Quantitative morphological changes in neurons and glia in the frontal lobe of the aging rat

Peinado, María Ángeles; Martínez, Manuel; Pedrosa, Juan Ángel; Quesada, Adoracion; Peinado, J.M.

doi:10.1002/ar.1092370110

Cited by 45 publications

(29 citation statements)

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“…In an earlier study, using the same methods and animal model as in the present work, we found no changes in neuronal density in the frontal cortex with age, with the exception of layer I. In addition, our data for perikaryon size showed no significant changes with age, although neuronal nuclear area was reduced (Peinado et al, 1993).…”

Section: Discussionsupporting

confidence: 64%

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Light microscopic quantification of morphological changes during aging in neurons and glia of the rat parietal cortex

et al. 1997

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Background: Different changes in neuronal and glial population of the aging brain have been described; however, the degree and extent of these changes are controversial. This study evaluates the quantitative and cytomorphometric effects of aging on neuronal and glial populations in the parietal cortex of the rat.Methods: The study was performed in two groups of rats aged 4-6 and 30-32 months. Cortical volume, neuronal density, glial density, and neuronal area, and shapes of the soma and nucleus were analyzed in cortical layers I, II-IV, V, and VI using serial sections stained with cresyl-fastviolet, and quantitative morphometric techniques.Results: No changes with age were found in volume of the cortex or neuronal density. Glial density increased significantly (mean for all layers 17%) in older rats. Layers II-IV, V, and VI showed an age-related decrease in the area of the neuronal soma. Neuronal shape, as revealed by the major/minor diameter ratio, also showed a decrease in old rats but only in layer II-IV. Nuclear area decreased with age only in layer VI.Conclusions: The stability of neuronal density together with the increased number of glial cells and the changes in neuronal soma size suggest that aged-related cognitive impairment could be a consequence of neuronal dysfunction rather than actual neuronal losses.

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Section: Discussionsupporting

confidence: 64%

“…In the rat substantia nigra, cell loss is not as prominent as has been reported in humans (Morgan et al, 1987). However, an earlier study (Peinado et al, 1993) found no evidence of neuronal loss, which confirmed similar findings in cortical barrels of aged mice (Curcio and Coleman, 1982).…”

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confidence: 81%

Light microscopic quantification of morphological changes during aging in neurons and glia of the rat parietal cortex

et al. 1997

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“…Considering that astrocytes contain a threefold to fourfold lower amount of mitochondria than neurons (Alano et al 2007), their eventual slight increase with aging should not particularly affect the content of mtDNA and of mitochondrial proteins such as TFAM. For what concerns neurons, it is now widely accepted that brain aging does not imply a loss of neurons, especially in the rat frontal cortex, but rather structural changes of neurons that alter their function (Grill and Riddle 2002;Peinado et al 1993;Turlejski and Djavadian 2002). Therefore, we can conclude that the changes in TFAM and mtDNA content are not the result of a variation in cellular population during aging, but are truly due to the effect of age.…”

Section: Discussionmentioning

confidence: 82%

Age- and calorie restriction-related changes in rat brain mitochondrial DNA and TFAM binding

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Fracasso

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et al. 2012

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Aging markedly affects mitochondrial biogenesis and functions particularly in tissues highly dependent on the organelle's bioenergetics capability such as the brain's frontal cortex. Calorie restriction (CR) diet is, so far, the only intervention able to delay or prevent the onset of several age-related alterations in different organisms. We determined the contents of mitochondrial transcription factor A (TFAM), mitochondrial DNA (mtDNA), and the 4.8-kb mtDNA deletion in the frontal cortex from young (6-monthold) and aged (26-month-old), ad libitum-fed (AL) and calorie-restricted (CR), rats. We found a 70 % increase in TFAM amount, a 25 % loss in mtDNA content, and a 35 % increase in the 4.8-kb deletion content in the aged AL animals with respect to the young rats. TFAM-specific binding to six mtDNA regions was analyzed by mtDNA immunoprecipitation and semiquantitative polymerase chain reaction (PCR), showing a marked age-related decrease. Quantitative realtime PCR at two subregions involved in mtDNA replication demonstrated, in aged AL rats, a remarkable decrease (60-70 %) of TFAM-bound mtDNA. The decreased TFAM binding is a novel finding that may explain the mtDNA loss in spite of the compensatory TFAM increased amount. In aged CR rats, TFAM amount increased and mtDNA content decreased with respect to young rats' values, but the extent of the changes was smaller than in aged AL rats. Attenuation of the age-related effects due to the diet in the CR animals was further evidenced by the unchanged content of the 4.8-kb deletion with respect to that of young animals and by the partial prevention of the age-related decrease in TFAM binding to mtDNA.

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“…1991; Peinado et al, 1993;Rance et al, 1993). We also analysed shape parameters such as form factor with values ranging from 0 to 1, the latter being the definition of a sphere.…”

Section: Discussionmentioning

confidence: 99%

“…Thus there is no agreement regarding the different parameters currently under study, e.g., neuronal size, extension of the dendritic tree, or the number of synapses per cell (Curcio and Hinds, 1983;Coleman and Flood, 1986;Markus et al, 1987;Flood and Coleman, 1988;de Lacalle et al, 1991;Crespo et al, 1992;Stroessner-Johnson et al, 1992;Flood and Coleman, 1993;Peinado et al, 1993;Rance et al, 1993). Similarly, it is argued whether or not neuronal loss occurs during old age (Diamond et al, 1977;Curcio and Coleman, 1982;Satorre et al, 1985;Sturrock, 1989).…”

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confidence: 99%

Quantitative morphological changes in neurons from the dorsal lateral geniculate nucleus of young and old rats

et al. 1997

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Background: We studied the morphological changes occurring in neurons from the dorsal lateral geniculate nucleus (dLGN) during aging by analysing the size and shape of cell bodies and nuclei.Methods: Male albino Wistar rats, aged 3, 18, 24, and 30 months, were used. After appropriate tissue preparation and following the usual histological procedure, the profiles of 1,920 neuronal bodies and nuclei were drawn using a camera lucida. Data was later recorded and processed with a semiautomatic image analyser.Results and conclusions: We observed that dLGN neurons do not change in size from the age of 3-24 months. Between 24 and 30 months, the soma and nucleus of the cell undergo hypertrophy, 32.8% and 35.6%, respectively, when compared to those from 3-month-old animals (P F 0.01). Furthermore, we found a high correlation between cell body size/nucleus size, which does not disappear with age. The r values (correlation coefficient) were 0.7998, 0.8662, 0.8433 and 0.7304, and R 2 (determination coefficient) was equal to 0.6397, 0.7504, 0.7112, and 0.5335. These latter values show that in 63.97%, 75.04%, 71.12%, and 53.35% of cases, respectively, modifications in somata size were accompanied by similar changes in nucleus size, and vice-versa. The study of the shape of the soma and nucleus of the cell revealed that both structures have a rounded-oval configuration that does not change in a significant way from adulthood to old age. Anat.

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Quantitative morphological changes in neurons and glia in the frontal lobe of the aging rat

Cited by 45 publications

References 29 publications

Light microscopic quantification of morphological changes during aging in neurons and glia of the rat parietal cortex

Light microscopic quantification of morphological changes during aging in neurons and glia of the rat parietal cortex

Age- and calorie restriction-related changes in rat brain mitochondrial DNA and TFAM binding

Quantitative morphological changes in neurons from the dorsal lateral geniculate nucleus of young and old rats

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