The consideration of neurons as coupled mechanical-electrophysiological systems is supported by a growing body of experimental evidence, including observations that cell membranes mechanically deform during the propagation of an action potential. However, the short-term (seconds to minutes) influence of membrane voltage on the mechanical properties of a neuron at the single-cell level remains unknown. Here, we use microscale dynamic mechanical analysis to demonstrate that changes in membrane potential induce changes in the mechanical properties of individual neurons. We simultaneously measured the membrane potential and mechanical properties of individual neurons through a multiphysics single-cell setup. Membrane voltage of a single neuron was measured through whole-cell patch clamp. The mechanical properties of the same neuron were measured through a nanoindenter, which applied a dynamic indentation to the neuron at different frequencies. Neuronal storage and loss moduli were lower for positive voltages than negative voltages. The observed effects of membrane voltage on neuron mechanics could be due to piezoelectric or flexoelectric effects and altered ion distributions under the applied voltage. Such effects could change cell mechanics by changing the intermolecular interactions between ions and the various biomolecules within the membrane and cytoskeleton.

Osteoarthritis (OA) is the most common joint disease. In the last years, the research community has focused on understanding the molecular mechanisms that led to the pathogenesis of the disease, trying to identify different molecular and clinical phenotypes along with the discovery of new therapeutic opportunities. Different types of cell-to-cell communication mechanisms have been proposed to contribute to OA progression, including mechanisms mediated by connexin43 (Cx43) channels or by small extracellular vesicles. Furthermore, changes in the chondrocyte phenotype such as cellular senescence have been proposed as new contributors of the OA progression, changing the paradigm of the disease. The use of different drugs able to restore chondrocyte phenotype, to reduce cellular senescence and senescence-associated secretory phenotype components, and to modulate ion channel activity or Cx43 appears to be promising therapeutic strategies for the different types of OA. In this review, we aim to summarize the current knowledge in OA phenotypes related with aging and tissue damage and the new therapeutic opportunities currently available.

The delivery of pulsed electric fields to biological cells for regenerative research and therapeutic applications is a field that has been widely explored. Picosecond pulsed electric fields have been shown to induce intracellular effects and directly target cell membrane proteins as well as being able to induce cell permeabilization and death by apoptosis. Additionally, ultrashort pulses can be focused and delivered in a noncontact manner for possible targeting of deep and inaccessible tissues. The unique characteristics of picosecond pulses make them a possible approach for treatment of Huntington's and Alzheimer's diseases, both characterized by progressive neuronal degeneration and death, and presence of intracellular and extracellular protein aggregates. In this study, the defining characteristics of picosecond pulses and neurodegenerative diseases are reviewed, and a description of how picosecond pulsed electric fields can be applied to disrupt protein aggregates, can target neural stem cell differentiation, and can be delivered to neurological tissue is provided.

Background: Voltage-gated sodium channels (VGSCs) are upregulated during cancer progression and promote metastatic cell behaviors. In contrast, voltage-gated potassium channels (VGPCs) that control proliferation, among other roles, are downregulated. In this study, we tested the effects of blocking VGPCs on the Matrigel invasiveness specifically of strongly metastatic cancer cells. Materials and Methods: The rat prostate cancer Mat-LyLu cell line and the human breast cancer MDA-MB-231 cell line, both strongly metastatic and expressing functional VGSCs, were adopted as models. Matrigel invasion assays and patch-clamp electrophysiology were used to monitor pharmacological effects of VGPC blockage. Results: Margatoxin (MGTX) significantly suppressed the outward currents in Mat-LyLu cells, consistent with K v 1.3 being the predominant VGPC in these cells. For the MDA-MB-231 cells, 4-aminopyridine (4-AP) was used as a general blocker of VGPCs. Treatment with the respective blocker significantly increased the cellular invasiveness under conditions wherein proliferative activity was not affected. As expected, invasiveness was reduced by treating the cells with the VGSC blocker tetrodotoxin (TTX). Importantly, the proinvasive effect of MGTX was suppressed completely by cotreating the MDA-MB-231 cells with TTX. Conclusions: (1) VGPC blockage promotes invasiveness in strongly metastatic carcinoma cell lines and this is associated with functional VGSC expression well known to occur in such cells. (2) The available data taken together are supportive of the Celex Hypothesis, proposing that the electrical excitability of cancer cells (resulting from functional VGSC upregulation and concomitant VGPC downregulation) promotes metastatic invasiveness.

BioelectricityVol. 2, No. 4 Bioelectricity BuzzRecent Bioelectricity-Related Articles Selected by Ann M. Rajnicek, Media Editor of BioelectricityAnn M. RajnicekAnn M. RajnicekAnn M. Rajnicek, BS, PhD, FRSB, Institute of Medical Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, AB25 2ZD Aberdeen, Scotland, Media Editor, Bioelectricity E-mail Address: a.m.rajnicek@abdn.ac.ukSearch for more papers by this authorPublished Online:16 Dec 2020https://doi.org/10.1089/bioe.2020.0049AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View articleFiguresReferencesRelatedDetails Volume 2Issue 4Dec 2020 InformationCopyright 2020, Mary Ann Liebert, Inc., publishersTo cite this article:Ann M. Rajnicek.Recent Bioelectricity-Related Articles Selected by Ann M. Rajnicek, Media Editor of Bioelectricity.Bioelectricity.Dec 2020.405-410.http://doi.org/10.1089/bioe.2020.0049Published in Volume: 2 Issue 4: December 16, 2020Online Ahead of Print:December 3, 2020PDF download

BioelectricityVol. 2, No. 3 Book ReviewWhat Is Life? By Paul NurseMustafa B.A. DjamgozMustafa B.A. DjamgozAddress correspondence to: Mustafa B.A. Djamgoz, PhD, Department of Life Sciences, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, London SW7 2AZ, United Kingdom E-mail Address: m.djamgoz@imperial.ac.ukDepartment of Life Sciences, Imperial College London, London, United Kingdom.Search for more papers by this authorPublished Online:16 Sep 2020https://doi.org/10.1089/bioe.2020.0038AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View article"What Is Life? By Paul Nurse." Bioelectricity, 2(3), pp. 314–315FiguresReferencesRelatedDetails Volume 2Issue 3Sep 2020 InformationCopyright 2020, Mary Ann Liebert, Inc., publishersTo cite this article:Mustafa B.A. Djamgoz.What Is Life? By Paul Nurse.Bioelectricity.Sep 2020.314-315.http://doi.org/10.1089/bioe.2020.0038Published in Volume: 2 Issue 3: September 16, 2020Online Ahead of Print:September 3, 2020PDF download

Background:Pulsed electric field has been widely used to facilitate molecular cargo transfer into cells. However, the cell viability is often decreased when trying to increase the electrotransfer efficiency. We hypothesize that the decrease is due to electropermeabilization of cell membrane that disrupts homeostasis of intracellular microenvironment. Thus, a reduction in the membrane permeabilization may increase the cell viability.Materials and Methods:Different compounds were supplemented into the pulsing buffer prior to electrotransfer for reduction of cell membrane damage. Extent of the damage was quantified by leakiness of the membrane to a fluorescent dye, calcein, preloaded into cells. At 24 hours post electrotransfer, cell viability and electrotransfer efficiency were quantified with flow cytometry.Results:The cell viability could be substantially increased by supplementation of either type B gelatin or bovine serum albumin (BSA), without compromising the electrotransfer efficiency. The supplementation also decreased the amount of calcein leaking out of the cells, suggesting that the improvement in cell viability was due to the reduction in electrotransfer-induced membrane damage.Conclusion:Data from the study demonstrate that type B gelatin and BSA can be used as inexpensive supplements for improving cell viability in electrotransfer.