Histology and histopathology Vol. 7, nº 1 (1992)

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  • Publication
    Open Access
    Expression of major histocompatibility complex antigens and CR3 complement receptors in activated microglia following an injection of ricin into the sciatic nerve in rats
    (Murcia : F. Hernández, 1992) Ling, E. A.; Kaur, C.; Wong, W. C.
    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 postinjection 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.
  • Publication
    Open Access
    The effect of mesulergine on prolactin secretion and anterior pituitary cells morphology in diethylstilboestrol-treated female Wistar rats
    (Murcia : F. Hernández, 1992) Pisarek, Hanna; Stepien, Henryk
    Mesulergine (Cu32-085) is an active semisynthetic ergot alkaloid with unusual biphasic antagonistic-agonistic effect on dopamine (DA) turnover in the rat striatum. The present study has been made to elucidate the influence of the long-term treatment of this drug on prolactin secretion and prolactin cells morphology in the female Wistar rats with experimentally-induced hyperprolactinemia. Additionally, the effect of this drug was compared with bromocriptine and pergolide activity, applied in the same experimental conditions. It has been shown that prolonged mesulergine treatment attenuated the stimulatory effect of stilboestrol on prolactin secretion in vivo. It also decreased mean prolactin cells density, above all cells and lactotroph mitotic indexes, estimated in immunohistochemically-stained slides. However, antiproliferative activity of Cu 32-085 was weaker, when compared with bromocriptine and pergolide.
  • Publication
    Open Access
    Effect of ascitic liquid on growth in vitro of embryoid bodies derived from teratocarcinoma
    (Murcia : F. Hernández, 1992) Monzó, M.; Martínez Rubio, G.; de Anta, J.M.; Saltó, C.; Ruano-Gil, D.
    Embryoid bodies (EB) derived from teratocarcinoma (TC) OTT6050 were cultured with ascitic liquids (AL) from animals carrying 16-, 22- and 35-day evolved EB. At the same time the presence of fibronectin (FN) in AL were analyzed by immunoblotting. Results indicate the . probable existence of growth-stimulatory factors for EB, as well as the presence of FN in the 22-day AL.
  • Publication
    Open Access
    Ageing of the human entorhinal cortex and subicular complex
    (Murcia : F. Hernández, 1992) Trillo, L.; Gonzalo, L. M.
    Age-dependent changes in the entorhinal cortex (EC) and subicular complex (SC) were studied in 30 brains of patients who died between 14 and 86 years of age, without CNS impairment, as determined by macro- and microscopic examination. The brains were fixed in 10% formalin and embedded in paraffin. Three series of corona1 EC and SC sections (7 pm) were stained by Nissl, PAS or hematoxylin-eosin. Using neuronal count and Kariometry, age-dependent modifications were studied in layers 11, 111 and V of the lateral area of the EC; in the pyramidal layer of the subiculum (S), and in layer 11 of the presubiculum (PS). Al1 EC layers studied presented a slight (11-20%) although significant reduction up to 35 years, but from 35 to 75 years the decrease was not significant. After 75 years the neuronal loss increased slightly. The nuclear area decreased up to the age of 40-45 years, (10-18%) and augmented from this age up to 75 years (10-14%). During the last period of life, the nuclear area did not change. From 30-60 years, pyramidal layer in the S showed a significant neuronal loss (30%), thereafter, neuronal reduction was less. At early years, the nuclear area decreased insignificantly (15%), and from 35 years up to the most advanced age studied, it increased significantly (13%). In the PS, layer 11 manifested a cell loss throughout the lifespan (32.9%) and the changes in the nuclear area did not reach statistical significance due to the dispersions of its values. These results lead to the conclusion that the neuronal loss in EC is notably less than in S and PS and, in general, than in other centres. The sequence of neuronal loss is also different in the EC and in the S. While in EC the maximal loss occurs up to 35 years of age, in S the most pronounced loss begins precisely after this age.
  • Publication
    Open Access
    Axonal and transsynaptic (transneuronal) spread of Herpesvirus simiae (B virus) in experimentally infected mice
    (Murcia : F. Hernández, 1992) Gosztonyi, Georg; Falke, Dietrich; Ludwig, Hanns
    In order to study the pathogenesis of B virus infection of the nervous system, newborn and young mice were inoculated by four different routes: 1. Intramuscular (i.m.) in the forelimb; 2. 1.m. in the hindlimb; 3. Subcutaneous (S.C.) in the abdominal wall; 4. Intraperitoneal (i.p.).Spread of virus was followed by immunohistochemical demonstration of vira1 antigen in tissue sections of the peripheral and central nervous system. Three distinct patterns emerged: 1. After i.m. limb inoculations, virus progressed along the ipsilateral dorsal column, the bilateral spinothalamic and bilateral spinoreticular systems and along central autonomic pathways. 2. After S.C. inoculation, the dorsal column was spared, otherwise the spread was similar to that following i.m. inoculations. 3. After i.p. inoculation, virus spread in the spinal cord bilaterally, mainly along spinothalamic and central autonomic pathways. The peripheral motoneurons were conspicuously spared, even in the i.m. inoculation mode. In the brain stem, B virus antigen appeared bilaterally, at multiple sites. In the cerebrum, virus infected cells appeared first in the thalamus, hypothalamus and the motor cortex. The mode of spread from spinal levels was mainly orthograde along the ascending systems (dorsal columns, spinothalamic, spinoreticular tracts), but also retrograde along descending systems (pyramidal tract, central autonomic pathways). Oligosynaptic systems transmitted virus more quickly than the polysynaptic ones. In the involvement of various neurona1 systems in virus spread, a certain selectivity, sparing the peripheral motoneuron and the cerebellar systems, could be assessed.