Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl
Ograniczanie wyników
Czasopisma help
Lata help
Autorzy help
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 46

Liczba wyników na stronie
first rewind previous Strona / 3 next fast forward last
Wyniki wyszukiwania
Wyszukiwano:
w słowach kluczowych:  astrocyte
help Sortuj według:

help Ogranicz wyniki do:
first rewind previous Strona / 3 next fast forward last
1
Content available remote On String Languages Generated by Spiking Neural P Systems with Astrocytes
100%
EN
Spiking neural P systems with astrocytes (SNPA systems, for short) are a class of distributed parallel computing devices inspired from the way spikes pass along the synapses between neurons. In this work, we investigate the computational power of SNPA systems as language generators. Specifically, representations of recursively enumerable languages and of regular languages are given by means of SNPA systems without forgetting rules. Furthermore, a simple finite language is produced which can be generated by SNPA systems, while it cannot be generated by usual spiking neural P systems. These results show that the astrocytes are a powerful ingredient for spiking neural P systems as language generators.
2
Content available remote Reversible Spiking Neural P Systems with Astrocytes
100%
EN
Spiking neural P systems with astrocytes (SNPA systems, for short) are a class of distributed parallel computing devices inspired from the way neurons communicate by means of spikes. In this work, we investigate the reversibility in SNPA systems as well as the computational power of reversible SNPA systems. It is proved that reversible SNPA systems are universal, where the forgetting rules and the feature of delay in spiking rules are not used, and each neuron contains only one spiking rule. The result suggests that the astrocytes play a key role in the functioning of reversible SNPA systems.
EN
40 adult Wistar rats were divided into two groups depending on the applied anaesthesia. In both groups animals were generally anaesthetized with fentanyl, dehydrobenzperidol administered intraperitoneally and midazolam given intramuscularly. In the second group (SEVO) animals received sevoflurane of 2.2 vol% end-tidal concentration. Intracerebral haematoma was produced through infusion of 100 µl of autologous blood into the striatum. Each group was divided into five subgroups depending on the length of survival period: 1, 3, 7, 14, 21 days. The astrocytic population was studied by means of anti-GFAP staining. Stereological analysis was applied to estimate the numerical density of immunoreactive cells and the distribution of their types. On 7th day of observation the density of GFAP-immunoreactive astrocytes in SEVO was lower (p<0,05) than that in the control group. In the control group, the increase (p<0.05) of per cent of activated astrocytes between the 1st and 3rd survival day was noted, which remained at this level till the end of observation. In SEVO group, the increase (p<0.05) of per cent of activated astrocytes between the 3rd and 7th day and the decrease (p<0.05) between the 14th and 21st survival day were observed. During days of observation the per cent of activated astrocytes was lower (p<0.05) in the SEVO group than that in the control group. Administration of sevoflurane during anaesthesia to animals with intracerebral haemorrhage has evoked not only the delay of the activation of astrocytes but also decrease in its level.
6
Content available remote Glial scar instability after brain injury
75%
|
|
tom 57
|
nr 4
97-102
EN
Glial scar is formed following surgical damage to the cerebral cortex. In the present study we examined the ultrastructural status of the cerebral cortex 14 to 180 days following surgical damage to cerebral parenchyma. The results showed a contribution of astrocytes, but also mesodermal cells, to the process of scar formation. Furthermore, our study showed that the process initiated by trauma did not terminate with the formation of a glial scar. Late phases of repair following tissue damage were associated with lytic processes and a disassembly of the cerebral parenchyma. These findings indicate a changing and unstable nature of the glial scar and its components.
EN
Astrocytes are glial cells prone to morphological changes associated with age. The aim of the study was to investigate the immunoreactivity of glial fibrillary acidic protein (GFAP) in astrocytes of the periaqueductal gray matter (PAG) of the midbrain in adult and old male rats to demonstrate morphological changes associated with age and to assess morphometrically the number of astrocytes and the digital immunostaining intensity of the examined protein in PAG astrocytes of both groups of animals. In the study, 10 male Wistar rats in two age groups were used. The first group consisted of five 100-day-old animals, whereas the second comprised five 3-year-old rats. After euthanasia, the midbrain, containing PAG, was collected and embedded in paraffin blocks. Immnunohistochemical peroxidase-antiperoxidase reaction was carried out on coronal tissue sections with the use of the specific primary antibody against GFAP, goat anti-mouse IgG, peroxidase-antiperoxidase complex, and diaminobenzidine chromogen. GFAP-immunopositive PAG astrocytes were observed under a light microscope and subjected to morphometric analysis to determine their number and digital immunostaining intensity for the protein examined. GFAP-immunoreactive PAG astrocytes in 100-day-old rats showed uniform distribution. Numerous processes branching into secondary ones protruded from intensely GFAP-immunostained stellate cells. In contrast, in 3-year-old rats a significantly lower number of glial cells of different morphology was observed compared to young animals. Astrocytes had fewer primary processes without secondary branches. Morphometric analysis confirmed microscopic observations. Our findings indicate that PAG astrocytes are prone to quantitative and morphological changes with age, which, in turn, can cause disorders in emotional, pain, and defensive reactions.
EN
The aim of the study was to trace the ERα immunoreactivity in the hippocampal astrocytes of ovariectomized rabbits with and without the application of 17β-estradiol. The study comprised sexually mature female rabbits that had undergone ovariectomy. The animals were divided into two experimental groups. Group I comprised of the ovariectomized rabbits and group II . the ovariectomized animals treated with 17β -estradiol. The immunocytochemical reaction was conducted with the application of two antibodies against estrogen receptors a. In the ovariectomized rabbits which did not receive 17β -estradiol the astrocytes were characterized by ERα immunoreactivity. Similarly in group II expression of ERα was found in the hippocampus astrocytes following the application of 17β -estradiol. In astrocytes, these receptors are located in the cell body and initial processes and rarely in cell nuclei. The results suggest that astrocytes are the target cells for estrogens, changing their function and modulating hippocampal neuron activity.
EN
Glial pathology and energy metabolism changes in the brain precede symptoms of Parkinson’s disease (PD) and multiple other neurodegenerative diseases. Astrocytes govern and regulate a large part of the energy metabolism in the brain. Prolonged impairment of astrocytic functions could increase the vulnerability of dopaminergic neurons in the substantia nigra (SN). In this model, 40‑50% of dopaminergic neurons were selectively killed, causing transient locomotor disability compensated with time. We also induced death of astrocytes in the SN, simultaneously activating microglia but sparing the dopaminergic neurons. The astrocytes replenished after toxin withdrawal. We studied multiple markers of energy metabolism and mitochondrial oxidative phosphorylation (OxPhos) complex and supercomplex functioning during the early stages of neurodegeneration and compensation in the SN and striatum (STR). Death of astrocytes diminished the capability of the dopaminergic system to compensate for the degeneration of neurons. It caused a local energy deprivation, a shift in the usage of energy substrates, via increased glycogenolysis and glycolysis markers, ketone bodies availability, and fatty acid transport in remaining glial cells. Increased neuronal expression of CPT1c and astrocytic expression of CPT1a suggest adaptation in fatty acid use. On the other hand, lesion of dopaminergic neurons influenced OxPhos system and enhanced its functioning. Microglia activation also plays an important role in the processes of degeneration, compensation, and energy metabolism regulation. Modulation of its activation phenotypes might be beneficial towards the indicated processes. Astrocyte and microglia energetic influence is one of the factors in the neuronal compensatory mechanisms of dopaminergic system and might have a leading role in presymptomatic PD stages.
16
63%
|
|
tom 57
|
nr 4
91-96
EN
Recent studies suggest that capillaries, neurons, and astrocytes form a functional unit that serves to maintain cerebral homeostasis. Physiological interactions between all these components of the neurovascular unit control cerebral microcirculation, while abnormal regulatory mechanisms lead to cerebral dysfunction and disease states, such as Alzheimer’s disease (AD). Using electron microscopy, we studied a fragment of the frontotemporal cortex obtained intraoperatively from a patient with established AD. The objective of our study was to assess the ultrastructure of the components of the neurovascular unit. Such ultrastructural studies allow analyzing the structural process of new blood vessels formation and also the appearance of neurons and astrocytes contributing to the neurovascular unit. We suggest that dysfunction of particular components of the neurovascular unit underlies AD and ultimately leads to neurodegeneration.
EN
Leukemia inhibitory factor (LIF) is a neuroprotective cytokine that is necessary for the normal development of astrocytes. Oxygen-glucose deprivation (OGD) can induce astrocyte proliferation by increasing hypoxia-inducible factor alpha (HIF- 1a) and vascular endothelial growth factor (VEGF). Here, we studied whether LIF affects the proliferation of cultured primary rat astrocytes under OGD conditions by measuring EdU incorporation into astrocyte DNA and the expression of proliferating cell nuclear antigen (PCNA) mRNA and protein. Our findings show that low concentrations of LIF (5 and 10 ng/mL) significantly decreased EdU incorporation and downregulated the expression of PCNA mRNA and PCNA protein in astrocytes subjected to OGD. A low concentration of LIF (10 ng/mL) clearly inhibited astrocyte proliferation induced by OGD, while a higher concentration (50 ng/mL) had no effect. To investigate the mechanism of this inhibition by LIF (10 ng/ mL), the expression of 3 related genes (LIF receptor, HIF-1a, and VEGF) was assessed using real-time PCR; VEGF protein expression was measured by Western blot. Our results indicate that LIFR mRNA was downregulated in astrocytes subjected to OGD. Interestingly, treatment with LIF further reduced LIFR mRNA expression in these cells. LIF treatment also decreased the expression of HIF-1a mRNA, VEGF mRNA, and VEGF protein induced by OGD. Low concentrations of LIF were observed to inhibit astrocyte proliferation induced by OGD.
EN
Using 13C labeled compounds and 13C magnetic resonance spectroscopy (MRS) it is possible to monitor cellular metabolism and astrocyte-neuronal interactions. Various 13C labeled substrates are used to unravel different aspects of cerebral metabolism. This presentation will focus on [1-13C]glucose, [U-13C] glucose, [2-13C]glucose and [3-13C]glucose metabolism in cerebellar and cerebro-cortical neurons and astrocytes in culture. [1-13C]Glucose is metabolized by both astrocytes and neurons and labeling of metabolites from this isotopomer of glucose will not be affected by the pentose phosphate pathway (PPP). Using [U-13C]glucose and 3-nitropropionic acid it could be confirmed that pyruvate carboxylation takes place in cortical astrocytes but not neurons. This carboxylation leads to the formation of oxaloacetate, which condenses with acetyl coenzyme A to form citrate. However, oxaloacetate may also be converted to malate and fumarate before being regenerated. This redundant pathway is termed the oxaloacetate-fumarate-flux, or backflux and has been shown to be extensive using [2-13C]- and [3-13C]glucose in cultured cerebral cortical and cerebellar cultures. It could also be calculated to be present in vivo. [2-13C]- and [3-13C]glucose can also be used to probe the PPP in neurons where pyruvate carboxylation is not present. Indeed, the PPP contributed to labeling of glutamate and other metabolites.
first rewind previous Strona / 3 next fast forward last
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.