysosome-like dense granules and vacuoles. In longer surviving animals, the cells became elongated with scanty cytoplasm showing relatively fewer dense granules and cytoplasmic vacuoles. It is postulated from this study that the cells attached to the crotoxin-coated beads are derived from the intraventricular macrophages. These are functionally active initially in response to the beads injected. With time, however, they undergo morphological alteration and regress into quiescent cells which are microglia-like.

Animals↗

PubMed1990

Lectin labelling of amoeboid microglial cells in the brain of postnatal rats.

The labelling of amoeboid microglial cells in the postnatal (2-10 days old) rat brain was studied by intracerebral injection of various lectins, including peroxidase-labelled Ricinus communis agglutinin (RCA), peroxidase-labelled isolectin Griffonia simplicifolia (GSA1-B4) and gold-labelled concanavalin A (Con A). Three to six hours after the injection of RCA and GSA1-B4, the amoeboid microglial cells in the supraventricular corpus callosum were selectively labelled. Most of the labelled cells were round, showing dense black reaction products. With the electron microscope the reaction of the binding sites for RCA and GSA1-B4 was localised on the plasma membrane, in the plasmalemmal invaginations, in the limiting membrane of the cytoplasmic vacuoles and in the dense granules identified as lysosomes. The binding sites for gold-labelled Con A were initially (one hour) observed at the plasma membrane. With time (3-6 hours) the gold particles occurred in the invaginations of the plasma membrane and consequently in the cytoplasmic vacuoles and in the dense granules. It appears therefore that the lectins first bind to their specific carbohydrate receptors on the plasma membrane and are later internalised by the cells. It is suggested that the receptors play an active role in phagocytic function. Furthermore, the fact that the amoeboid microglial cells show similar membrane lectin receptors as the monocyte-derived tissue macrophage supports the hypothesis of their origin from blood monocytes.

Animals↗

PubMed1989

Development of the various glial cell types in the cerebral cortex of postnatal rats.

The present quantitative study in the postnatal rats showed the rapid growth of the various glial cell types in the cerebral cortex. Among them, the increase of microglia was most dramatic. The increase was about 15 times, covering a period of 15 days extending from 5 days of age to 20 days. The majority of the microglia observed were in the outer third of the cortex. During the same period, the number of oligodendrocytes and astrocytes also showed a steady but moderate increase. The increase of oligodendrocytes was most significant between 5 and 10 days. Their density was greater in the inner third of the cortex. Astrocytes were distributed uniformly throughout. Examination of the cerebral cortex in 1- to 3-day-old rats by electron microscopy showed sporadic ameboid microglia cells and glioblasts. The possibility that they served as the precursor cells of microglia and macroglia (astrocytes and oligodendrocytes), respectively, was considered.

Animals↗

PubMed1989

Scanning electron microscopy of transitory subependymal cysts in the developing midbrain of postnatal rats.

Transitory cystic cavities, associated with the subependymal region of the aqueduct in the midbrain of postnatal rats aged 1-15 days, were studied by light and scanning electron microscopy. The walls of these cysts, as observed in scanning electron microscopy, were lined by a dense feltwork of nerve fibres. Two types of cells were identified in the cysts: smaller glioblasts and larger amoeboid microglial cells. The glioblasts were characterized by a smoother cell body with radiating long processes. The amoeboid microglial cells showed blebs and pseudopodia on their surface. They either adhered to the walls or floated freely in the lumen. It is postulated that the formation of the subependymal cysts in the developing brain resulted following the cleavage or breakdown of the nervous tissue due to the expansion of the aqueduct and the brain as a whole. The amoeboid microglial cells in the cysts were probably derived from the extravasated blood monocytes in response to the physical damage ensuing during the formation of the cysts.

Animals↗

PubMed1987

Localisation of thiamine pyrophosphatase in the amoeboid microglial cells in the brain of postnatal rats.

The activity of TPPase in amoeboid microglial cells has been studied in postnatal rats. When examined with the light microscope such cells in 1-10 days old rats perfused with 4% paraformaldehyde were round and showed a dark brown reaction in their cytoplasm. In older rats (10-30 days), the reactive amoeboid microglial cells were oval, flattened or branched. Electron microscopic examination revealed that the reaction product was seen on the plasma membrane, in the subplasmalemmal vacuoles, in tubular invaginations of plasma membrane and in the transface of the Golgi saccules. In rats perfused with the mixed aldehyde solution, the amoeboid microglial cells did not show a positive TPPase reaction with the light microscope but at the ultrastructural level a weak reaction was seen in some cytoplasmic vacuoles and in the Golgi saccules.

Animals↗

PubMed1987

Origin and fate of neural macrophages in a stab wound of the brain of the young rat.

Colloidal carbon was injected intravenously into young rats to label circulating monocytes before making a stab wound in the brain. The rats were killed 3-16 days after the stab wound. Demonstration of non-specific esterase, thiamine pyrophosphatase and 5'-nucleotidase was carried out on the carbon-labelled macrophages at the site of lesion at various survival times. In rats killed 3-5 days after the injury numerous carbon-labelled macrophages were present in the needle passage as well as in the marginal area of the lesion and they showed a positive reaction for non-specific esterase. The reaction of the enzyme was found in some of the dense bodies in the form of punctate precipitates. The reaction for thiamine pyrophosphatase was seen in the Golgi saccules as well as on the plasma membrane, although in the latter the reaction was weaker. Intense reaction for 5'-nucleotidase was localised over the plasma membrane as well as over the dense bodies. The carbon-labelled macrophages displaying the activities of the above enzymes in the 3-5 days postoperative group were of the round type. However, in the 8-16 postoperative days animals, the cells were either oval or had assumed an elongated outline resembling the microglial cells seen in the tissue taken from the normal side. It is concluded that circulating monocytes are a main source of brain macrophage in traumatic brain lesions. In the healing process of the wound some of the cells regress to become microglial cells as shown by the presence of the carbon particles as well as non-specific esterase, thiamine pyrophosphatase and 5'-nucleotidase activity in the various stages of structural transformation.

Animals↗

PubMed1986

Labelling of amoeboid microglial cells in rats of various ages following an intravenous injection of horseradish peroxidase.

The macrophagic amoeboid microglial cells in the corpus callosum of postnatal rats were labelled following an intravenous injection of horseradish peroxidase (HRP). The earliest time when these cells were labelled was 3 h after the injection of HRP in postnatal (1-10 days) rats. Similar cells around the mesencephalic aqueduct and the fourth ventricle were also labelled. These cells, however, were weakly labelled in developing (11-20 days) and unlabelled in weaning (21-30 days) rats. The results suggest that in the postnatal rats, the HRP passed through the endothelial lining of the blood vessels and was then ingested by the amoeboid microglial cells. In the developing and older rats, the wall of blood vessels had developed fully thereby preventing the free passage of HRP into the brain tissues.

Aging↗

PubMed1985

Transformation of amoeboid microglial cells into microglia in the corpus callosum of the postnatal rat brain. An electron microscopical study.

An electron microscope study of the corpus callosum in postnatal rats of various ages was carried out to elucidate the fate of the amoeboid microglial cells. The cells present in the corpus callosum of younger rats (3-5 days) were round and showed an eccentric nucleus with marginal chromatin. They displayed numerous lysosomal granules and vacuoles in the cytoplasm. In older animals, i.e., from 7 days onwards some of the cells became oval so that by 15-20 days of age most of the cells were elongated and branched. In the latter, the cells showed a flattened or angular nucleus with dense chromatin clumps. The cytoplasm showed fewer lysosomal granules and vacuoles which were absent in cells of 20 day old animals. Quantitative measurements showed that there was a gradual diminution in the amount of cytoplasm at the cell body of amoeboid microglial cells with age, so that by the age of 20 days the cells were reduced to less than one-third of their original size as seen in 3 day old rats. The reduction of cytoplasm at the cell body is probably because it is channelled to the cytoplasmic processes which are evident in older rats. Some cytoplasm may have been extruded and phagocytosed by companion cell types.

Age Factors↗

PubMed1984

Cytochemical localisation of 5'-nucleotidase in amoeboid microglial cells in postnatal rats.

The activity of the enzyme 5'-nucleotidase has been studied in postnatal rats. In 5 days old rats, under the light microscope, round amoeboid microglial cells were stained for the enzyme. The cytoplasm was stained dark brown, with a clear nucleus. In older rats, the reactive amoeboid microglial cells assumed an oval or flattened form. In the electron microscope, in 5 days old rat, reaction product was deposited at various sites in the cytoplasm of the amoeboid microglial cells: over lysosomes in subplasmalemmal vacuoles as well as in saccules of the Golgi apparatus. In older rats the cells showed reaction over the lysosomes. The cells became oval and elongated.

5'-Nucleotidase↗

PubMed1983

An inhibitory role for morphine on the release of dopamine into hypophysial portal blood and on the synthesis of dopamine in tuberoinfundibular neurons.

The intracerebroventricular administration of morphine to ovariectomized rats resulted in a marked decrease in the concentration of dopamine in plasma of hypophysial portal blood. A 90% reduction in the rate of release of hypothalamic dopamine into hypophysial portal blood occurred during the 60 min following the intraventricular administration of 60 ng of morphine sulfate. A dose-related decrease in the rate of release of dopamine into the portal vasculature was observed between 7.5 ng and 60 ng of morphine sulfate. Regardless of the quantity of morphine sulfate (1-500 ng) given to the animals, the concentrations of norepinephrine and epinephrine in hypophysial portal plasma and femoral arterial plasma remained unchanged. The efficacy of morphine on the release of dopamine into hypophysial portal blood was not associated with an equal efficacy of the drug on the synthesis of dopamine in tuberoinfundibular neurons, as evaluated by the accumulation of dihydroxyphenylalanine (DOPA) in the median eminence of rats given 3-hydroxybenzylhydrazine (NSD 1015). No effect of morphine was observed on DOPA accumulation in the median eminence of NSD-treated rats that had received 50 ng of morphine sulfate intracerebroventricularly, and only a 50% reduction was observed in the accumulation of DOPA in the median eminence of rats given 500 ng of morphine sulfate. These findings are supportive of the view that morphine inhibits both the release and synthesis of dopamine but is more effective in inhibiting the release than synthesis of dopamine.

Animals↗