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

Peinado, María Ángeles; Quesada, Adoracion; Pedrosa, Juan Ángel; Martı́nez, Manuel; Esteban, Francisco J.; Moral, Marı́a Luisa Del; Peinado, J.M.

doi:10.1002/(sici)1097-0185(199703)247:3<420::aid-ar14>3.3.co;2-o

Cited by 14 publications

(19 citation statements)

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“…Nonsynaptic mitochondria originate from both neurons and nonneuronal cells. In rat parietal cortex, glial cell density is approximately double the neuronal density, and mitochondria occupy a smaller percentage of the cytosol in glia as compared with neurons (50). Using a similar method to that used in the present study to isolate nonsynaptic mitochondria, Kristian and colleagues (51) found faint peripheral benzodiazepine receptor immunoreactivity, a marker of astrocytic mitochondria (52), in the nonsynaptic mitochondrial fraction in contrast to strong immunoreactivity in mitochondria isolated from cultured astrocytes.…”

Section: Discussionsupporting

confidence: 50%

Synaptic Mitochondria Are More Susceptible to Ca2+Overload than Nonsynaptic Mitochondria

Brown

Sullivan

Geddes

2006

Journal of Biological Chemistry

261

228

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Mitochondria in nerve terminals are subjected to extensive Ca 2؉ fluxes and high energy demands, but the extent to which the synaptic mitochondria buffer Ca 2؉ is unclear. In this study, we identified a difference in the Ca 2؉ clearance ability of nonsynaptic versus synaptic mitochondrial populations enriched from rat cerebral cortex. Mitochondria were isolated using Percoll discontinuous gradients in combination with high pressure nitrogen cell disruption. Mitochondria in the nonsynaptic fraction originate from neurons and other cell types including glia, whereas mitochondria enriched from a synaptosomal fraction are predominantly neuronal and presynaptic in origin. There were no differences in respiration or initial Ca 2؉ loads between nonsynaptic and synaptic mitochondrial populations. Following both bolus and infusion Ca 2؉ addition, nonsynaptic mitochondria were able to accumulate significantly more exogenously added Ca 2؉ than the synaptic mitochondria before undergoing mitochondrial permeability transition, observed as a loss in mitochondrial membrane potential and decreased Ca 2؉ uptake. The limited ability of synaptic mitochondria to accumulate Ca 2؉ could result from several factors including a primary function of ATP production to support the high energy demand of presynaptic terminals, their relative isolation in comparison with the threads or clusters of mitochondria found in the soma of neurons and glia, or the older age and increased exposure to oxidative damage of synaptic versus nonsynaptic mitochondria. By more readily undergoing permeability transition, synaptic mitochondria may initiate neuron death in response to insults that elevate synaptic levels of intracellular Ca 2؉ , consistent with the early degeneration of distal axon segments in neurodegenerative disorders.Mitochondria are important regulators of cellular Ca 2ϩ homeostasis, producers of ATP via oxidative phosphorylation, and regulators of cell death pathways (for reviews see Refs. 1 and 2). Mitochondria assist in maintaining Ca 2ϩ homeostasis by sequestering and releasing Ca 2ϩ (2-4). Normal Ca 2ϩ cycling occurs by the movement of Ca 2ϩ into mitochondria via the Ca 2ϩ uniporter and slow efflux via the Na ϩ /Ca 2ϩ antiporter or by Na ϩ -independent mechanisms (1, 3). Isolated mitochondria in the presence of phosphate take up Ca 2ϩ to a fixed capacity, in a membrane potential (⌬⌿ m )-dependent fashion (5-7). When the mitochondria become overloaded with Ca 2ϩ , they undergo the cataclysmic mitochondrial permeability transition (mPT) 3 via formation of a nonselective pore that allows solutes of 1500 daltons or smaller to pass through the usually impermeable inner mitochondrial membrane with a resultant rupture of the outer mitochondrial membrane caused by osmotic swelling (2, 8 -12).Previous studies have demonstrated substantial mitochondrial heterogeneity that exists among organs and within the CNS. Nonsynaptic brain mitochondria are more resistant to Ca 2ϩ -induced opening of mPT, assessed by mitochondrial swelling, when compared w...

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Section: Discussionsupporting

confidence: 50%

Synaptic Mitochondria Are More Susceptible to Ca2+Overload than Nonsynaptic Mitochondria

Brown

Sullivan

Geddes

2006

Journal of Biological Chemistry

261

228

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“…Although data on the ratio between neurons and glia in rat MC is not readily available, parietal and occipital cortices are estimated to have two times more neurons than glial cells on PD10 (Mooney and Napper, 2005). This ratio is decreased significantly by PD115 due to the increase in glial cell number (not a decrease in neuronal counts) with age (Mooney and Napper, 2005; Peinado et al, 1997). …”

Section: Discussionmentioning

confidence: 97%

Binge‐like postnatal alcohol exposure triggers cortical gliogenesis in adolescent rats

Helfer

Calizo

Dong

et al. 2009

J of Comparative Neurology

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The long-term effects of binge-like alcohol exposure on cell proliferation and differentiation in the adolescent rat neocortex were examined. Unlike the hippocampal dentate gyrus, where proliferation of progenitors results primarily in addition of granule cells in adulthood, the vast majority of newly generated cells in the intact mature rodent neocortex appear to be glial cells. The current study examined cytogenesis in the motor cortex of adolescent and adult rats that were exposed to 5.25 g/kg/day of alcohol on postnatal days (PD) 4-9 in a binge manner. Cytogenesis was examined at PD 50 (through bromodeoxyuridine, BrdU, labeling) and survival of these newly generated cells was evaluated at PD80. At PD50, significantly more BrdU positive cells were present in the motor cortex of alcohol-exposed rats than controls. Confocal analysis revealed that the majority (>60%) of these labeled cells also expressed NG2 chondroitin sulfate proteoglycan (NG2 glia). Additionally, survival of these newly generated cortical cells was affected by neonatal alcohol exposure, based on the greater reduction in the number of BrdU-labeled cells from PD50 to PD80 in the alcohol-exposed animals compared to controls. These findings demonstrate that neonatal alcohol exposure triggers an increase in gliogenesis in the adult motor cortex.

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“…There is conflicting data in the literature as to whether astrocyte number changes with advancing age. For instance, age-related increases in astrocyte number have been documented in the cerebral cortex (Vaughan and Peters, 1974; Peinado et al, 1997; Peinado et al, 1998), the molecular layer of the dentate gyrus (Pilegaard and Ladefoged, 1996), the dorsal lateral geniculate nucleus (Satorre et al, 1985), and the neostriatum (Sturrock, 1980). In contrast, other studies were unable to detect significant changes in astrocyte number in cerebral cortex (Hansen et al, 1987; Peters et al, 1991; Peters et al, 1994) and the hippocampus (Landfield et al, 1977; Geinisman et al, 1978; Landfield et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

Age-related changes in glial cells of dopamine midbrain subregions in rhesus monkeys

Kanaan

Kordower

Collier

2010

Neurobiology of Aging

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Aging remains the strongest risk factor for developing Parkinson's disease (PD), and there is selective vulnerability in midbrain DA neuron degeneration in PD. By tracking normal aging-related changes with an emphasis on regional specificity, factors involved in selective vulnerability and resistance to degeneration can be studied. Towards this end, we sought to determine whether age-related changes in microglia and astrocytes in rhesus monkeys are region-specific, suggestive of involvement in regional differences in vulnerability to degeneration that may be relevant to PD pathogenesis. Gliosis in midbrain DA subregions was measured by estimating glia number using unbiased stereology, assessing fluorescence intensity for proteins upregulated during activation, and rating morphology. With normal aging, microglia exhibited increased staining intensity and a shift to more activated morphologies preferentially in the vulnerable substantia nigra-ventral tier (vtSN). Astrocytes did not exhibit age-related changes consistent with an involvement in regional vulnerability in any measure. Our results suggest advancing age is associated with chronic mild inflammation in the vtSN, which may render these DA neurons more vulnerable to degeneration.

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

Abstract: 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.

Cited by 14 publications

References 0 publications

Synaptic Mitochondria Are More Susceptible to Ca2+Overload than Nonsynaptic Mitochondria

Synaptic Mitochondria Are More Susceptible to Ca2+Overload than Nonsynaptic Mitochondria

Binge‐like postnatal alcohol exposure triggers cortical gliogenesis in adolescent rats

Age-related changes in glial cells of dopamine midbrain subregions in rhesus monkeys

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