Simultaneous mapping of nanoscale topography and surface potential of charged surfaces by scanning ion conductance microscopy

Nanoscale ◽  
2020 ◽  
Vol 12 (40) ◽  
pp. 20737-20748
Author(s):  
Feng Chen ◽  
Namuna Panday ◽  
Xiaoshuang Li ◽  
Tao Ma ◽  
Jing Guo ◽  
...  

Simultaneous mapping of nanoscale topography and surface potential of soft, rough and heterogeneously charged surfaces under physiological conditions.

Nanoscale ◽  
2021 ◽  
Author(s):  
Feng Chen ◽  
Jin He ◽  
Prakash Manandhar ◽  
Yizi Yang ◽  
Peidang Liu ◽  
...  

The distribution of surface charge and potential of cell membrane plays an indispensable role in cellular activities. However, probing surface charge of live cells in physiological conditions, until recently, remains...


2021 ◽  
Vol 11 (12) ◽  
pp. 5689
Author(s):  
Martina Gruening ◽  
Jonathan E. Dawson ◽  
Christian Voelkner ◽  
Sven Neuber ◽  
Katja Fricke ◽  
...  

Surface charges at the cell–biomaterial interface are known to determine cellular functions. Previous findings on cell signaling indicate that osteoblastic cells favor certain moderately positive surface charges, whereas highly positive charges are not tolerated. In this study, we aimed to gain deeper insights into the influence exerted by surface charges on the actin cytoskeleton and the cell shape. We analyzed surfaces with a negative, moderately positive, and highly positive zeta (ζ) potential: titanium (Ti), Ti with plasma polymerized allylamine (PPAAm), and Ti with a polydiallyldimethylammonium chloride (PDADMA) multilayer, respectively. We used the software FilaQuant for automatic actin filament quantification of osteoblastic MG-63s, analyzed the cell edge height with scanning ion conductance microscopy (SICM), and described the cellular shape via a mathematical vertex model. A significant enhancement of actin filament formation was achieved on moderately positive (+7 mV) compared with negative ζ-potentials (−87 mV). A hampered cell spreading was reflected in a diminished actin filament number and length on highly positively charged surfaces (+50 mV). Mathematical simulations suggested that in these cells, cortical tension forces dominate the cell–substrate adhesion forces. Our findings present new insights into the impact of surface charges on the overall cell shape and even intracellular structures.


The Analyst ◽  
2018 ◽  
Vol 143 (5) ◽  
pp. 1087-1093 ◽  
Author(s):  
Cheng Zhu ◽  
Wenqing Shi ◽  
David L. Daleke ◽  
Lane A. Baker

Scanning ion conductance microscopy (SICM) is an ideal method to study dynamic phospholipid-induced morphological changes of RBCs in physiological conditions.


2021 ◽  
Vol 27 (S1) ◽  
pp. 500-502
Author(s):  
Oleg Suchalko ◽  
Roman Timoshenko ◽  
Alexander Vaneev ◽  
Vasilii Kolmogorov ◽  
Nikita Savin ◽  
...  

2013 ◽  
Vol 104 (2) ◽  
pp. 317a
Author(s):  
Yusuke Mizutani ◽  
Zen Ishikura ◽  
Myung-Hoon Choi ◽  
Sang-Joon Cho ◽  
Takaharu Okajima

2017 ◽  
Vol 114 (9) ◽  
pp. 2395-2400 ◽  
Author(s):  
Umesh Vivekananda ◽  
Pavel Novak ◽  
Oscar D. Bello ◽  
Yuri E. Korchev ◽  
Shyam S. Krishnakumar ◽  
...  

Although action potentials propagate along axons in an all-or-none manner, subthreshold membrane potential fluctuations at the soma affect neurotransmitter release from synaptic boutons. An important mechanism underlying analog–digital modulation is depolarization-mediated inactivation of presynaptic Kv1-family potassium channels, leading to action potential broadening and increased calcium influx. Previous studies have relied heavily on recordings from blebs formed after axon transection, which may exaggerate the passive propagation of somatic depolarization. We recorded instead from small boutons supplied by intact axons identified with scanning ion conductance microscopy in primary hippocampal cultures and asked how distinct potassium channels interact in determining the basal spike width and its modulation by subthreshold somatic depolarization. Pharmacological or genetic deletion of Kv1.1 broadened presynaptic spikes without preventing further prolongation by brief depolarizing somatic prepulses. A heterozygous mouse model of episodic ataxia type 1 harboring a dominant Kv1.1 mutation had a similar broadening effect on basal spike shape as deletion of Kv1.1; however, spike modulation by somatic prepulses was abolished. These results argue that the Kv1.1 subunit is not necessary for subthreshold modulation of spike width. However, a disease-associated mutant subunit prevents the interplay of analog and digital transmission, possibly by disrupting the normal stoichiometry of presynaptic potassium channels.


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