1,721,011 research outputs found
Increased intracellular ionic content is correlated with a decreased perichromatin granule density in old neurones
No full textThe intracellular content of monovalent ions (Na+, Cl -, and K+) in brain cortical cells from young, adult, and old rats was measured by X-ray microanalysis. By referring the peak of each ion to the respective value of the dry mass, we obtained the intracellular content as a percentage of dry mass. A significant increase of the intracellular content of Na+, Cl-, and K+ was found in old animals. In the same type of cells from rats of different ages, we estimated the density of perichromatin granules (PGs), the RNA structural correlates containing ribonucleoproteins (RNPs). PGs were discovered by Bernhard's method, which allows the preferential staining of RNPs. The PG density (i.e., the number of PGs/μm2 of nuclear area) was significantly lower (-27.8%) in the neurons of old animals. Taken together, the present findings document that in the nuclei of brain cortical cells of old animals the ionic strength is markedly increased and that this alteration may affect chromatin functions (e.g., DNA template activity). The ionic content of the nucleoplasm is reported to modulate the structure of chromatin molecules and regulate gene expression; thus, the increased content of the three ions found by us in old animals, by increasing the viscosity of the nucleoplasm, may affect gene expression by disturbing the inhibition (negative regulation) or potentiation (positive regulation) of RNA polymerase binding. In physiological aging, increased ionic strength may lead to age-related DNA dysfunction as well as to alterations in the processing of RNA structural constituents, such as PGs. © 2004 New York Academy of Sciences
Structural and functional features of skeletal muscle cell nuclei are modulated by physical exercise in old mice
No full textThe work describes the structural and functional features of skeletal muscle cell nuclei after physical exercise in old mic
Effect of a mild physical exercise on the activation and differentiation potential of satellite cells from skeletal muscles of old mice.
No full textThe work describes the effect of a mild physical exercise on the activation and differentiation potential of satellite cells from skeletal muscles of old mice
Ultrastructural histochemistry is a valuable tool for investigating cell nuclear alterations in skeletal muscle wasting
No full textEffects of ageing on the fine distribution of the circadian CLOCK protein in reticular formation neurons
No full textMany biochemical, physiological and behavioural
processes, from bacteria to human, exhibit roughly
24 h cyclic oscillations deWned as circadian rhythms. However,
during ageing, numerous aspects of the circadian biology
undergo alterations; in particular, the sleep pattern
changes, with more frequent awakenings and shorter sleep
time. The basic mechanism of the circadian clock relies on
intracellular molecular pathways involving interlocking
transcriptional/translational feedback loops, and CLOCK
protein, a transcription factor, is essential for normal circadian
rhythms. In this study, the Wne distribution of CLOCK
protein has been analysed, in adult and old rats, at diVerent
phases of the daily cycle in the neurons of the medullary
reticular formation, involved in the control of the sleep–
wake cycle. The results demonstrate quali–quantitative
modiWcations of CLOCK protein in the neurons of old animals,
suggesting that such a deregulation of the intracellular
clock mechanism may play some role in the
degeneration of the sleep–wake circadian cycle
Quantification of G6PD in small and large intestine of rat during aging.
No full textNumerous studies have demonstrated a decrease in glucose-6-phosphate dehydrogenase (G6PD) activity during aging in many cell types, including red blood cells, fibroblasts and lens cells. Moreover, the intracellular activity of G6PD has been shown to be regulated by binding to cell organelles. To investigate whether binding of G6PD to cell organelles is related with the decrease in its activity during aging, distribution patterns of G6PD activity and protein were assessed in small (SI) and large (LI) intestine of 3-month-old and 28-month-old rats. Enzyme activity, as measured spectrophotometrically, did not show any significant change with aging in SI or LI. Enzyme histochemistry, performed by subtracting activity staining of 6-phosphogluconate dehydrogenase (6PGD) from that of G6PD, showed a lower net G6PD activity in SI and LI epithelium of old rats in comparison with young rats. G6PD activity did not change significantly with aging in the muscularis externa of SI and LI. Immunoelectr..
Aging affects the distribution of the circadian CLOCK protein in rat hepatocytes.
No full textSeveral biochemical, physiological, and behavioral processes exhibit cyclic oscillations of about 24 h, which have been defined as circadian rhythms. In mammals, the primary circadian pacemaker resides in the suprachiasmatic nuclei; however, cell-autonomous circadian oscillators occur also in extraneural tissues, including the liver. CLOCK protein is a transcription factor essential for normal circadian rhythms and recent studies have demonstrated that it undergoes intranuclear redistribution in hepatocytes, along the daily cycle. It is known that aging leads to a progressive deterioration of the circadian rhythm at the behavioral, physiological, and cellular levels; in addition, aging affects the organization of nuclear structural components involved in transcription and splicing. In this view, we carried out ultrastructural immunocytochemical analyses on hepatocytes of adult and old rats, so as to investigate possible qualitative and quantitative modifications of CLOCK protein, in relation to the aging process. Our observations demonstrated that most CLOCK protein was always located in the cell nucleus, where it accumulated on perichromatin fibrils (the sites of premRNA transcription and early splicing); in addition, CLOCK showed daily oscillations in the different nuclear compartments, but these oscillations differed significantly between adult and old animals. This unusual distribution of CLOCK protein during aging could be related to the prolonged diurnal activity of old animals and/or to altered nuclear pathways. © 2005 Wiley-Liss, Inc
Early impairment of long-term depression in the perirhinal cortex of a mouse model of Alzheimer’s disease.
No full textTg2576 is one of the most widely used mouse transgenic line in Alzheimer’s disease (AD) research. It carries a double missense mutation on the amyloid precursor protein gene (APP), resulting in marked increases in b-amyloid (Ab) 1–40 and Ab1–42 in the plasma and brain by 3–5 months of age, decrease in spine density in the outer molecular layer of the dentate gyrus at 4
months, decline in long-term potentiation of synaptic transmission
in the dentate gyrus associated with impairment in contextual
fear conditioning by 5 months, and plaque deposition in
brain starting at 8 months. Visual recognition memory is seriously
impaired in patients in the early stages of AD. The perirhinal
cortex (Prh), a multimodal associative cortex of the
temporal lobe, is critically involved in this form of memory;
long-term depression of synaptic transmission (LTD) in this
cortical region is regarded as its cellular correlate. The present
work was aimed at evaluating if LTD in Prh of Tg2576 mice is
already compromised at 3 months of age. Field excitatory postsynaptic
potentials evoked by afferent pathways stimulation
were recorded in layer II/III of Prh in horizontal brain slices
obtained from 3 month old Tg2576 mice and littermate controls.
We found that a single train of 3000 pulses delivered at 5 Hz
induced LTD in slices from control mice, but not in those from
Tg2576 mice. This result is consistent with the early visual recognition
impairment observed in AD patients, and is particularly
interesting because no changes in synaptic plasticity have
previously been found so early in this transgenic line. Indeed,
one of the major goals in AD research is to characterize the
mechanisms leading to early functional impairments in order to improve diagnostic and therapeutic tools
Physical exercise positively affects activation and differentiation in vitro of satellite cells from skeletal muscles of sarcopenic mice
No full textAgeing is associated with a progressive loss of muscle mass,
strength and function: this condition is known as sarcopenia
and represents an important risk factor for physical disability
in elderly. The mechanisms leading to sarcopenia are still
largely unknown and no specific therapy is presently available
to counteract its onset or progress. Many studies have stressed
the importance of physical exercise as an effective approach
to prevent/limit the age-related muscle mass loss. We evaluated
the effects of physical exercise on the activation and differentiation
potential of cultured satellite-cell-derived
myoblasts obtained from quadriceps muscles of old exercised,
old sedentary and adult sedentary (control) mice.
Cytochemical and immunocytochemical techniques were
applied at light and transmission electron microscopy. Our
results demonstrated that: a) physical exercise induces an
increase in number of activated satellite cells; b) myoblasts
from exercised muscles show morphological features quite
similar to myoblasts from adult subjects, whereas myoblasts
from non exercised muscles exhibit nuclear and cytoplasmic
alterations suggestive of a reduced metabolic activity; c)
myotubes differentiated from myoblasts of exercised muscles
resemble the myotubes from adult myoblasts, whereas
myotubes from non exercised muscles show marked structural
alterations, especially in the cytoskeletal apparatus
The effect of comprehensive intervention on plasmatic BDNF in Alzheimer’s disease patients.
No full textA comprehensive intervention (CI) on patients with Alzheimer's disease was assessed by measuring plasmabrain-derived neurotrophic factor (pBDNF) and ADAS-Cog score (ADAS-Cogscore) before, immediately after (FU1), and 6 (FU2) and 24 months (FU3) after the CI. Baseline pBDNF was higher in patients with moderate AD (but not mild AD) than in healthy controls. At FU1, pBDNF and ADAS-Cogscore decreased significantly. At FU2 and FU3, patients' cognitive status worsened and pBDNF further increased versus baseline, suggesting that CI interruption may be a stress event that prevents return to homeostasis. CI exerted positive short-term effects, but more information is needed on long-term consequence
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