scholarly journals Drosophila Mechanical Nociceptors Preferentially Sense Localized Poking

2022 ◽  
Author(s):  
Zhen Liu ◽  
Qi-Xuan Wang ◽  
Meng-Hua Wu ◽  
Shao-Zhen Lin ◽  
Xi-Xiao Feng ◽  
...  
Keyword(s):  
Neural Circuits ◽  
Signal Propagation ◽  
Cellular Level ◽  
Cellular Mechanisms ◽  
Force Detection ◽  
Lateral Tension ◽  
Sensory Features ◽  
Evolutionarily Conserved ◽  
Living Organisms ◽  
Sensory Process

Mechanical nociception is an evolutionarily conserved sensory process required for the survival of living organisms. Previous studies have revealed much about the neural circuits and key sensory molecules in mechanical nociception, but the cellular mechanisms adopted by nociceptors in force detection remain elusive. To address this issue, we study the mechanosensation of a fly larval nociceptor (class IV da neurons, c4da) using a customized mechanical device. We find that c4da are sensitive to mN-scale forces and make uniform responses to the forces applied at different dendritic regions. Moreover, c4da showed a greater sensitivity to more localized forces, consistent with them being able to sense the poking of sharp objects, such as wasp ovipositor. Further analysis reveals that high morphological complexity, mechanosensitivity to lateral tension and active signal propagation in the dendrites altogether facilitate the mechanosensitivity and sensory features of c4da. In particular, we discover that Piezo and Ppk1/Ppk26, two key mechanosensory molecules, make differential but additive contributions to the mechanosensation of c4da. In all, our results provide updates into understanding how c4da process mechanical signals at the cellular level and reveal the contributions of key molecules.

Magnitude and variation of ratio of total body potassium to fat-free mass: a cellular level modeling study

2001 ◽  
Vol 281 (1) ◽  
pp. E1-E7 ◽  
Author(s):  
Zimian Wang ◽  
F. Xavier Pi-Sunyer ◽  
Donald P. Kotler ◽  
Jack Wang ◽  
Richard N. Pierson ◽  
...  
Keyword(s):  
Body Fat ◽  
Essential Element ◽  
Physiological Model ◽  
Cellular Level ◽  
Fat Free Mass ◽  
Total Body Potassium ◽  
Fluid Compartment ◽  
Total Body Fat ◽  
Total Body ◽  
Living Organisms

Potassium is an essential element of living organisms that is found almost exclusively in the intracellular fluid compartment. The assumed constant ratio of total body potassium (TBK) to fat-free mass (FFM) is a cornerstone of the TBK method of estimating total body fat. Although the TBK-to-FFM (TBK/FFM) ratio has been assumed constant, a large range of individual and group values is recognized. The purpose of the present study was to undertake a comprehensive analysis of biological factors that cause variation in the TBK/FFM ratio. A theoretical TBK/FFM model was developed on the cellular body composition level. This physiological model includes six factors that combine to produce the observed TBK/FFM ratio. The ratio magnitude and range, as well as the differences in the TBK/FFM ratio between men and women and variation with growth, were examined with the proposed model. The ratio of extracellular water to intracellular water ( E/I) is the major factor leading to between-individual variation in the TBK/FFM ratio. The present study provides a conceptual framework for examining the separate TBK/FFM determinants and suggests important limitations of the TBK/FFM method used in estimating total body fat in humans and other mammals.

Activins, Inhibins, and Follistatins: From Endocrinology to Signaling. A Paradigm for the New Millennium

2002 ◽  
Vol 227 (9) ◽  
pp. 724-752 ◽  
Author(s):  
Corrine Welt ◽  
Yisrael Sidis ◽  
Henry Keutmann ◽  
Alan Schneyer
Keyword(s):  
Hormone Secretion ◽  
Signal Propagation ◽  
Cellular Level ◽  
Model Systems ◽  
Pituitary Hormone ◽  
New Paradigm ◽  
Activin Signaling ◽  
Physiological Relevance ◽  
Paracrine Growth Factor

It has been 70 years since the name inhibin was used to describe a gonadal factor that negatively regulated pituitary hormone secretion. The majority of this period was required to achieve purification and definitive characterization of inhibin, an event closely followed by identification and characterization of activin and follistatin (FS). In contrast, the last 15–20 years saw a virtual explosion of information regarding the biochemistry, physiology, and biosynthesis of these proteins, as well as identification of activin receptors, and a unique mechanism for FS action—the nearly irreversible binding and neutralization of activin. Many of these discoveries have been previously summarized; therefore, this review will cover the period from the mid 1990s to present, with particular emphasis on emerging themes and recent advances. As the field has matured, recent efforts have focused more on human studies, so the endocrinology of inhibin, activin, and FS in the human is summarized first. Another area receiving significant recent attention is local actions of activin and its regulation by both FS and inhibin. Because activin and FS are produced in many tissues, we chose to focus on a few particular examples with the most extensive experimental support, the pituitary and the developing follicle, although nonreproductive actions of activin and FS are also discussed. At the cellular level, it now seems that activin acts largely as an autocrine and/or paracrine growth factor, similar to other members of the transforming growh factor β superfamily. As we discuss in the next section, its actions are regulated extracellularly by both inhibin and FS. In the final section, intracellular mediators and modulators of activin signaling are reviewed in detail. Many of these are shared with other transforming growh factor β superfamily members as well as unrelated molecules, and in a number of cases, their physiological relevance to activin signal propagation remains to be elucidated. Nevertheless, taken together, recent findings suggest that it may be more appropriate to consider a new paradigm for inhibin, activin, and FS in which activin signaling is regulated extracellularly by both inhibin and FS whereas a number of intracellular proteins act to modulate cellular responses to these activin signals. It is therefore the balance between activin and all of its modulators, rather than the actions of any one component, that determines the final biological outcome. As technology and model systems become more sophisticated in the next few years, it should become possible to test this concept directly to more clearly define the role of activin, inhibin, and FS in reproductive physiology.

5-HT Prolongs Ventral Root Bursting Via Presynaptic Inhibition of Synaptic Activity During Fictive Locomotion in Lamprey

2005 ◽  
Vol 93 (2) ◽  
pp. 980-988 ◽  
Author(s):  
Eric J. Schwartz ◽  
Tatyana Gerachshenko ◽  
Simon Alford
Keyword(s):  
Synaptic Transmission ◽  
Presynaptic Inhibition ◽  
Cellular Level ◽  
Ventral Horn ◽  
Pattern Generation ◽  
Ventral Root ◽  
Synaptic Activity ◽  
Fictive Locomotion ◽  
Cellular Mechanisms ◽  
Bath Application

Locomotor pattern generation is maintained by integration of the intrinsic properties of spinal central pattern generator (CPG) neurons in conjunction with synaptic activity of the neural network. In the lamprey, the spinal locomotor CPG is modulated by 5-HT. On a cellular level, 5-HT presynaptically inhibits synaptic transmission and postsynaptically inhibits a Ca2+-activated K+ current responsible for the slow afterhyperpolarization (sAHP) that follows action potentials in ventral horn neurons. To understand the contribution of these cellular mechanisms to the modulation of the spinal CPG, we have tested the effect of selective 5-HT analogues against fictive locomotion initiated by bath application of N-methyl-d-aspartate (NMDA). We found that the 5-HT1D agonist, L694-247, dramatically prolongs the frequency of ventral root bursting. Furthermore, we show that L694-247 presynaptically inhibits synaptic transmission without altering postsynaptic Ca2+ -activated K+ currents. We also confirm that 5-HT inhibits synaptic transmission at concentrations that modulate locomotion. To examine the mechanism by which selective presynaptic inhibition modulates the frequency of fictive locomotion, we performed voltage- and current-clamp recordings of CPG neurons during locomotion. Our results show that 5-HT decreases glutamatergic synaptic drive within the locomotor CPG during fictive locomotion. Thus we conclude that presynaptic inhibition of neurotransmitter release contributes to 5-HT–mediated modulation of locomotor activity.

The Neural Basis of Escape Behavior in Vertebrates

2020 ◽  
Vol 43 (1) ◽  
pp. 417-439 ◽  
Author(s):  
Tiago Branco ◽  
Peter Redgrave
Keyword(s):  
Neural Circuits ◽  
Escape Behavior ◽  
Building Blocks ◽  
Normative Theory ◽  
Neural Systems ◽  
Adaptive Behaviors ◽  
Neural Basis ◽  
Sensory Stimuli ◽  
Evolutionarily Conserved ◽  
Escape Behaviors

Escape is one of the most studied animal behaviors, and there is a rich normative theory that links threat properties to evasive actions and their timing. The behavioral principles of escape are evolutionarily conserved and rely on elementary computational steps such as classifying sensory stimuli and executing appropriate movements. These are common building blocks of general adaptive behaviors. Here we consider the computational challenges required for escape behaviors to be implemented, discuss possible algorithmic solutions, and review some of the underlying neural circuits and mechanisms. We outline shared neural principles that can be implemented by evolutionarily ancient neural systems to generate escape behavior, to which cortical encephalization has been added to allow for increased sophistication and flexibility in responding to threat.

scholarly journals Wnt signalling at the crossroads of nutritional regulation

2008 ◽  
Vol 416 (2) ◽  
pp. e11-e13 ◽  
Author(s):  
Jaswinder K. Sethi ◽  
Antonio J. Vidal-Puig
Keyword(s):  
Protein Kinase ◽  
Glucose Sensing ◽  
Cellular Level ◽  
Wnt Signalling ◽  
Nutritional Regulation ◽  
Biochemical Journal ◽  
Hexosamine Pathway ◽  
Attractive Therapeutic Target ◽  
Sense And Respond ◽  
Living Organisms

The ability to sense and respond to nutritional cues is among the most fundamental processes that support life in living organisms. At the cellular level, a number of biochemical mechanisms have been proposed to mediate cellular glucose sensing. These include ATP-sensitive potassium channels, AMP-activated protein kinase, activation of PKC (protein kinase C), and flux through the hexosamine pathway. Less well known is how cellularly heterogenous organs couple nutrient availability to prioritization of cell autonomous functions and appropriate growth of the entire organ. Yet what is clear is that when such mechanisms fail or become inappropriately active they can lead to dire consequences such as diabetes, metabolic syndromes, cardiovascular diseases and cancer. In this issue of the Biochemical Journal, Anagnostou and Shepherd report the identification of an important link between cellular glucose sensing and the Wnt/β-catenin signalling pathway in macrophages. Their data strongly indicate that the Wnt/β-catenin pathway of Wnt signalling is responsive to physiological concentrations of nutrients but also suggests that that this system could be inappropriately activated in the diabetic (hyperglycaemic) or other metabolically compromised pathological states. This opens the exciting possibility that organ-selective modulation of Wnt signalling may become an attractive therapeutic target to treat these diseases.

scholarly journals Mechanisms of spreading depolarization in vertebrate and insect central nervous systems

2016 ◽  
Vol 116 (3) ◽  
pp. 1117-1127 ◽  
Author(s):  
Kristin E. Spong ◽  
R. David Andrew ◽  
R. Meldrum Robertson
Keyword(s):  
Locusta Migratoria ◽  
Model Systems ◽  
Control Mechanisms ◽  
Cellular Mechanisms ◽  
Nervous Systems ◽  
Spreading Depolarization ◽  
Metathoracic Ganglion ◽  
Evolutionarily Conserved ◽  
Central Nervous Systems ◽  
The Central Nervous System

Spreading depolarization (SD) is generated in the central nervous systems of both vertebrates and invertebrates. SD manifests as a propagating wave of electrical depression caused by a massive redistribution of ions. Mammalian SD underlies a continuum of human pathologies from migraine to stroke damage, whereas insect SD is associated with environmental stress-induced neural shutdown. The general cellular mechanisms underlying SD seem to be evolutionarily conserved throughout the animal kingdom. In particular, SD in the central nervous system of Locusta migratoria and Drosophila melanogaster has all the hallmarks of mammalian SD. Locust SD is easily induced and monitored within the metathoracic ganglion (MTG) and can be modulated both pharmacologically and by preconditioning treatments. The finding that the fly brain supports repetitive waves of SD is relatively recent but noteworthy, since it provides a genetically tractable model system. Due to the human suffering caused by SD manifestations, elucidating control mechanisms that could ultimately attenuate brain susceptibility is essential. Here we review mechanisms of SD focusing on the similarities between mammalian and insect systems. Additionally we discuss advantages of using invertebrate model systems and propose insect SD as a valuable model for providing new insights to mammalian SD.

scholarly journals Minireview: The Circadian Clockwork of the Suprachiasmatic Nuclei—Analysis of a Cellular Oscillator that Drives Endocrine Rhythms

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5624-5634 ◽  
Author(s):  
Elizabeth S. Maywood ◽  
John S. O’Neill ◽  
Johanna E. Chesham ◽  
Michael H. Hastings
Keyword(s):  
Neural Circuits ◽  
Clock Genes ◽  
Time Base ◽  
Suprachiasmatic Nuclei ◽  
Dark Cycle ◽  
Cellular Mechanisms ◽  
Circadian Control ◽  
Daily Cycles ◽  
Central Clock ◽  
Retinal Afferents

The secretion of hormones is temporally precise and periodic, oscillating over hours, days, and months. The circadian timekeeper within the suprachiasmatic nuclei (SCN) is central to this coordination, modulating the frequency of pulsatile release, maintaining daily cycles of secretion, and defining the time base for longer-term rhythms. This central clock is driven by cell-autonomous, transcriptional/posttranslational feedback loops incorporating Period (Per) and other clock genes. SCN neurons exist, however, within neural circuits, and an unresolved question is how SCN clock cells interact. By monitoring the SCN molecular clockwork using fluorescence and bioluminescence videomicroscopy of organotypic slices from mPer1::GFP and mPer1::luciferase transgenic mice, we show that interneuronal neuropeptidergic signaling via the vasoactive intestinal peptide (VIP)/PACAP2 (VPAC2) receptor for VIP (an abundant SCN neuropeptide) is necessary to maintain both the amplitude and the synchrony of clock cells in the SCN. Acute induction of mPer1 by light is, however, independent of VIP/VPAC2 signaling, demonstrating dissociation between cellular mechanisms mediating circadian control of the clockwork and those mediating its retinally dependent entrainment to the light/dark cycle. The latter likely involves the Ca2+/cAMP response elements of mPer genes, triggered by a MAPK cascade activated by retinal afferents to the SCN. In the absence of VPAC2 signaling, however, this cascade is inappropriately responsive to light during circadian daytime. Hence VPAC2-mediated signaling sustains the SCN cellular clockwork and is necessary both for interneuronal synchronization and appropriate entrainment to the light/dark cycle. In its absence, behavioral and endocrine rhythms are severely compromised.

Autophagy Defects in Skeletal Myopathies

2020 ◽  
Vol 15 (1) ◽  
pp. 261-285 ◽  
Author(s):  
Marta Margeta
Keyword(s):  
Clinical Presentation ◽  
Critical Role ◽  
Lysosomal Degradation ◽  
Cellular Mechanisms ◽  
Biological Stress ◽  
Evolutionarily Conserved ◽  
Different Types ◽  
Muscle Homeostasis ◽  
Catabolic Process ◽  
Cellular Organelles

Autophagy is an evolutionarily conserved catabolic process that targets different types of cytoplasmic cargo (such as bulk cytoplasm, damaged cellular organelles, and misfolded protein aggregates) for lysosomal degradation. Autophagy is activated in response to biological stress and also plays a critical role in the maintenance of normal cellular homeostasis; the latter function is particularly important for the integrity of postmitotic, metabolically active tissues, such as skeletal muscle. Through impairment of muscle homeostasis, autophagy dysfunction contributes to the pathogenesis of many different skeletal myopathies; the observed autophagy defects differ from disease to disease but have been shown to involve all steps of the autophagic cascade (from induction to lysosomal cargo degradation) and to impair both bulk and selective autophagy. To highlight the molecular and cellular mechanisms that are shared among different myopathies with deficient autophagy, these disorders are discussed based on the nature of the underlying autophagic defect rather than etiology or clinical presentation.

scholarly journals Growth dynamics of the Arabidopsis fruit is mediated by cell expansion

2019 ◽  
Vol 116 (50) ◽  
pp. 25333-25342 ◽  
Author(s):  
Juan-José Ripoll ◽  
Mingyuan Zhu ◽  
Stephanie Brocke ◽  
Cindy T. Hon ◽  
Martin F. Yanofsky ◽  
...  
Keyword(s):  
Computational Modeling ◽  
Cell Expansion ◽  
Growth Dynamics ◽  
Spatial Separation ◽  
Cellular Level ◽  
Fruit Growth ◽  
Signaling Cascades ◽  
Comprehensive Understanding ◽  
Cellular Mechanisms ◽  
Plant Reproductive Success

Fruit have evolved a sophisticated tissue and cellular architecture to secure plant reproductive success. Postfertilization growth is perhaps the most dramatic event during fruit morphogenesis. Several studies have proposed that fertilized ovules and developing seeds initiate signaling cascades to coordinate and promote the growth of the accompanying fruit tissues. This dynamic process allows the fruit to conspicuously increase its size and acquire its final shape and means for seed dispersal. All these features are key for plant survival and crop yield. Despite its importance, we lack a high-resolution spatiotemporal map of how postfertilization fruit growth proceeds at the cellular level. In this study, we have combined live imaging, mutant backgrounds in which fertilization can be controlled, and computational modeling to monitor and predict postfertilization fruit growth in Arabidopsis. We have uncovered that, unlike leaves, sepals, or roots, fruit do not exhibit a spatial separation of cell division and expansion domains; instead, there is a separation into temporal stages with fertilization as the trigger for transitioning to cell expansion, which drives postfertilization fruit growth. We quantified the coordination between fertilization and fruit growth by imaging no transmitting tract (ntt) mutants, in which fertilization fails in the bottom half of the fruit. By combining our experimental data with computational modeling, we delineated the mobility properties of the seed-derived signaling cascades promoting growth in the fruit. Our study provides the basis for generating a comprehensive understanding of the molecular and cellular mechanisms governing fruit growth and shape.

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