The Journal of Physiology publishes research in all areas of physiology and pathophysiology that illustrates new physiological principles, mechanisms or premises. Papers on work at the molecular level, cell membrane, single cells, tissues or organs, and on systems physiology are all encouraged. We are particularly keen on research that has a clinical or translational focus, to help further our understanding of the role physiology plays in health and disease.

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Inhibitory actions of melanin‐concentrating hormone in the lateral septum

  •  14 June 2024

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Abstract figure legend Melanin-concentrating hormone (MCH) neurons (blue) project to the lateral septum (LS) where they overlapped with the expression of MCH receptors (MCHR1) at the ventrolateral LS region (red). MCHR1 activation at LS cells elicited a protein-kinase C-dependent chloride conductance at GABAA receptors that hyperpolarized LS cells.

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Issue Information

  •  2675-2676
  •  13 June 2024
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Ion channel signalling mechanisms in physiology and disease

  •  12 June 2024
No abstract is available for this article.

Short‐term aerobic exercise prevents development of glucocorticoid myopathic features in aged skeletal muscle in a sex‐dependent manner

  •  11 June 2024

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Abstract figure legend Daily 1 mg/kg dexamethasone (DEX) treatment in 24-month-old female and male mice results in sexually dimorphic effects on skeletal muscle physiology. Short-term treadmill exercise mitigates the DEX-induced myopathic features in a sex-dependent manner. DEX-treated aged female mice expressed greater sub-tetanic contractility without an influence of exercise. Exercise protected against DEX-induced fatigue and losses in muscle mass and soluble protein content in aged females. DEX treatment in aged male mice resulted in a prolonged tetanic half-relaxation time, increased fatigue and losses in soluble protein content, which were not affected by exercise.

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The mitochondrial calcium uniporter: Balancing tumourigenic and anti‐tumourigenic responses

  •  10 June 2024

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Abstract figure legend A solid tumour schematic is shown on the right, highlighting enhanced or suppressed mitochondrial Ca2+ uptake in cancer. Enhanced mitochondrial Ca2+ uniporter complex (mtCU)-mediated Ca2+ uptake (top) is implicated in colorectal cancer, breast cancer, oral squamous cell carcinoma, pancreatic cancer, hepatocellular carcinoma and embryonal rhabdomyosarcoma. Decreased mtCU-mediated mitochondrial Ca2+ uptake (bottom) has been associated with melanoma but remains uncharacterized in glioblastoma. The mitochondrion shown above the tumour depicts enhanced mitochondrial Ca2+ uptake as a result of mtCU channels comprised of 3 × mitochondrial Ca2+ uniporter (MCU) (teal):1 × MCU dominant-negative beta (MCUb) (violet):2 ×  essential MCU regulator (EMRE) (beige):1 ×  mitochondrial Ca2+ uptake (MICU)1 (green):1 × MICU2 (pink) subunits, with Ca2+ ions shown in grey. The mitochondrion shown below the tumour depicts suppressed mitochondrial Ca2+ uptake as a result of mtCU channels comprised of 1 × MCU (teal):3 × MCUb (violet) subunits. The dysregulated oncogenic/anti-oncogenic microRNAs (miRNAs), small-molecule inhibitors and post-translational modifications correlated with mtCU-mediated mitochondrial Ca2+ dysfunction are indicated as future avenues and considerations for therapeutic intervention. Created with BioRender.com.

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Sex disparities of human neuromuscular decline in older humans

  •  10 June 2024

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Abstract figure legend Intramuscular electromyography applied to the vastus lateralis of older males (pink) and females (purple) during low- and mid-level voluntary contractions reveal higher motor unit firing rates in females. In both sexes the decline of neuromuscular from early to late elderly follow similar trajectories yet is consistently higher in males.

Renal handling of albumin in rats with early stage diabetes: A theoretical analysis

  •  10 June 2024

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Abstract figure legend In early-stage diabetes, several changes in renal tubular function impact the urinary excretion of albumin. Our computational model of albumin handing in the rat proximal tubule (PT) predicts that decreased abundance of albumin receptors markedly lowers endocytic uptake capacity and raises albumin excretion, whereas increases in PT diameter and length exert similarly large, but opposite effects. The elevated glomerular filtration rate increases albumin filtration, and the resulting increase in tubular flow reduces fractional albumin uptake (as a result of a shorter residence time), thereby significantly raising albumin excretion. By contrast, our simulations suggest that glucose-elicited osmotic diuresis per se raises tubular flow and albumin excretion only slightly. The residence time effects of high flow are partially counterbalanced by shear stress-induced stimulation of endocytosis (not shown).

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More than the clock: distinct regulation of muscle function and metabolism by PER2 and RORα

  •  8 June 2024

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Abstract figure legend This study evaluates the functional and molecular consequences of modulating different regulatory loops of the muscle-intrinsic clock, through extensive phenotypic, transcriptomic, proteomic and metabolomic profiling of the muscle around the clock. Overall, deletion of PER2 and RORα and, as a proxy, modulation of the primary or secondary feedback arms, leads to shared but distinct outcomes in terms of the transcriptome, proteome and phenotype. Perturbations of both the primary (PER2 MKO) and secondary arms (RORα MKO) of the core clock dampen the amplitude of expression of many clock and clock-associated genes but do not affect their phase, thereby maintaining basic circadian oscillation in the muscle. The deletion of PER2 and RORα affects muscle metabolism and homeostasis in a circadian manner, through modulation of metabolic and mitochondrial genes, which encode proteins involved in amino acid metabolism, the tricarboxylic acid (TCA) cycle and mitochondrial biogenesis, thereby affecting amino acid and ion homeostasis. As a result, glucose and lipid metabolism, in addition to amino acid metabolism, are impacted in these knockouts, highlighting the central role of the molecular clock in modulating muscle plasticity. ATP: adenosine triphosphate, ETC: electron transport chain.

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Bayliss Starling Prize Lecture 2023: Neuropeptide‐Y being ‘unsympathetic’ to the broken hearted

  •  7 June 2024

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Abstract figure legend The hallmark of cardiac disease is autonomic dysregulation, characterised by a state of chronic sympathoexcitation. Neuropeptide-Y (NPY) is a sympathetic co-transmitter that is released by sympathetic neurons and circulating venous levels are elevated in a range of cardiac disease, such as myocardial infarction and chronic heart failure. NPY has direct effects on cardiomyocytes, vascular smooth muscle cells and autonomic nerves through its Y receptors, resulting in adverse cardiac remodelling, pro-arrhythmic electrophysiological changes, vasoconstriction and parasympathetic inhibition. Large prospective cohort studies have demonstrated that these effects ultimately lead to adverse cardiac events and increased mortality in patients. An understanding of the role of co-transmitters such as NPY may ultimately lead to novel therapeutic targets and biomarkers to improve risk stratification and prognostication in patients with cardiac disease.

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