Relevant bibliographies by topics / Intrinsic homeostasis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Intrinsic homeostasis'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Intrinsic homeostasis"

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D’Angelo, Egidio. "Homeostasis of intrinsic excitability: making the point." Journal of Physiology 588, no. 6 (March 12, 2010): 901–2. http://dx.doi.org/10.1113/jphysiol.2010.187559.

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Butler, Colin, Martin Birchall, and Adam Giangreco. "Interventional and Intrinsic Airway Homeostasis and Repair." Physiology 27, no. 3 (June 2012): 140–47. http://dx.doi.org/10.1152/physiol.00001.2012.

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Human airways are a paragon of intrinsic engineering. They experience 7,000–10,000 liters of airflow/day, have a 70-m2 surface area, and undergo complete renewal every 100–400 days. Despite this, airways are susceptible to aging, injury, and diseases that are major causes of mortality. Current airway regeneration research is focused both on understanding the cells and strategies responsible for maintaining intrinsic tissue homeostasis as well as on establishing clinical interventions for improving repair.
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Gainey, Melanie A., and Daniel E. Feldman. "Multiple shared mechanisms for homeostatic plasticity in rodent somatosensory and visual cortex." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1715 (March 5, 2017): 20160157. http://dx.doi.org/10.1098/rstb.2016.0157.

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We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.
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Hoyes, Thomas W., Neville A. Stanton, and R. G. Taylor. "Risk homeostasis theory: A study of intrinsic compensation." Safety Science 22, no. 1-3 (February 1996): 77–86. http://dx.doi.org/10.1016/0925-7535(96)00007-0.

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Wu, Yue Kris, Keith B. Hengen, Gina G. Turrigiano, and Julijana Gjorgjieva. "Homeostatic mechanisms regulate distinct aspects of cortical circuit dynamics." Proceedings of the National Academy of Sciences 117, no. 39 (September 11, 2020): 24514–25. http://dx.doi.org/10.1073/pnas.1918368117.

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Homeostasis is indispensable to counteract the destabilizing effects of Hebbian plasticity. Although it is commonly assumed that homeostasis modulates synaptic strength, membrane excitability, and firing rates, its role at the neural circuit and network level is unknown. Here, we identify changes in higher-order network properties of freely behaving rodents during prolonged visual deprivation. Strikingly, our data reveal that functional pairwise correlations and their structure are subject to homeostatic regulation. Using a computational model, we demonstrate that the interplay of different plasticity and homeostatic mechanisms can capture the initial drop and delayed recovery of firing rates and correlations observed experimentally. Moreover, our model indicates that synaptic scaling is crucial for the recovery of correlations and network structure, while intrinsic plasticity is essential for the rebound of firing rates, suggesting that synaptic scaling and intrinsic plasticity can serve distinct functions in homeostatically regulating network dynamics.
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Cannon, Jonathan, and Paul Miller. "Synaptic and intrinsic homeostasis cooperate to optimize single neuron response properties and tune integrator circuits." Journal of Neurophysiology 116, no. 5 (November 1, 2016): 2004–22. http://dx.doi.org/10.1152/jn.00253.2016.

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Homeostatic processes that provide negative feedback to regulate neuronal firing rate are essential for normal brain function, and observations suggest that multiple such processes may operate simultaneously in the same network. We pose two questions: why might a diversity of homeostatic pathways be necessary, and how can they operate in concert without opposing and undermining each other? To address these questions, we perform a computational and analytical study of cell-intrinsic homeostasis and synaptic homeostasis in single-neuron and recurrent circuit models. We demonstrate analytically and in simulation that when two such mechanisms are controlled on a long time scale by firing rate via simple and general feedback rules, they can robustly operate in tandem to tune the mean and variance of single neuron's firing rate to desired goals. This property allows the system to recover desired behavior after chronic changes in input statistics. We illustrate the power of this homeostatic tuning scheme by using it to regain high mutual information between neuronal input and output after major changes in input statistics. We then show that such dual homeostasis can be applied to tune the behavior of a neural integrator, a system that is notoriously sensitive to variation in parameters. These results are robust to variation in goals and model parameters. We argue that a set of homeostatic processes that appear to redundantly regulate mean firing rate may work together to control firing rate mean and variance and thus maintain performance in a parameter-sensitive task such as integration.
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Ge, Rongjing, Na Chen, and Jin-Hui Wang. "Real-time neuronal homeostasis by coordinating VGSC intrinsic properties." Biochemical and Biophysical Research Communications 387, no. 3 (September 2009): 585–89. http://dx.doi.org/10.1016/j.bbrc.2009.07.066.

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Niemeyer, Nelson, Jan-Hendrik Schleimer, and Susanne Schreiber. "Biophysical models of intrinsic homeostasis: Firing rates and beyond." Current Opinion in Neurobiology 70 (October 2021): 81–88. http://dx.doi.org/10.1016/j.conb.2021.07.011.

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Ferri, Francesca, Fabio Olivieri, Roberto Cannataro, Maria Cristina Caroleo, and Erika Cione. "Phytomelatonin Regulates Keratinocytes Homeostasis Counteracting Aging Process." Cosmetics 6, no. 2 (April 18, 2019): 27. http://dx.doi.org/10.3390/cosmetics6020027.

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Phytomelatonin (PM) gained the greatest interest for its application in agriculture and its use to improve human health conditions. PM based supplement has been shown to possess antioxidant capabilities because it functions as a free radical scavenger. Reactive Oxygen Species (ROS), induced by both intrinsic (peroxide production) and extrinsic (UV-radiation) factors are biochemical mediators crucial in skin aging. Skin aging is also regulated by specific microRNAs (miRs). Herein we have shown the effect of PM free radical scavengers on the human keratinocyte cell line HaCat and on ROS formation induced by both extrinsic and intrinsic factors as well as their capability to positively modulate a member of the hsa-miR-29 family linked to aging. Our result highlights the regulatory role of PM for the keratinocytes homeostasis.
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Verheijden, Simon, and Guy E. Boeckxstaens. "Neuroimmune interaction and the regulation of intestinal immune homeostasis." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 1 (January 1, 2018): G75—G80. http://dx.doi.org/10.1152/ajpgi.00425.2016.

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Many essential gastrointestinal functions, including motility, secretion, and blood flow, are regulated by the autonomic nervous system (ANS), both through intrinsic enteric neurons and extrinsic (sympathetic and parasympathetic) innervation. Recently identified neuroimmune mechanisms, in particular the interplay between enteric neurons and muscularis macrophages, are now considered to be essential for fine-tuning peristalsis. These findings shed new light on how intestinal immune cells can support enteric nervous function. In addition, both intrinsic and extrinsic neural mechanisms control intestinal immune homeostasis in different layers of the intestine, mainly by affecting macrophage activation through neurotransmitter release. In this mini-review, we discuss recent insights on immunomodulation by intrinsic enteric neurons and extrinsic innervation, with a particular focus on intestinal macrophages. In addition, we discuss the relevance of these novel mechanisms for intestinal immune homeostasis in physiological and pathological conditions, mainly focusing on motility disorders (gastroparesis and postoperative ileus) and inflammatory disorders (colitis).
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Dissertations / Theses on the topic "Intrinsic homeostasis"

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Sweeney, Yann Aodh. "Functional relevance of homeostatic intrinsic plasticity in neurons and networks." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/20982.

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Maintaining the intrinsic excitability of neurons is crucial for stable brain activity. This can be achieved by the homeostatic regulation of membrane ion channel conductances, although it is not well understood how these processes influence broader aspects of neuron and network function. One of the many mechanisms which contribute towards this task is the modulation of potassium channel conductances by activity-dependent nitric oxide signalling. Here, we first investigate this mechanism in a conductance-based neuron model. By fitting the model to experimental data we find that nitric oxide signalling improves synaptic transmission fidelity at high firing rates, but that there is an increase in the metabolic cost of action potentials associated with this improvement. Although the improvement in function had been observed previously in experiment, the metabolic constraint was unknown. This additional constraint provides a plausible explanation for the selective activation of nitric oxide signalling only at high firing rates. In addition to mediating homeostatic control of intrinsic excitability, nitric oxide can diffuse freely across cell membranes, providing a unique mechanism for neurons to communicate within a network, independent of synaptic connectivity. We next conduct a theoretical investigation of the distinguishing roles of diffusive homeostasis mediated by nitric oxide in comparison with canonical non-diffusive homeostasis in cortical networks. We find that both forms of homeostasis robustly maintain stable activity. However, the resulting networks differ, with diffusive homeostasis maintaining substantial heterogeneity in activity levels of individual neurons, a feature disrupted in networks with non-diffusive homeostasis. This results in networks capable of representing input heterogeneity, and linearly responding over a broader range of inputs than those undergoing non-diffusive homeostasis. We further show that diffusive homeostasis interferes less than non-diffusive homeostasis in the synaptic weight dynamics of networks undergoing Hebbian plasticity. Overall, these results suggest a novel homeostatic mechanism for maintaining stable network activity while simultaneously minimising metabolic cost and conserving network functionality.
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Symonds, Alistair. "The zinc finger transcription factor Early Growth Response 2 (Egr-2) is an intrinsic regulator of T cell tolerance and homeostasis." Thesis, Queen Mary, University of London, 2009. http://qmro.qmul.ac.uk/xmlui/handle/123456789/409.

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Tolerance of T cells to self-antigen is crucial to prevent the development of autoimmune disease. How self-tolerance is controlled at the transcriptional level is, however, unknown. We discovered that the transcription factor Early Growth Response 2 (Egr-2) was expressed by tolerant T cells, and by CD4+CD44high T cells in the absence of overt antigen stimulation, in vivo. To investigate the roles of Egr-2 in T cells, we generated CD2 cell specific Egr-2 deficient (Egr-2 cKO) mice. The proliferation of Egr-2 cKO CD44high T cells in vivo was markedly increased leading to progressive accumulation as the mice aged. By 15 months of age CD4+CD44high cells constituted the predominant T cell population in the peripheral lymphoid organs of Egr-2 cKO mice and expressed high levels of the activation markers CD25 and CD69. In addition to this lymphoproliferative disorder, 15 month old Egr-2 cKO mice showed signs of lupus-like autoimmune disease. This autoimmune syndrome was characterised by glomerulonephritis and proteinuria, infiltration of T cells into internal organs and, crucially, auto-antibodies directed against nuclear components; the hallmark of lupus. We observed decreased expression of the cyclin-dependent kinase inhibitor p21cip1 in Egr-2 cKO CD4+CD44high T cells while TCR stimulation induced IFN-γ, and, in particular, IL-17A and IL-17F expression was markedly increased. Consistent with these findings, we observed increased numbers of IFN-γ and IL-17 producing CD4+ T cells in Egr-2 cKO mice. The numbers of IFN-γ and IL-17 producing CD4+ T cells further increased as the mice aged in parallel with the gradual development of symptoms of lupus-like disease. These results demonstrate that Egr-2 is an intrinsic regulator of both T cell homeostasis and T cell tolerance.
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Kimme, Peter. "Intrinsic and extrinsic protection of the brain : an experimental and clinical study examining some aspects of autoregulation and complications of hypothermia /." Linköping : Univ, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med897s.pdf.

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Susin, Eduarda Demori. "Plasticidade sináptica e homeostase intrínseca em uma rede neural in silico : propriedades globais e de resposta a estímulos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/143172.

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Recentemente observou-se experimentalmente, Johnson et al. (2010), que fatias organotípicas corticais de rato são capazes de completar padrões espaço-temporais, após serem treinadas. Embora se especule que mecanismos de plasticidade sináptica e homeostática estejam por trás do fenômeno, ainda não existe nenhuma explicação detalhada sobre o assunto. Com o intuito de propor uma explicação clara e consistente para os mecanismos que permeiam a resposta da rede aos estímulos como um todo, nos propomos a estudar este fenômeno por meio de uma rede de neurônios de integração-e-disparo dotada de mecanismos de homeostase intrínseca e de plasticidade sináptica dependente de disparos. O sistema construído foi explorado, de modo a determinar em que condições a rede poderia comportar-se como o sistema real, e treinado de forma similar `a realizada experimentalmente por Johnson et al. (2010).
Recently it has been observed experimentally, Johnson et al. (2010), that organotypic cortical slices of rat are capable of completing spatio-temporal patterns after training. Although it is speculated that synaptic and homeostatic plasticity may have an important role in this phenomenon, there is still no detailed explanation about this subject. In order to propose a clear and consistent explanation for the mechanisms that underlie the network response to stimuli as a whole, we propose to study this phenomenon through a network of integrate-and-fire neurons endowed with intrinsic homeostasis and spike-timing dependent plasticity mechanisms. The constructed system was explored, aiming to determine in which conditions the network could behave as the real system, and trained in a way similar as the experimental one done by Johnson et al. (2010).
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O'Leary, Timothy S. "Homeostatic regulation of intrinsic excitability in hippocampal neurons." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/3079.

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The proper functioning of nervous systems requires electrical activity to be tightly regulated. Perturbations in the intrinsic properties of neurons, and in excitatory input, are imposed throughout nervous system development as cell morphology and network activity evolve. In mature nervous systems these changes continue as a result of synaptic plasticity and external stimuli. It is therefore likely that homeostatic mechanisms exist to regulate membrane conductances that determine the excitability of individual neurons, and several mechanisms have been characterised to date. This thesis characterises a novel in vitro model for homeostatic control of intrinsic excitability. The principal finding is that cultured hippocampal neurons respond to chronic depolarisation over a period of days by attenuating their response to injected current. This effect was found to depend on the level of depolarisation and the length of treatment, and is accompanied by changes in both active and passive membrane conductances. In addition, the effect is reversible and dependent on L-type calcium channel activity. Using experimental data to parameterise a conductance-based computer model suggests that the changes in conductance properties account for the observed differences in excitability.
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Gasselin, Célia. "Plasticités hebbienne et homéostatique de l'excitabilité intrinsèque des neurones de la région CA1 de l'hippocampe=hebbian and homeostatic plasticity of intrinsic excitability in hippocampal CA1 neurons." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5047.

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Pendant des décennies, la plasticité synaptique a été considérée comme le substrat principal de la plasticité fonctionnelle cérébrale. Récemment, plusieurs études expérimentales indiquent que des régulations à long terme de l’excitabilité intrinsèque participent à la plasticité dépendante de l’activité. En effet, la modulation des canaux ioniques dépendants du potentiel, lesquels régulent fortement l’excitabilité intrinsèque et l’intégration des entrées synaptiques, a été démontrée essentielle dans les processus d’apprentissage. Cependant, la régulation, dépendante de l’activité, du courant ionique activé par l’hyperpolarisation (Ih) et ses conséquences sur l’induction de futures plasticités reste à éclaircir, tout comme la présence d’une régulation de conductances dépendantes du potentiel dans les neurones inhibiteurs. Dans la première partie de ma thèse, nous caractérisons les mécanismes d’induction et d’expression de la plasticité à long terme de l’excitabilité (LTP-IE) dans les interneurons en panier de la région CA1 exprimant la parvalbumine. Dans une seconde partie, le rôle de Ih dans la régulation homéostatique de l’excitabilité neuronale induite par des manipulations de l’activité neuronale dans sa globalité a été étudié. Dans la troisième étude, nous montrons que la magnitude de la Dépression à Long Terme (LTD) détermine le sens de la régulation de Ih dans les neurones pyramidaux de CA1. En conclusion, cette thèse montre qu’à la fois dans les neurones excitateurs et inhibiteurs, les régulations des conductances dépendantes du potentiel aident à maintenir une relative stabilité dans l’activité du réseau
Synaptic plasticity has been considered for decades as the main substrate of functional plasticity in the brain. Recently, experimental evidences suggest that long-lasting regulation of intrinsic neuronal excitability may also account for activity-dependent plasticity. Indeed, voltage-dependent ionic channels strongly regulate intrinsic excitability and inputs integration and their regulation was found to be essential in learning process. However, activity-dependent regulation of the hyperpolarization-activated ionic current (Ih) and its consequences for future plasticity remain unclear, so as the presence of any voltage-dependent conductances regulation in inhibitory neurons. In the first part of this thesis, we report the characterization of the induction and expression mechanisms of Long-Term Potentiation of Intrinsic Excitability (LTP-IE) in CA1 parvalbumin-positive basket interneurons. In a second part, the role of Ih in the homeostatic regulation of intrinsic neuronal excitability induced by global manipulations of neuronal activity was reported. In the third experimental study, we showed that the magnitude of Long-term Depression (LTD) determines the sign of Ih regulation in CA1 pyramidal neurons. In conclusion, this thesis shows that in both excitatory and inhibitory neurons, activity-dependent regulations of voltage-dependent conductances help to maintain a relative stability in the network activity
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O'Brien, Thomas Francis. "Intrinsic Mechanisms that Regulate T Cell Homeostasis and Function." Diss., 2011. http://hdl.handle.net/10161/5011.

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The unique functional attributes possessed by T cells are initiated after stimulation via their T cell receptor (TCR). Due to the T cell's integral role in immune function, the regulation of signaling events downstream of the TCR have been, and continue to be, an area of intense research. An effective T cell immune response is dependent upon the proper relaying of the signals initiated by the TCR-antigen-MHC interaction, whereas a disruption in the signaling cascades downstream of the TCR can result in the inability to control pathogen replication or the initiation of T cell mediated autoimmunity. The discovery of specific pharmacological inhibitors and the generation of genetically modified mouse models have allowed investigators to take a stepwise approach in understanding TCR induced signaling hierarchies.

In this study, we have utilized genetically modified mouse models, in which the targets of gene deletion, TSC1 and DGK, are molecules that regulate signals emanating from the TCR. Additionally, we have demonstrated that both of these molecules negatively regulate the mammalian target of rapamycin (mTOR) in both naïve and activated T cells. mTOR is a critical regulator of cell growth and metabolism. By virtue of its kinase ability, mTOR has been shown to initiate signaling in response to a variety of extracellular signals including cytokines, growth factors, amino acids, and toll-like receptor (TLR) ligands. The versatility with which this protein kinase interprets multiple signaling inputs simultaneously has led to mTOR being referred to as the "rheostat" of the cell. Recent investigation has begun to elucidate the role of the mTOR pathway in basic T cell biology, however, the mechanisms by which mTOR controls basic T cell homeostasis and function is unclear, and the importance of tight control of the TSC-mTOR pathway in T cells is not known.

In the first model, mice were strategically bred so that TSC1 was deleted exclusively in the murine T cell lineage. TSC1, in complex with TSC2, acts as an inhibitor of mTOR by inhibiting Rheb, an activator of mTORC1. Using this model we found that deletion of TSC1 at the double-positive (DP) stage of thymocyte development has several profound effects on T cell signaling, homeostasis and survival. Specifically, the loss TSC1 in T cells results in constitutive activation of mTORC1 and decreased activation of mTORC2. Reduced T cell numbers were also observed in the peripheral lymphoid organs, which correlated with the finding of increased cell death ex vivo as well as after TCR stimulation in vitro. Furthermore, we found that TSC1 deficiency resulted in altered mitochondrial homeostasis and function, which could be rescued in vitro with co-stimulation and/or antioxidants. These observations give us clear evidence that the TSC-mTOR pathway regulates T cell survival and normal mitochondrial homeostasis.

In the second model, I utilized diacylglycerol kinase (DGK) deficient mice in our examination of the mechanisms by which the TCR affects T cell biology. To date, ten DGK isoforms have been identified in mammals, with DGKα and DGKζ being expressed in T cells. Immediately following TCR stimulation, PIP2 is hydrolyzed into the secondary messengers inostitol triphosphate (IP3) and diacylglycerol (DAG). By converting DAG into phosphatidic acid, DGKs effectively terminate signaling mediated by DAG and serve to dampen T cell activation. Additionally, previous work from our lab has shown that mTOR kinase activity is negatively regulated in T cells by DGKs, and reveals a novel signaling relationship between the TCR, DGKs, and mTOR kinase activation. Given the ability of DGKα and ζ to regulate mTOR and other signaling cascades, we hypothesized that DGK activity may play an important role during an anti-viral immune response. Using DGKα- and DGKζ-deficient (germline) mice in conjunction with MHC class I restricted tetramers and synthetically generated viral antigens, we were able to enumerate the primary and memory CD8+ anti-viral immune response in the absence of diacylglycerol (DAG) metabolism and enhanced mTOR activity. In response to LCMV infection, DGK-deficient CD8+ T cells expand more aggressively and produce elevated amounts of anti-viral cytokines, which results in reduced viral titers in DGK-deficient mice 7 days after infection. Additionally, we found that while DGK activity serves to suppress the CD8+ T cell response during the primary infection phase, it promotes the expansion of antigen specific CD8+ T cells during the memory phase of an immune response. The diminished response by DGK-deficient memory CD8+ T cells highlights opposing roles for DAG metabolism during the primary and memory immune phases.

The studies reported in this dissertation provide novel insights into the intrinsic mechanisms that regulate T cell homeostasis and function.


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Corey, Joseph Harrod. "Homeostasis and synaptic scaling : a theoretical perspective." 2012. http://hdl.handle.net/2152/20010.

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Abstract The synaptic input received by neurons in cortical circuits is in constant flux. From both environmental sensory changes and learning mechanisms that modify synaptic strengths, the excitatory and inhibitory signals received by a post-synaptic cell vary on a continuum of time scales. These variable inputs inherent in different sensory environments, as well as inputs changed by Hebbian learning mechanisms (which have been shown to destabilize the activity of neural circuits) serve to limit the input ranges over which a neural network can effectively operate. To avoid circuit behavior which is either quiescent or epileptic, there are a variety of homeostatic mechanisms in place to maintain proper levels of circuit activity. This article provides a basic overview of the biological mechanisms, and consider the advantages and disadvantages of homeostasis on a theoretical level.
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George, Andrew Anthony. "Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity." Thesis, 2009. http://hdl.handle.net/2152/ETD-UT-2009-12-407.

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Although the processes used for temporarily storing and manipulating neural information have been extensively studied at the synaptic level far less attention has been given to the underlying cellular and molecular mechanisms that contribute to change in the intrinsic excitability of neurons. More importantly, how do these mechanisms of plasticity integrate with ongoing mechanisms of regulation of neural intrinsic excitability and, in turn, homeostasis of entire neural circuits? In this dissertation I describe the underlying mechanisms that contribute to persistent neural activity and, more globally, sensorimotor adaptation using weakly electric fish as my model system. Weakly electric fish have evolved a behavior adaptation known as the jamming avoidance response (JAR), and it is this adaptation that allows the organism to elevate its own electrical discharge in response to intraspecific interactions and subsequent distortions of the animal’s electric field. The elevation operates over a wide range and in vivo can last tens of hours upon cessation of a jamming stimulus. I demonstrate that the underlying mechanisms of the adaptation are mediated by calcium-dependent signaling in the pacemaker nucleus and that calcium-mediated phosphorylation plays an important role in the regulation of the long-term frequency elevation (LTFE). I demonstrate using an in vitro brain slice preparation from the weakly electric fish, Apteronotus leptorhynchus that the engram of memory formation depends on the cooperativity of calcium-dependent protein kinases and protein phosphatases. In addition, I show that the memory formation (in the form of LTFE) does not depend on the continued flux of calcium, but rather the phosphorylation events downstream of NMDA receptor activation. Moreover, I describe the differences in the expression of protein phosphatases and protein kinases as they relate to species-specific differences in sensorimotor adaptation. It is important to note that this is the first time that the cooperativity between different isoforms of protein kinase C (PKC) have been shown to play a role in graded long-term change in neuronal activity and, in turn, providing the neural basis of species-specific behavior. The neural adaptation of the electromotor system in weakly electric fish provides an excellent model system to study the underlying cellular and molecular events of vertebrate memory formation.
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Sweeney, Yann. "Functional Relevance of Homeostatic Intrinsic Plasticity in Neurons and Networks." Doctoral thesis, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-185747.

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Maintaining the intrinsic excitability of neurons is crucial for stable brain activity. This can be achieved by the homeostatic regulation of membrane ion channel conductances, although it is not well understood how these processes influence broader aspects of neuron and network function. One of the many mechanisms which contribute towards this task is the modulation of potassium channel conductances by activity-dependent nitric oxide signalling. Here, we first investigate this mechanism in a conductance-based neuron model. By fitting the model to experimental data we find that nitric oxide signalling improves synaptic transmission fidelity at high firing rates, but that there is an increase in the metabolic cost of action potentials associated with this improvement. Although the improvement in function had been observed previously in experiment, the metabolic constraint was unknown. This additional constraint provides a plausible explanation for the selective activation of nitric oxide signalling only at high firing rates. In addition to mediating homeostatic control of intrinsic excitability, nitric oxide can diffuse freely across cell membranes, providing a unique mechanism for neurons to communicate within a network, independent of synaptic connectivity. We next conduct a theoretical investigation of the distinguishing roles of diffusive homeostasis mediated by nitric oxide in comparison with canonical non-diffusive homeostasis in cortical networks. We find that both forms of homeostasis robustly maintain stable activity. However, the resulting networks differ, with diffusive homeostasis maintaining substantial heterogeneity in activity levels of individual neurons, a feature disrupted in networks with non-diffusive homeostasis. This results in networks capable of representing input heterogeneity, and linearly responding over a broader range of inputs than those undergoing non-diffusive homeostasis. We further show that diffusive homeostasis interferes less than non-diffusive homeostasis in the synaptic weight dynamics of networks undergoing Hebbian plasticity. Overall, these results suggest a novel homeostatic mechanism for maintaining stable network activity while simultaneously minimising metabolic cost and conserving network functionality.

Joint Doctoral Program in Neuroinformatics.  https://www.kth.se/eurospin

Public defence Monday, 23 May 2016, at 9.00 a.m. in Room 1,15, Meeting and Training suite, 1st Floor, Library, Univ Edinburgh, School of Informatics (can be joined via videoconference from Konstantinbågen, Drottning Kristinas väg 4, Kungliga Tekniska högskolan, Stockholm.

QC 20160426

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Books on the topic "Intrinsic homeostasis"

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Shaffu, Shireen, and James Taylor. Normal function of the musculoskeletal system. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0263.

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The musculoskeletal system consists of specialized connective tissue whose primary function is to allow locomotion. The tissues of the musculoskeletal system are bones, muscles, tendons, and ligaments. In particular, the bony skeleton also has the task of protecting vital internal organs, contains the bone marrow, and is an intrinsic part of the metabolic pathways involved in calcium homeostasis. Motion is allowed by specialized articulating structures, the joints.
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Book chapters on the topic "Intrinsic homeostasis"

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Meier, Jochen, Marcus Semtner, and Jakob Wolfart. "Homeostasis of Neuronal Excitability Via Synaptic and Intrinsic Inhibitory Mechanisms." In Homeostatic Control of Brain Function, 51–72. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199322299.003.0004.

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del Rey, Adriana, and Hugo Besedovsky. "The Immune System as a Sensor Able to Affect Other Homeostatic Systems." In Immunopsychiatry, 83–102. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.003.0005.

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This chapter deals with the capacity of the immune system to sense the intrusion of external challenges and modifications of self-components, and to provide information to the brain about these disturbances. These properties allow us to classify the immune system as a classical sensory organ. Besides its intrinsic function directed at the elimination of dangerous stimuli, the activation of the immune system also affects the functioning of other homeostatic systems, such as the endocrine and the nervous systems. We also discuss our view of how immune-derived information could be processed by the brain and integrated with other inputs that it permanently receives, leading to a resetting of regulatory adaptive systems. Due to the high energetic cost of immunity, we discuss how brain-borne cytokines, in particular IL-1, could affect glucose homeostasis. Deregulation of these immune-neuroendocrine interactions can affect brain mechanisms that include behavior, cognition, mood, and personality.
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Smith, Moyra. "Maintaining homeostasis and mitigating effects of harmful factors in the intrinsic or extrinsic environment." In Gene Environment Interactions, 139–75. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-819613-7.00006-2.

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Yasin, Durdana, Md Zafaryab, Khalid Umar Fakhri, Shaheen Husain, Bushra Afzal, Neha Sami, Hemlata Hemlata, M. Moshahid Alam Rizvi, and Tasneem Fatma. "Apoptotic Pathway." In Handbook of Research on Advancements in Cancer Therapeutics, 290–311. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-6530-8.ch009.

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Cancer is a major killer disease caused by uncontrolled growth and invasion of cells. Apoptosis is the cell's natural mechanism of death, which maintains tissue homeostasis. Any mutation that disturbs the apoptotic pathway leads to deregulated proliferation, resistance, and evasion of apoptosis. This evasion is one of the hallmarks of malignant developments. Apoptosis takes place via two distinct pathways i.e. the intrinsic and the extrinsic pathways. These pathways use cleaved caspases to execute apoptosis which in turn cleave many downstream proteins to kill the cells. They can also be inhibited through various means that include up-regulation of anti-apoptotic and down-regulation of pro-apoptotic factors. The authors here aim to impart a comprehensive understanding of the biochemical characteristics of these pathways that render scientists target these pathways and assess apoptosis restoring abilities of the novel drugs and natural products for cancer treatment.
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Kalkan, Hilal. "The Program Cell Death (Apoptosis) and the Therapy of Cancer." In Regulation and Dysfunction of Apoptosis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97289.

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Apoptosis plays many vital roles in maintaining organ homeostasis and represents type I programmed cell death. Programmed cell death happens when the DNA damage is irremediable and has two important pathways, the intrinsic death pathway also known as the mitochondrial pathway, and the extrinsic programmed cell death pathway. Any defects in the regulation of these crucial pathways have been associated with many disorders, most importantly cancer. Therefore, understanding the molecular basis of apoptosis is essential for the treatment of incurable cancer. To date, several anti-cancer drugs have been developed by targeting anti-apoptotic proteins, which are upregulated in many cancers. Nonetheless, a disease progression often time warranted due to the deregulation of several anti or pro-apoptotic proteins which also contribute to drug resistance. Hence, it is important to understand the maintenance and counteraction of apoptosis and improve successful new pharmacological applications of cell death mechanisms for future therapies. This chapter discusses the mechanism of apoptosis and emerging principles of drug resistance in cancer.
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Becker, Richard C., and Frederick A. Spencer. "Fibrinolytic Agents." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0011.

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The fibrinolytic system plays a vital role in maintaining vital organ homeostasis. Fibrinolysis, defined as the dissolution of fibrin (the major scaffold for intravascular thrombus), is the process that regulates thrombus growth after hemostasis has been achieved, thus preserving tissue perfusion. An understanding of fibrinolysis has led to the development of pharmacologic agents that can be used in the treatment of arterial and venous thrombotic disorders, including acute myocardial infarction, acute ischemic stroke, and pulmonary embolism. Fibrinolytic therapy makes use of the vascular system’s intrinsic defense mechanism by accelerating and amplifying the conversion of an inactive enzyme precursor (zymogen), plasminogen, to the active enzyme plasmin. In turn, plasmin hydrolyzes several key bonds in the fibrin (clot) matrix, causing dissolution (lysis). A single-chain glycoprotein consisting of 790 amino acids, plasminogen is converted to plasmin by cleavage of the Arg560–Val561 peptide bond. The plasminogen molecule also contains specific lysine binding sites, which mediate its interaction with fibrin and α2-plasmin inhibitor. A serine protease with trypsinlike activity, plasmin attacks lysyl and arginyl bonds of fibrin at two principal sites: (1) the carboxyterminal portion α-chain (polar region) and (2) the coiled coil connectors containing α-, β-, and γ-chains. The ability of a fibrinolytic agent to dissolve an occlusive thrombus is determined by several factors. After administration the agent must be delivered to, perfuse, and ultimately infiltrate the thrombus while concomitantly being provided with an adequate amount of substrate (plasminogen) and the appropriate metabolic environment for an enzymatic reaction (conversion of plasminogen to plasmin) to take place. The intrinsic composition or ultrastructure of a thrombus also affects its lysability. Changes in the total amount and distribution of blood flow determine oxygen delivery to metabolically active tissues. They also determine the delivery of enzymatic substrate and plasminogen activators to the occlusive thrombus. In the heart, coronary blood flow correlates directly with mean arterial pressure. The flow-pressure curve is relatively flat above 65 to 70 mmHg, but becomes steeper as the mean arterial pressure decreases below this point. The relationship within the brain is more complex.
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Sharma, Maryada, Kavita Kaushal, Sanjay Singh Rawat, Manjul Muraleedharan, Seema Chhabra, Nipun Verma, Anupam Mittal, et al. "The Cellular Stress Response Interactome and Extracellular Matrix Cross-Talk during Fibrosis: A Stressed Extra-Matrix Affair." In Extracellular Matrix - Developments and Therapeutics [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95066.

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Diverse internal and external pathologic stimuli can trigger cellular stress response pathways (CSRPs) that are usually counteracted by intrinsic homeostatic machinery, which responds to stress by initiating complex signaling mechanisms to eliminate either the stressor or the damaged cells. There is growing evidence that CSRPs can have context-dependent homeostatic or pathologic functions that may result in tissue fibrosis under persistence of stress. CSRPs can drive intercellular communications through exosomes (trafficking and secretory pathway determinants) secreted in response to stress-induced proteostasis rebalancing. The injured tissue environment upon sensing the stress turns on a precisely orchestrated network of immune responses by regulating cytokine-chemokine production, recruitment of immune cells, and modulating fibrogenic niche and extracellular matrix (ECM) cross-talk during fibrotic pathologies like cardiac fibrosis, liver fibrosis, laryngotracheal stenosis, systemic scleroderma, interstitial lung disease and inflammatory bowel disease. Immunostimulatory RNAs (like double stranded RNAs) generated through deregulated RNA processing pathways along with RNA binding proteins (RBPs) of RNA helicase (RNA sensors) family are emerging as important components of immune response pathways during sterile inflammation. The paradigm-shift in RNA metabolism associated interactome has begun to offer new therapeutic windows by unravelling the novel RBPs and splicing factors in context of developmental and fibrotic pathways. We would like to review emerging regulatory nodes and their interaction with CSRPs, and tissue remodeling with major focus on cardiac fibrosis, and inflammatory responses underlying upper airway fibrosis.
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Conference papers on the topic "Intrinsic homeostasis"

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Rahbar, Elaheh, Beth A. Placette, and James E. Moore. "Modeling of Lymphatic Contractility." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19604.

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The lymphatic system is responsible for maintaining fluid and protein homeostasis, collecting approximately 4 liters of interstitial fluid per day and returning it to the venous system. Transporting this fluid, however, is no trivial task. Given that the point of return is located in the upper torso, most of the body’s lymph is pumped “uphill”. Furthermore, tissue pressures are very low, no higher than 15 mmHg, suggesting that lymph flow is not solely pressure driven. In fact, lymphatic vessels rely on intrinsic and extrinsic pumping mechanisms to propel lymph.
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Gu, Xiang, Daniel Leong, Rashal Mahammud, Yong Hui Li, Hui Bin Sun, and Luis Cardoso. "Continuous Passive Motion and Loading System Design for the Study of Pro- and Anti-Inflamatory Mediators in Articular Cartilage." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206753.

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Joint diseases are common causes of disability worldwide. Physical activity and weight bearing conditions play an important role in the regulation of joint homeostasis throughout life. The parametric characterization of deleterious and beneficial joint loading regimens influencing the homeostasis of articular cartilage is of great interest from both a basic research and clinical practice point of view. The development of in vivo animal models is critical to investigate the underlying mechanisms mediating the biological response of articular joints to external mechanical stimuli. For this purpose, the design of a device capable of accurately control the joint motion and loading in a small animal is needed. In the present work, an assisted motion system was conceived to perform continuous passive motion (CPM) and continuous loaded motion (CLM) on the knee joint of a small animal in vivo. A major purpose of this system is the study of the inflammatory and anti-inflammatory response of cartilage under several biomechanical environments. Therefore, a key design criterion was to avoid any invasive intervention (i.e. intraskeletal fixators) that may produce an intrinsic inflammatory response and then obscure/mislead the assessment of the biological markers of interest. Other important design criteria include real time control of the knee joint position, angular displacement, cyclic motion frequency and custom load magnitude applied in the axial direction along the tibia.
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You might also be interested in the extended bibliographies on the topic 'Intrinsic homeostasis' for particular source types:
Journal articles
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