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] |
It is known that injures produced in the adult mammalian brain are able to induce degeneration in the nervous tissue, even in remote places from the lesions (Jones and Cowan, 1983). However, the discussion of our results about induced lesions is difficult because the literature about this type of lesions is scarce.
Our results showed no loss of neurons in the contralateral frontal cortex of the lesioned rats. In contrast, most of the quantitative studies of neuronal population have been performed with lesions due to ischemic damage, which produces important neuronal loss (Hanyu et al., 1993). The most affected zones are CA1 hippocampal areas, cortical layers II, V and VI, the Purkinje cells in the cerebellum and striatal neurons (Pulsinelli et al., 1982; Gallyas et al.,1992c). In this situation, the neuronal loss is dependent on the duration of the ischemic period and the time between repeated ischemics (Tomida et al.,87; Nakano et al.,89; kato y Kogure,90; Hanyu et al.,93). However, this neuronal death is progressive, as has been described in gerbils (Kirino, 1982; Lin et al., 1990; Ito et al., 1987) and in rats (Nakano et al., 1990). In the same way, different neuronal loss areas have been described in cortex and hippocampus after chronical cerebral hypoperfusions (Kudo et al., 1993). All these studies were performed in ipsilateral levels. Waite and col. (1992) described a decrease in neuronal population and in the ventrobasal volume after contralateral lesions in the infraorbital nerve. Also, lesions by aspiration of the frontal or parietal cortex made in cat fetuses, produced loss of about 25% of neurons in the ipsilateral levels but the changes in contralateral side were insignificant (Loopuijt et al.,1995).
Although our results showed no changes in contralateral neuronal populations, some degenerative marks like presence of dark neurons, have been observed. Traditionally, these neurons have been related with poor fixative processes (Cammermeyer, 1961; Mugnaini, 1965; Jones y Powell, 1970), with postmortem manipulation of the tissue and with perfusion with hypertonic fluids (Cammermeyer, 1979). More recent studies revealed that these neurons are generated in vivo as an acute or delayed consequence of several pathological situations and lesions (Kleiner et al., 1986; Gallyas et al., 1992a; 1993; Ong and Garey, 1993; Czurko and Nishino, 1993). However, although the morphological characteristics are perfectly known, only one hypothesis explains their appearance (Gallyas et al., 1992a): an initial and localized damage is extending to all neuronal structure, producing a global deorganization. This theory could explain the presence of dark neurons with similar morphological characteristics in processes with different etiology.
In our study, the increase in SDN is parallel to a reduction in NN, but no neuronal loss have been detected, so it could be possible that the NN are replaced by SDN. Furthermore, we distinguished a third neuronal population (LDN). No changes were observed in the number of these neurons with a light hyperchromasia and without estructural changes. This stability could indicate that these neurons are not an intermediate between NN and SDN. We unknown exactly their significance although it may be possible that they appear spontaneously in all the animals, and it could be possible too, that these neurons could be consequence of manipulation of the tissue, although the animals used in this study were perfused and fixed.
The distribution of the different neuronal types considered in our study, across the cortical thickness showed a decrease in the number of NN and an increase in SDN in practically all the layers. It could be consequence of the inespecifity of the lesion. Clarke and Nussbaumer (1987) observed an increase in the SDN population in some cerebral areas after global ischemic processes. These increase was especially significant in cortical layers II, III and V in ipsi and contralateral hemispheres.
By other hand, it is known that neuronal degeneration is accompanied with an atrophy proccess characterized by a decrease in soma, nucleus and nucleolus areas (Finch, 93). In accordance with our results, the SDN could be considered atrophy neurons. In fact, these neurons presented slower values of soma, nucleus and nucleolus areas. Finally, the NN of lesioned animals showed increases in these parameters and it could be related with some reaction capacity. Other significative results are the values obtained for form index. SDN presented values higher than one; it could be indicative to the structural deorganization and atrophy.
In summary, the quantitative and morphological changes reported here may be responsible for some of the neurophysiological impairments associated with cortical lesions.
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[Cell Biology & Cytology] |
[Neuroscience] |
[Physiology] |
