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Intracellular Ca2+ pools in PC12 cells: three intracellular pools are distinguished for their turnover and mechanisms of Ca2+ accumulation, storage and release
No full textThree, non-cytosolic Ca2+ pools were characterized in intact PC12 cells. The first pool, sensitive to both inositol 1,4,5-trisphosphate and caffeine (Zacchetti, D., Clementi, E., Fasolato, C., Zottini, M., Grohovaz, F., Fumagalli, G., Pozzan, T., and Meldolesi, J. (1991) J. Biol. Chem. 266, 20152-20158) accounts for approximately equal to 200 microM of Ca2+/liter of cell water (less than 30% of total exchangeable Ca2+) and takes up Ca2+ from the cytosol via a Ca(2+)-ATPase, blocked by thapsigargin. A second pool, approximately equal to 400 microM/liter, is insensitive to both inositol 1,4,5-trisphosphate, caffeine, and thapsigargin and is released by the Ca2+ ionophore ionomycin. This pool is probably heterogeneous and its intracellular localization and physiological roles remain undefined. The third pool, approximately equal to 170 mumoles of Ca2+/liter, was discharged by the combination of ionomycin together with a substance that collapsed intracellular pH gradients, such as monensin or NH4Cl. This indicates that the pool is acidic, at variance with the first two. When exocytosis was stimulated, the size of this pool declined, indicating its primary residence within secretory granules. In the conditions of our experiments no major transfer of Ca2+ among the pools seemed to occur. This is the first comprehensive description of non-cytosolic Ca2+ pools investigated in intact neurosecretory cells by non-invasive procedures
Distribuzione e consistenza di una popolazione di Pernice rossa (Alectoris rufa) nell'Appennino settentrionale
No full textHabitat use by partridges (Perdix perdix and Alectoris rufa) in an area of northern Apennines, Italy
No full textValutazione del successo dell'immissione di starne ( Perdix perdix ) nell'Appennino settentrionale
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The significance of cyclic EEG changes in Creutzfeldt-Jakob disease: prognostic value of their course in 9 patients.
No full textThe diagnostic value of the EEG in Creutzfeldt-Jakob disease is based not only on the presence of a typical pattern of periodic discharges but also on the appearance of cyclic changes in the EEG. The pattern of the cyclic EEG changes was analysed in 9 patients with Creutzfeldt-Jakob disease. The changes appear when the level of wakefulness is reduced. The alternating pattern rate increases as the disease progresses and accounts for as much as 100 per cent of the tracing when the patient is in coma. During the cyclic changes the cardiorespiratory rate is always higher in phase A than in phase B. Hypertonic fits and most myoclonic jerks are present only in the A-phase, whereas partial myoclonus and fasciculations are present in both phases. The cyclic change pattern in Creutzfeldt-Jakob disease reveals a progressive. The cyclic change pattern in Creutzfeldt-Jakob disease reveals a progressive, serious involvement of the waking system
Iron entry in neurons and astrocytes: a link with synaptic activity
No full textIron plays a fundamental role in the development of the central nervous system (CNS) as well as in several neuronal functions including synaptic plasticity. Accordingly, neuronal iron supply is tightly controlled: it depends not only on transferrin-bound iron but also on non-transferrin-bound iron (NTBI), which represents a relevant quote of the iron physiologically present in the cerebrospinal fluid (CSF). Different calcium permeable channels as well as the divalent metal transporter 1 (DMT1) have been proposed to sustain NTBI entry in neurons and astrocytes even though it remains an open issue. In both cases, it emerges that the control of iron entry is tightly linked to synaptic activity. The iron-induced oxidative tone can, in physiological conditions, positively influence the calcium levels and thus the synaptic plasticity. On the other hand, an excess of iron, with the ensuing uncontrolled production of reactive oxygen species (ROS), is detrimental for neuronal survival. A protective mechanism can be played by astrocytes that, more resistant to oxidative stress, can uptake iron, thereby buffering its concentration in the synaptic environment. This competence is potentiated when astrocytes undergo activation during neuroinflammation and neurodegenerative processes. In this minireview we focus on the mechanisms responsible for NTBI entry in neurons and astrocytes and on how they can be modulated during synaptic activity. Finally, we speculate on the relevance they may have in both physiological and pathological conditions
Mechnism of [Ca2+]i oscillations in rat chromaffin cells: the intracellular oscillator operates within a useful range of [Ca2+]i
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