Poster | 6th Internet World Congress for Biomedical Sciences |
María Jesús Ramírez-Expósito(1), José Manuel Martínez-Martos(2)
(1)Unit of Physiology. University of Jaen - Jaén. Spain
(2)Unit of Physiology. University of Jaén - Jaén. Spain
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[Cell Biology & Cytology]![]() |
[Neuroscience]![]() |
[Physiology]![]() |
Since the clasical studies of Ramón y Cajal (1913) and Del Rio Hortega (1920) about astrocytes, microglial cells and oligodendrocytes, the interest of glial cells has increased. In this way, in the last 20 years a radical change in the CNS studies has been observed. Actually, the interest is not only on neurons but also in the role of glial cells in the neuronal functions. This fact is been performed by the development of the new technologies as specific stained, cell cultures and autorradiographic techniques which allow a better and bigger knolodge about these cells and the functional role of glia in the noervous system (Raine, 1989; Noremberg, 1994).
In the last years, many atention has been payed to the changes observed in the glial cells during lesions, traumas, degenerative illness and also aging. Damage in the CNSs breaks the physical and functional juntions of the nervous tissues, disrupts in this way, the interactions between neuronal and glial cells (Nieto.Sanpedro, 1998). This fact could be the responsive mechanism of the described reactivity of glial cells, especially for astrocytes and microglial cells in some lesions (Hajos et al., 1990; Landis, 1994; Nieto Sanpedro et al., 1985; Ramírez Expósito y Martínez Martos 1998a, b, 1999).
Astroglial changes are widely recognized to be one of the earliest and most remarkable cellular responses following a wide variety of insults to the CNS. These changes are known as reactive astrogliosis. Reactive astrocytes are characterized by a hypertrophy including pericaryon and processes. In some instances, increased cell size may be related to a requirement for increased astrocytic metabolic activity (Landis, 1994) and the increase in the processes may be related with the formation of the glial scar (Norenber, 1994). However, the most extensively studied aspect of reactive astrocytic is the increase in GFAP inmunoreactivity observed after lesions (Nathanial and Nathanial, 1984; Eng, 1988; Steward et al., 1993; Neary et al., 1994).
By other hand, proliferation of astrocytes after an injury is still uncertain, although it is known that the possibilities of mitosis are limited (Miyake et al., 1988, 1992) evidences suggest that astrocytes may arise in injured brain (Landis, 1994). However, some authors considered that proliferation anly exits in lesions affected BBB (Nieto Sanpedro, 1998; Kimelberg y Noremberg, 1994). All these changes induced by lesions are similar to those observed during aging (Hansen et al., 1987; Bronson et al., 1993; Finch, 1993; Berciano et al., 1995). The role of oligodendrocytes in cerebral lesions is unknown due to the problems of their identification (Giordana et al., 1994; Bartholdi and Schwab, 1998). The quantitative changes in astrocytes and oligodendrocytes population may be related with the neuronal death and axonic and dendritic degeneration (Peters et al., 1991).
Microglial cells are the other glial cell type more affected by lesions. In this situation, microglial cells are able to increase their number by division of their precursor o migration (Kreutzberg, 1996), and resting microglial cells rapidly transform into an activated form with a rounded morphology (Akiyama et al., 1988) and phagocitic activity (Streit, 1988). Reactive microglia also cann regulate the reactive gliosis (Giulian and Baker, 1986; Giulian et al.,1989). Increase in the number of microglial cells could be related with elimination of lipofuscine and death neurons.
The aim of present work is to study the changes of glial cells in different neurodegenerative process, so we analyzed the effects of aging and lesions. The quantitative changes of glial population observed in the different cortical layer of the frontal cortex were analyzed.
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[Cell Biology & Cytology]![]() |
[Neuroscience]![]() |
[Physiology]![]() |