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T Cecchini

Publications and source records attributed to T Cecchini.

At least 19 recordsLinked to original sources
PubMed2001

Alpha-tocopherol controls cell proliferation in the adult rat dentate gyrus.

The effect of alpha-tocopherol on cell proliferation and proliferated cell survival was investigated in the dentate gyrus of adult rats. Adult rats were supplemented with alpha-tocopherol, injected with 5-bromo-2'-deoxyuridine (BrdU), that is incorporated into DNA during the S-phase, and killed at different time after BrdU injection. The number of newborn cells decreased after alpha-tocopherol supplementation, confirming the hypothesis that alpha-tocopherol is able to depress cell proliferation in vivo. Most newborn cells die within few days; more newborn cells survive in alpha-tocopherol-treated rats, suggesting the hypothesis that alpha-tocopherol decreases cell death.

Age Factors↗
PubMed2000

Spatial learning affects immature granule cell survival in adult rat dentate gyrus.

Neurogenesis occurs throughout life in mammalian dentate gyrus. The effect of learning on newborn cell survival was studied in rat. Rats were trained on a hippocampus-dependent spatial learning task by using Morris water maze. Neurogenesis was evaluated by 5-bromo-2'deoxyuridine administered before learning. Several newborn cells expressed the immature neuron marker TOAD-64. The main findings were as follows: (1) the survival of newborn cells was enhanced by learning at early stage of differentiation; (2) the newborn cells saved by learning were mainly located in the rostral part of external blade of granule cell layer and (3) there was a correlation between the actual individual learning and newborn cell survival.

Age Factors↗
PubMed2000

Are there proliferating neuronal precursors in adult rat dorsal root ganglia?

The origin of new neurons in dorsal root ganglia of adult rat was investigated using an experimental model in which postnatal neurogenesis naturally occurring is enhanced and restricted in a brief period of life. Possible mitotic origin of new neurons was investigated by means of 5-bromo-2-deoxyuridine, anti-NF 200 antibody was used to detect if proliferated cells showed a neuronal phenotype. The results suggest that postnatal neurogenesis in dorsal root ganglia could depend only in part on precursor proliferation and that normally new neurons derive from the late differentiation of postmitotic cells.

Animals↗
PubMed1999

Postnatal proliferation of DRG non-neuronal cells in vitamin E-deficient rats.

Changes in the number of satellite cells in neuron body sheaths in dorsal root ganglia (DRGs) were studied from 1 to 5 months of age in control and in vitamin E-deficient rats; furthermore, the satellite cell proliferation rate was detected in the same groups of animals with immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU). The number of satellite cells in sheaths of DRG neurons increased in the period of life considered both in control and in vitamin E-deficient rats. Satellite cell proliferation was observed in both groups, but its rate was found to be higher in vitamin E-deficient rats. The results obtained in control rats confirm that mitotic ability is retained by satellite cells in adulthood and show that at least some of newborn satellite cells add to the pre-existing population. The results obtained in vitamin E-deficient rats suggest that a faster turnover in satellite cell population takes place in these animals and support the idea that vitamin E could be an exogenous factor controlling cell proliferation.

Animals↗
PubMed1999

Neurogenesis in the adult rat dentate gyrus is enhanced by vitamin E deficiency.

Neurogenesis occurs throughout adult life in rat dentate gyrus. Factors and mechanisms of adult neurogenesis regulation are not well known. Vitamin E deficiency has been found to deliver a neurogenetic potential in rat dorsal root ganglia. To determine whether the role of tocopherols in adult neurogenesis may be generalized to the central nervous system, changes in adult rat dentate gyrus neurogenesis were investigated in vitamin E deficiency. Neurogenesis was quantitatively studied by determination of the density of 5-bromo-2'-deoxyuridine (BrdU)-labeled cells and by determination of the total number of cells in the granule cell layer. The BrdU-labeled cells were immunocytochemically characterized by demonstration of neuronal marker calbindin D28K. The following results were found: (1) the volume of the granule layer increased in controls from 1 to 5 months of age, mainly due to cell density decrease; (2) the volume increased by a similar amount in vitamin E-deficient rats, mainly because of an increase in cell number; (3) BrdU-positive cells were more numerous in vitamin E-deficient rats in comparison to age-matched controls; (4) the increase in proliferated cells was located in the hilus and in the plexiform layer. This study confirms that neurogenesis occurs within adult dentate gyrus and demonstrates that this process is enhanced in vitamin E deficiency. This finding indicates that vitamin E may be an exogenous factor regulating adult neurogenesis.

Animals↗
PubMed1998

Neuron and glial cells in neocortex after methylazoxymethanol treatment in early development.

The quantitative changes were investigated in neuron and glia density in the different cortical layers of the frontal cortex of 3 and 12 month old mice, exposed to methylazoxymethanol on embryonic day 13 (MAM13). No loss of cortical neurons was found between young and adult animals. MAM exposure on the 13th day of development induced a neuron density decrease throughout on the entire cortical depth and did not produce changes in the density of glial cells with respect to the controls and to age. Consequently, at 3 months of age we observe a glia/neuron ratio greater than that of controls and at 12 months a similar value. In the neocortex of MAM-mice at this numerical uniformity of glial cell density, did not correspond to a similar proportional composition: the frequency of the astrocytes is lower, adapting to the decreased neuron density; the greater oligodendrocyte percentage may be related to disturbed layering and to the hyperinnervation of the hypoplastic cortex; the microglia shows a trend similar to that of the controls. These results, together with those of other studies, suggest that prenatal exposure to MAM causes a cortical compensatory response regulating glial cells proliferation.

Alkylating Agents↗
PubMed1997

Vitamin E affects quantitative age changes in lumbar motoneurons and in their peripheral projections.

Vitamin E deficiency was previously found to induce plastic changes in the number of primary sensory neurons and in motoneuron peripheral field projections. In this work, quantitative changes in motoneurons of lumbar segments, in nerve fibres constituting ventral roots and in innervating leg motor fibres were studied in normal and vitamin E deficient rats from 1 to 5 months of age. The number of lumbar motoneurons was found to decrease, while there were no changes in the number of ventral root fibres. An increase in the number of innervating leg motor fibres was observed during ageing in control rats; in vitamin E deficient rats the number of fibres in the ventral roots did not change, as occurred in controls, but the decrease in the number of motoneurons was smaller and the number of innervating leg motor fibres increased further in comparison to the controls. The findings are consistent with the idea that vitamin E deficiency causes a decrease in motoneuron death or, alternatively, that it induces some process partially compensating naturally occurring motoneuron death.

Aging↗
PubMed1996

Quantitative changes in neuron and glial cells of neocortex following prenatal exposure to methylazoxymethanol.

The quantitative changes in neuron and glial cell density were analyzed in different cortical layers from frontal cortex of 3 and 12 months old mice exposed to Methylazoxymethanol (MAM) on embryonic day 15 (MAM 15) or 17 (MAM 17). An increase was found in glial cell density in all cortical layers from 3 months old MAM 17 compared to the age-matched controls. In particular, electron microscopic analysis showed that the only cells to increase in all cortical layers were the microglia cells. When the young and adult mice were compared it was noted that the glia increased significantly in all cortical layers of controls, whereas it did not change the older MAM 17. In the older MAM 15 the increase in glial density was similar to that observed in controls. No loss of cortical neurons was found between young and adult animals. In addition, the different trend of glial cell density between control and MAM 17 mice during aging was accompanied by a decline in the mean nuclear area in neurons of treated mice with respect to the controls. The hypothesis that MAM treatment seems to produce events similar to those normally occurring in aging finds support in the data of glial density and neuron size.

Alkylating Agents↗
PubMed1995

Changes in the number of primary sensory neurons in normal and vitamin-E-deficient rats during aging.

In the dorsal root ganglia (DRGs) of vitamin-E-deficient rats, we previously found an increase in the number of neurons during the first 5 months of life (Cecchini et al., 1993, 1994). This neurogenetic event seems to bring forward in time the increase in the number of primary sensory neurons that Devor et al. (1985) found in normal rats aged more than 1 year, but that other authors have not confirmed. The present study had two aims: first, to verify whether neurogenesis spontaneously occurs in DRGs of 14-month-old Sprague-Dawley rats; and, second, to determine whether the neurogenesis enhanced by vitamin E deficiency continues further in the long run, or whether it stops or reverses into neuron loss. A quantitative and morphometric analysis was performed on neurons of L3-L6 DRGs in 14-month-old normal and vitamin-E-deficient rats: the results obtained were compared to those previously obtained in 1-month-old and 5-month-old animals of both dietetic treatment groups, in order to observe the effects of aging on these neuronal populations. The total number of DRG neurons in the control group was higher in older than in younger animals, whereas the value in the vitamin-E-deficient group was lower in older than in younger animals. The present data confirm that neurogenesis occurs in DRGs of normal rats during adult life. Moreover, they show that once the premature neurogenesis in the deficient rats is completed, no further increase in the number of neurons takes place.

Age Factors↗
PubMed1995

Cell death and cell number in the developing cerebral cortex of MAM treated mice.

The postnatal cell death decline in microencephalic mice produced after methylazoxymethanol-acetate injection during embryonic development may adjust the final cell number of treated animals in the mature neocortex. Quantitative observations of cortical cell number in normal and treated mice, from 5 days to adult age were carried out. The proportion of cortical dead cells per 1000 live cells in a standardized cortical column and the cumulative cell death across time were studied in mice aged 5-10-20-30 days. Two main results were obtained. First, the mature neocortex of treated animals shows a number of cells which is significantly lower with respect to the controls but the difference is less accentuated than in the developing neocortex. Secondly, the proportion of cortical dead cells per 1000 live cells at every date studied and the cumulative cell death across time decreased in cerebral cortex of treated mice when compared with age-matched controls. Our data show that decreasing initial cell number by prenatal MAM injection is correlated to an increase in the survival of cortical cells.

Acetates↗
PubMed1994

Increased number of sciatic sensory neurons in vitamin-E-deficient rats.

The number and morphometric characteristics of sciatic sensory neurons were studied in Vitamin-E-deficient rats. Horseradish peroxidase (HRP) was injected into the sciatic nerves of normal and vitamin-E-deficient rats of the same age, and retrogradely labeled sensory neurons were counted and measured. The study was also carried out in rats that had previously undergone sciatic nerve crush, in order to observe the effects of axotomy on primary sensory neurons. In vitamin-E-deficient rats the number of sciatic sensory neurons was significantly higher than normal, with an increase of about 30%, in agreement with a previous finding concerning total population of primary sensory neurons in lumbar dorsal root ganglia (DRGs) of vitamin-E-deficient rats. The increase involved the small cell classes in particular. Axotomy induced similar percentages of neuron loss in normal and in vitamin-E-deficient rats (about 40%). In the latter, death affected small cell classes in particular--that is, the same classes that had increased in number in vitamin-E-deficient rats by comparison with controls. These results, together with previous findings, suggest that neurogenesis may occur in DRGs of vitamin-E-deficient rats.

Afferent Pathways↗
PubMed1994

[A fatal case of postpartum Budd-Chiari syndrome in a woman with SLA].

We report a case of Budd Chiari syndrome with clinical onset during post partum in a patient with SLE. Etiopathogenetic correlations between pregnancy and BDS and between SLE and BDS are discussed, with particular regard to lupus anticoagulant factor. Furthermore, the diagnostic role of abdominal CT is emphasized.

Adult↗
PubMed1994

[Segmentary veno-occlusive disease of the liver secondary to insecticide inhalation].

We report a case of venocclusive (VOD) disease secondary to inhalation of an insecticide. Pathological features of liver injury are illustrated with regard to patchy lesions shown by a new computer assisted colorimetric method. A possible role of immuno-complexes in the development of endothelium damage to centro-lobular veins is discussed.

Adult↗
PubMed1993

Nodal and terminal sprouting by regenerating nerve in vitamin E-deficient rats.

The increased number of poly-innervated cells in normal and reinnervated extensor digitorum longus (edl) muscle of vitamin E-deficient rats suggests enhanced sprouting by motor neurons in conditions of decreased protection against lipid peroxidation. End-plates and terminal axons were observed by a combined technique that shows both end-plate acetylcholinesterase area and axons. Quantitative observations of nodal and terminal sprouting in normally innervated and reinnervated edl muscles of vitamin E-deficient rats were carried out. Branch points of nerve terminal within end-plates were also observed. Three main results were obtained. First, a notable increase of both terminal and nodal sprouting was found in reinnervated muscles of normal and vitamin E-deficient rats; moreover, a relative increase in the number of nodal sprouts occurs in the long run. Second, in muscles of uninjured, vitamin E-deficient rats, nodal and terminal sprouting and branching within end-plate was greater than in controls. Third, nodal sprouting by regenerating axons was more affected by vitamin E-deficiency than terminal sprouting and branching within end-plates.

Acetylcholinesterase↗
PubMed1993

Regeneration of motor nerves in bilobalide-treated rats.

Bilobalide, a terpene extracted from the leaves of the Ginkgo biloba tree, has been proposed to exert trophic and protective effects on neurons and on Schwann's cells in various neuropathies. The reinnervation of the extensor digitorum longus muscle following traumatic nerve damage was investigated in rats by using electrophysiological and histological techniques. Evaluation parameters included the membrane resting potential of muscle cells, the spontaneous quantal release of acetylcholine, and the percentage of muscle cells receiving multiple innervation. The percentage of muscle cells receiving multiple innervation reached a peak more rapidly in treated animals and declined subsequently to values lower than those found in controls. These data suggest that the rearrangement of regenerated innervation occurs more rapidly in bilobalide-treated animals.

Animals↗
PubMed1993

Increased number of dorsal root ganglion neurons in vitamin-E-deficient rats.

Quantitative and morphometric observations were carried out on neurons of L3-L6 dorsal root ganglia (DRGs) in control and vitamin-E-deficient rats at different ages. Controls were fed a standard diet and sacrificed at 1 or at 5 months of age; deficient rats were fed a diet without vitamin E from 1 to 5 months of age and then sacrificed. No significant difference in total number of neurons was found, but an increase in neuron sizes, a decrease in nucleus-cytoplasm ratio, and a more circular neuron shape were found in controls with increasing age (from 1 to 5 months). In L3-L6 DRGs of vitamin-E-deficient rats (5 months of age), a higher number of neurons was found than in those of either young or adult controls. Moreover, some morphometric characteristics of neurons in the deficient rats were similar to those of neurons in 1-month-old controls. The findings suggest that vitamin E deficiency can trigger events resulting in appearance of new neurons, possibly anticipating phenomena that normally occur in aging.

Age Factors↗
PubMed1993

Morphological analysis on the adrenal zona fasciculata of Ginseng, Ginsenoside Rb1 and Ginsenoside Rg1 treated mice.

Morphological analysis was performed on the adrenal cortex of depressed mice which received repeated administrations of Ginseng extract or Ginsenoside Rb1 or Ginsenoside Rg1 in order to follow the behaviour of the gland. The left gland was fixed for usual stains and cell measurements of both treated and control adrenal cortex were made on twenty central sections. The outlines of cells from the zona fasciculata, in which nucleus was evident, were traced at 625X using a drawing tube. Cell areas were computed from these drawings by means of image analysis (Optilab software). Our results show that: 1) Ginseng extract administration produces a significant increase in the zona fasciculata cell size with respect to controls. The distribution of soma sizes is generally to the right of the spectrum showing a considerable decrease in cells of small size and a similar increase in cells of intermediate and large size with respect to controls; 2) in Ginsenoside-administered animals, although the mean cell areas is not significantly altered, the distribution of cell sizes shows significant differences between normal and treated animals. It is commonly recognized that mean cell area is in strict connection with cell activity: therefore Ginseng extract may be thought to stimulate adrenal cell activity while the two Ginsenosides have an effect which do not lead to significant changes in mean cell size.

Animals↗