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991.
Jean-Pierre Vilardaga Guillermo Romero Peter A. Friedman Thomas J. Gardella 《Cellular and molecular life sciences : CMLS》2011,68(1):1-13
The parathyroid hormone (PTH) receptor type 1 (PTHR), a G protein-coupled receptor (GPCR), transmits signals to two hormone
systems—PTH, endocrine and homeostatic, and PTH-related peptide (PTHrP), paracrine—to regulate different biological processes.
PTHR responds to these hormonal stimuli by activating heterotrimeric G proteins, such as GS that stimulates cAMP production. It was thought that the PTHR, as for all other GPCRs, is only active and signals through
G proteins on the cell membrane, and internalizes into a cell to be desensitized and eventually degraded or recycled. Recent
studies with cultured cell and animal models reveal a new pathway that involves sustained cAMP signaling from intracellular
domains. Not only do these studies challenge the paradigm that cAMP production triggered by activated GPCRs originates exclusively
at the cell membrane but they also advance a comprehensive model to account for the functional differences between PTH and
PTHrP acting through the same receptor. 相似文献
992.
Eoin E. Kelly Conor P. Horgan Mary W. McCaffrey Paul Young 《Cellular and molecular life sciences : CMLS》2011,68(2):185-194
Long-term potentiation (LTP) defines persistent increases in neurotransmission strength at synapses that are triggered by
specific patterns of neuronal activity. LTP, the most widely accepted molecular model for learning, is best characterised
at glutamatergic synapses on dendritic spines. In this context, LTP involves increases in dendritic spine size and the insertion
of glutamate receptors into the post-synaptic spine membrane, which together boost post-synaptic responsiveness to neurotransmitters.
In dendrites, the material required for LTP is sourced from an organelle termed the endosomal-recycling compartment (ERC),
which is localised to the base of dendritic spines. When LTP is induced, material derived from the recycling compartment,
which contains α-amino-3-hydroxy-5-methyl-4-isoxazole propionate-type glutamate receptors (AMPARs), is mobilised into dendritic
spines feeding the increased need for receptors and membrane at the spine neck and head. In this review, we discuss the importance
of endosomal-recycling and the role of key proteins which control these processes in the context of LTP. 相似文献
993.
994.
Alexander V. Zhdanov Ruslan I. Dmitriev Dmitri B. Papkovsky 《Cellular and molecular life sciences : CMLS》2011,68(5):903-917
Bafilomycin A1 (Baf) induces an elevation of cytosolic Ca2+ and acidification in neuronal cells via inhibition of the V-ATPase. Also, Baf uncouples mitochondria in differentiated PC12
(dPC12), dSH-SY5Y cells and cerebellar granule neurons, and markedly elevates their respiration. This respiratory response in dPC12 is accompanied by morphological changes in the mitochondria and decreases the mitochondrial pH, Ca2+ and ΔΨm. The response to Baf is regulated by cytosolic Ca2+ fluxes from the endoplasmic reticulum. Inhibition of permeability transition pore opening increases the depolarizing effect
of Baf on the ΔΨm. Baf induces stochastic flickering of the ΔΨm with a period of 20 ± 10 s. Under conditions of suppressed
ATP production by glycolysis, oxidative phosphorylation impaired by Baf does not provide cells with sufficient ATP levels.
Cells treated with Baf become more susceptible to excitation with KCl. Such mitochondrial uncoupling may play a role in a
number of (patho)physiological conditions induced by Baf. 相似文献
995.
996.
Lucas Matt Stylianos Michalakis Franz Hofmann Verena Hammelmann Andreas Ludwig Martin Biel Thomas Kleppisch 《Cellular and molecular life sciences : CMLS》2011,68(1):125-137
Neuronal hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are known to modulate spontaneous activity, resting
membrane potential, input resistance, afterpotential, rebound activity, and dendritic integration. To evaluate the role of
HCN2 for hippocampal synaptic plasticity, we recorded long-term potentiation (LTP) in the direct perforant path (PP) to CA1
pyramidal cells. LTP was enhanced in mice carrying a global deletion of the channel (HCN2−/−) but not in a pyramidal neuron-restricted knockout. This precludes an influence of HCN2 located in postsynaptic pyramidal
neurons. Additionally, the selective HCN blocker zatebradine reduced the activity of oriens-lacunosum moleculare interneurons
in wild-type but not HCN2−/− mice and decreased the frequency of spontaneous inhibitory currents in postsynaptic CA1 pyramidal cells. Finally, we found
amplified LTP in the PP of mice carrying an interneuron-specific deletion of HCN2. We conclude that HCN2 channels in inhibitory
interneurons modulate synaptic plasticity in the PP by facilitating the GABAergic output onto pyramidal neurons. 相似文献
997.
998.
Chia-Ching Lin Yuan-Ju Wu Bernd Heimrich Martin Schwemmle 《Cellular and molecular life sciences : CMLS》2013,70(22):4399-4410
Borna disease virus (BDV) persistently infects neurons of the central nervous system of various hosts, including rats. Since type I IFN-mediated antiviral response efficiently blocks BDV replication in primary rat embryo fibroblasts, it has been speculated that BDV is not effectively sensed by the host innate immune system in the nervous system. To test this assumption, organotypical rat hippocampal slice cultures were infected with BDV for up to 4 weeks. This resulted in the secretion of IFN and the up-regulation of IFN-stimulated genes. Using the rat Mx protein as a specific marker for IFN-induced gene expression, astrocytes and microglial cells were found to be Mx positive, whereas neurons, the major cell type in which BDV is replicating, lacked detectable levels of Mx protein. In uninfected cultures, neurons also remained Mx negative even after treatment with high concentrations of IFN-α. This non-responsiveness correlated with a lack of detectable nuclear translocation of both pSTAT1 and pSTAT2 in these cells. Consistently, neuronal dissemination of BDV was not prevented by treatment with IFN-α. These data suggest that the poor innate immune response in rat neurons renders this cell type highly susceptible to BDV infection even in the presence of exogenous IFN-α. Intriguingly, in contrast to rat neurons, IFN-α treatment of mouse neurons resulted in the up-regulation of Mx proteins and block of BDV replication, indicating species-specific differences in the type I IFN response of neurons between mice and rats. 相似文献
999.
Tsjalling Swierstra 《Foundations of Science》2017,22(2):275-278
In this review I argue that Puech draws on two important currents in modern thought: the criticism of the ontological and social priority of conflict, and the rehabilitation of praxis vis-à-vis theoria. Still, his plea for a non-confrontational art of living leaves important questions unanswered. What is the problem exactly? What does exactly count as (non)confrontational? What is non-confrontation exactly meant to solve? What is the antiposition here? And: how does this new (or rather: old) art of living relate to the political and ethical varieties of Technology Assessment? 相似文献
1000.
Multicellular organisms contain numerous symbiotic microorganisms, collectively called microbiomes. Recently, microbiomic research has shown that these microorganisms are responsible for the proper functioning of many of the systems (digestive, immune, nervous, etc.) of multicellular organisms. This has inclined some scholars to argue that it is about time to reconceptualise the organism and to develop a concept that would place the greatest emphasis on the vital role of microorganisms in the life of plants and animals. We believe that, unfortunately, there is a problem with this suggestion, since there is no such thing as a universal concept of the organism which could constitute a basis for all biological sciences. Rather, the opposite is true: numerous alternative definitions exist. Therefore, comprehending how microbiomics is changing our understanding of organisms may be a very complex matter. In this paper we will demonstrate that this pluralism proves that claims about a change in our understanding of organisms can be treated as both true and untrue. Mainly, we assert that the existing concepts differ substantially, and that only some of them have to be reconsidered in order to incorporate the discoveries of microbiomics, while others are already flexible enough to do so. Taking into account the plurality of conceptualisations within different branches of modern biology, we will conduct our discussion using the developmental and the cooperation–conflict concepts of the organism. Then we will explain our results by referring to the recent philosophical debate on the nature of the concept of the organism within biology. 相似文献