Poster
# 24
Poster |
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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] |
In the last years, studies performed in all the neurobiological fields had produced important knowledge about the neurodegenerative processes that are responsible for cell damaging and neuronal death. These processes seem to be originated by similar mechanisms, including deficiencies in energy levels (Lees,93), release of excitatory amino acids, particularly glutamic acid (Choi and Harley, 1993) and hyperproduction of free radicals such as nitric oxide (Lees, 1993; Moreno and Prior, 1992). All these disorders may be responsible of several pathologies such as those described in induced lesions, cerebrovascular accidents and neurodegenerative illness (Reinikainen et al., 1990; Lees, 1993). However, all these mechanism may occurs simultaneously, producing finally an increase in the intracellular free Ca2+ concentration (Choi, 1992; Khachaturian, 1994; Sun et al., 1997) that probably is the major responsible for cell damage and death.
It is known that neurodegeneration could produce quantitative and morphological changes in neurons and glial cells. Although traditionally, several types of degenerative disorders have been associated with neuronal loss, quantitative studies performed after induced lesions are very scarce; practically, all these studies are focused in the quantitative analysis of neuronal population after ischemic-reperfusion processes (Kudo et al.,1993; Hanyu et al., 1993). Neuronal loss in the cortex and in the CA1 hippocampal area have been described, but this neuronal death is selective and seems to be dependent of the duration of the lesion (Hanyu et al.,1993). Other induced lesions performed are aspiration of cortical areas, finding in this report selective neuronal loss too (Loopuijt et al.,1995).
In addition to the quantitative changes, the neurodegenerative processes also can induce structural changes in neurons; in fact, the presence of pyknotic neurons in the histological studies of the CNS is very well known. These neurons are characterized by their high affinity for several histological stains, like toluidine blue, cresil violet and acid fuschine. This affinity is the responsible of the dark appearance, so in the last years, these neurons were called dark neurons (Cammermeyer,1961; Cohen and Pappas,1969; Mugnaini,1965; Garey and Powell,1971; Cragg, 1975; Ong and Garey, 1991; Gallyas et al, 1992a; 93) hyperchromatic, cromophilic, contracted (Cammermeyer,1961) and more recently argyrophilic (Gallyas et al.,1992a) or collapsed neurons (Gallyas et al.,1992a; Czurko and Nishino, 1993). In semithin sections stained with toluidine blue, these neurons exhibit a retried soma and nucleus and strong staining. Occasionally, the nucleus is stained stronger than the nucleolus (Gallyas et al.,1990a). Although the structural characteristics of these neurons are well known, the quantitative studies performed are also scarce.
The aim of the present work is to study the quantitative and cytomorphometric changes in neurons in the Fr cortex of the rat during a neurodegenerative process induced by a stereotaxic lesion in the contralateral frontal cortex.
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[Cell Biology & Cytology] |
[Neuroscience] |
[Physiology] |
