J Comp Physiol B

[Abbie Buesing]

Journalof Comparative Physiology B publishes peer-reviewed original and review articles on the comparative physiology of invertebrate and vertebrate animals.Places special emphasis on integrative studies at various biological levels.Highlights adaptation and evolutionary aspects of physiology.Covers a broad range of physiological interests including metabolism, respiration, and exercise physiology.Reports on the current state of knowledge in comparative physiology and future research directions.

The Journal of Comparative Physiology A is dedicated to enhancing our understanding of physiological mechanisms at organismic, cellular, and molecular levels.Research disciplines covered include neuroethology, sensory physiology, neurophysiology, functional neuroanatomy, neuroendocrinology, and computational neuroscience.Publishes original papers, short communications, review and review-history articles, perspectives, obituaries, and book reviews.Color figures are included free in both print and online versions.There are no page charges for publication.

Have you ever wondered whether reviewers suggested during submission increase the chances to get your manuscript accepted for publication? Or have you suspected that the friend you recently suggested as a reviewer was actually a foe who recommended rejection of your paper?

If the answer is YES to either of these questions, then you should read the following editorial by Gnther K.H. Zupanc, Editor-in-Chief of the Journal of Comparative Physiology A:

Suggested Reviewers: Friends or Foes?

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Inhibition of the renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in treatment of chronic kidney diseases (CKD). However, reversal of the course of CKD or at least long-term stabilization of renal function are often difficult to achieve, and many patients still progress to end-stage renal disease. New treatments are needed to enhance protective actions of RAAS inhibitors (RAASis), such as angiotensin-converting enzyme (ACE) inhibitors (ACEIs) or angiotensin receptor blockers (ARBs), and improve prognosis in CKD patients. Inhibition of endothelin (ET) system in combination with established RAASis may represent such an approach. There are complex interactions between both systems and similarities in their renal physiological and pathophysiological actions that provide theoretical rationale for combined inhibition. This view is supported by some experimental studies in models of both diabetic and nondiabetic CKD showing that a combination of RAASis with ET receptor antagonists (ERAs) ameliorate proteinuria, renal structural changes, and molecular markers of glomerulosclerosis, renal fibrosis, or inflammation more effectively than RAASis or ERAs alone. Practically all clinical studies exploring the effects of RAASis and ERAs combination in nephroprotection have thus far applied add-on designs, in which an ERA is added to baseline treatment with ACEIs or ARBs. These studies, conducted mostly in patients with diabetic nephropathy, have shown that ERAs effectively reduce residual proteinuria in patients with baseline RAASis treatment. Long-term studies are currently being conducted to determine whether promising antiproteinuric effects of the dual blockade will be translated in long-term nephroprotection with acceptable safety profile.

Modified muscle use or injury can produce a stereotypic inflammatory response in which neutrophils rapidly invade, followed by macrophages. This inflammatory response coincides with muscle repair, regeneration, and growth, which involve activation and proliferation of satellite cells, followed by their terminal differentiation. Recent investigations have begun to explore the relationship between inflammatory cell functions and skeletal muscle injury and repair by using genetically modified animal models, antibody depletions of specific inflammatory cell populations, or expression profiling of inflamed muscle after injury. These studies have contributed to a complex picture in which inflammatory cells promote both injury and repair, through the combined actions of free radicals, growth factors, and chemokines. In this review, recent discoveries concerning the interactions between skeletal muscle and inflammatory cells are presented. New findings clearly show a role for neutrophils in promoting muscle damage soon after muscle injury or modified use. No direct evidence is yet available to show that neutrophils play a beneficial role in muscle repair or regeneration. Macrophages have also been shown capable of promoting muscle damage in vivo and in vitro through the release of free radicals, although other findings indicate that they may also play a role in muscle repair and regeneration through growth factors and cytokine-mediated signaling. However, this role for macrophages in muscle regeneration is still not definitive; other cells present in muscle can also produce the potentially regenerative factors, and it remains to be proven whether macrophage-derived factors are essential for muscle repair or regeneration in vivo. New evidence also shows that muscle cells can release positive and negative regulators of inflammatory cell invasion, and thereby play an active role in modulating the inflammatory process. In particular, muscle-derived nitric oxide can inhibit inflammatory cell invasion of healthy muscle and protect muscle from lysis by inflammatory cells in vivo and in vitro. On the other hand, muscle-derived cytokines can signal for inflammatory cell invasion, at least in vitro. The immediate challenge for advancing our current understanding of the relationships between muscle and inflammatory cells during muscle injury and repair is to place what has been learned in vitro into the complex and dynamic in vivo environment.

Neurophysiological and behavioral measures were obtained from 32 senescent (28--34 mo) and 32 mature adult (10--16 mo) rats. Extracellularly recorded synaptic responses were obtained from electrodes chronically implanted in the fascia dentata and perforant path. The rats were first tested on a circular platform, which favored the use of spatial cues for its solution, and the senescent rats were shown to exhibit poorer memory for the rewarded place. When granule cell synaptic responses were recorded after a single session of very brief high-frequency stimulation, the amount of elevation and time course of decline were equivalent between age groups. Af ter three repetitions, however, the young rats maintained the increased synaptic strength for at least 14 days, whereas the old rats declined after the first session. The amount of synaptic enhancement was statistically correlated with the ability to perform the circular platform task both within and between groups. Furthermore, the aftereffects of the high-frequency stimulation selectively impaired the old rats' spontaneous alternation behavior on a T-maze. Certain other neurophysiological and electroencephalographic measures did not distinguish between age groups. The results are discussed in terms of the synaptic theory of memory formation and of their relevance to the aging process.

This brief review summarizes features of the zebrafish, Danio rerio, that make it a suitable model organism for studies of regulatory physiology. The review presents the argument that random mutagenesis screens are a valuable gene-finding strategy to identify genes of functional importance and that their utility, although well established for developmental issues, will extend to a variety of topics of interest to the regulatory physiologist. Particular attention is drawn to the range of functional responses amenable to mutagenesis screens in larval zebrafish. Other virtues of the organism, the range of genomic tools, the potential for innovative optical methods, and the tractability for genetic and other experimental manipulations, are also described. Finally, the review provides examples of functional studies in zebrafish, including studies in sensory neurons, cardiac rhythm disturbances, gastrointestinal function, and studies of the developing kidney, that illustrate potential applications. Because of the relative ease with which combinatorial studies can be performed, the zebrafish may eventually be particularly valuable in understanding the functional interaction between subtle gene defects that cause polygenic disorders.

Neural, hormonal, and genetic regulation of cellular oxidative metabolism, energy balance, obesity, and thermogenesis. Extracellular signal reception/intracellular signal transduction and uncoupling proteins; physiological changes with obesity/aging.

Mikhailova, A, J Mack, N Vitagliano, JS Hamilton, JM Horowitz, BA Horwitz. Recovery of Syrian hamster hippocampal signaling following its depression during oxygen-glucose deprivation is enhanced by cold temperatures and by hibernation. Neurosci Lett 621:98-103, 2016.

Cell model of a Principal cell Aldosterone modulates ENaC in these cells by first affecting gene expression through the mineralocorticoid receptor and inducing expression of the Ki-Ras and Sgk signaling proteins, which then signal to ENaC to modulate ion channel activity. My laboratory uses a number of contemporary methodologies, including electrophysiology, molecular biology, biochemistry, genomics and proteomics, and fluorescence microscopy to investigate regulation of ENaC and aldosterone signaling. We routinely use yeast, bacteria, immortalized cell lines and animals in this regard. Our lab is equipped to perform real-time measurement of ion channel activity and fluorescence imaging, and performs biophysical analysis of ion channel activity and gating, creates point mutations and chimeric proteins and genes, investigates cellular signal transduction, reconstitutes signaling pathways in heterologous systems, and determines the molecular mechanisms modulating gene expression, and uses the power of yeast genetics in addition to immortalized mammalian cells to investigate ENaC targeting and regulation. The pictures below give some idea of the methods we employ. Flourescence Microscopy Targeting ENaC to different cellular locales. Fusion proteins were created by tagging the cytosolic domains of ENaC with GFP. Cellular localization was determined in a heterologous system by overexpressing these chimeric fusion proteins. Electrophysiology Single channel current recordings for ENaC in cell attached patches. A. ENaC activity in the presence of aldosterone is marked by long open states (downward deflections). B. The frequency of long openings in the presence of aldosterone can be decreased by pre-treating cells with inhibitors of Ki-Ras. C. This maneuver also leads to the shortening of openings. Molecular biology Idealized schematic showing one way that we test the molecular basis for modulation of gene expression by aldosterone. Two reporter constructs are challenged with aldosterone. Only the one containing the aldosterone-responsive DNA segment respond to hormonal treatment with increased expression of luciferase.

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