On cell surface deformation during an action potential

The excitation of many cells and tissues is associated with cell mechanical changes. The evidence presented herein corroborates that single cells deform during an action potential (AP). It is demonstrated that excitation of plant cells (Chara braunii internodes) is accompanied by out-of-plane displacements of the cell surface in the micrometer range (1-10 micron). The onset of cellular deformation coincides with the depolarization phase of the AP. The mechanical pulse (i) propagates with the same velocity as the electrical pulse (within experimental accuracy; 10 mm/s), (ii) is reversible, (iii) in most cases of biphasic nature (109 out of 152 experiments) and (iv) presumably independent of actin-myosin-motility. The existence of transient mechanical changes in the cell cortex is confirmed by micropipette aspiration experiments. A theoretical analysis demonstrates that this observation can be explained by a reversible change in the mechanical properties of the cell surface (transmembrane pressure, surface tension and bending rigidity). Taken together, these findings contribute to the ongoing debate about the physical nature of cellular excitability

An acoustically-driven biochip: particle-cell interactions under physiological flow conditions [Abstract]

Introduction: The interaction of particulate drug carriers with cells has generally been assessed in stationary microplate assays. These setups fail to reflect the flow conditions in vivo which generate substantial hydrodynamic drag forces [1]. In order to address this shortcoming, a microfluidic biochip with the capability of imitating a wide range of shear rates and pulsation modes has been developed. This device, which is based on an incorporated surface acoustic wave pump, was used to study the interaction of targeted microparticles with epithelial cells under flow conditions

On the Temperature Behavior of Pulse Propagation and Relaxation in Worms, Nerves and Gels

<div><p>The effect of temperature on pulse propagation in biological systems has been an important field of research. Environmental temperature not only affects a host of physiological processes <i>e.g.</i> in poikilotherms but also provides an experimental means to investigate the thermodynamic phenomenology of nerves and muscle. In the present work, the temperature dependence of blood vessel pulsation velocity and frequency was studied in the annelid <i>Lumbriculus variegatus</i>. The pulse velocity was found to vary linearily between 0°C and 30°C. In contrast, the pulse frequency increased non-linearly in the same temperature range. A heat block ultimately resulted in complete cessation of vessel pulsations at 37.2±2.7°C (lowest: 33°C, highest: 43°C). However, quick cooling of the animal led to restoration of regularly propagating pulses. This experimentally observed phenomenology of pulse propagation and frequency is interpreted without any assumptions about molecules in the excitable membrane (<i>e.g.</i> ion channels) or their temperature-dependent behaviour. By following Einstein’s approach to thermodynamics and diffusion, a relation between relaxation time τ and compressibility κ of the excitable medium is derived that can be tested experimentally (for κ_T ∼ κ_S). Without fitting parameters this theory predicts the temperature dependence of the limiting (<i>i.e.</i> highest) pulse frequency in good agreement with experimental data. The thermodynamic approach presented herein is neither limited to temperature nor to worms nor to living systems. It describes the coupling between pulse propagation and relaxation equally well in nerves and gels. The inherent consistency and universality of the concept underline its potential to explain the dependence of pulse propagation and relaxation on any thermodynamic observable.</p></div

Reversible heat-block of pulse propagation.

<p>Heating of a worm above a critical temperature (average threshold temperature: 37.2±2.7°C; min: 33°C, max: 43°C; number of worms studied = 17) led to cessation of blood vessel pulsations. Regular contractions reappeared upon quick cooling. Illustrated is a typical temperature-frequency response as obtained from a single worm. Dashed lines are guides to the eye.</p

Variation of pulse wave velocity with environmental temperature.

<p>Data was normalized to each individual worm’s pulse propagation velocity at 9.2±0.3°C (average: 0.19±0.05 mm s⁻¹). The black envelopes are guides to the eye. Each data point represents the average of at least 36 measurements. Number of worms studied = 29.</p

Variation of pulse frequency with environmental temperature.

<p>Data was normalized to each individual worm’s pulse frequency at 9.3±0.7°C (average: 4.4±0.8 beats min⁻¹). The black envelopes are guides to the eye. Each data point represents the average of six measurements. Number of worms studied = 68.</p

Study of pulse wave propagation in <i>Lumbriculus variegatus</i>.

<p>(<b>A</b>) Cross-sectional view of a <i>Lumbriculus</i> segment with intestine (I), ventral nerve chord (VNC), ventral (VBV) and dorsal blood vessel (DBV). The latter are partially connected by lateral vessels (LV). (<b>B</b>) A blackworm is aspirated into a buffer-filled glass capillary (WIC) and subsequently submersed in a temperature-controlled petri dish (TEMP). (<b>C</b>) Top view of WIC with the DBV (light-gray structure in the center) and a propagating pulse wave (arrow).</p

Lipid Membrane State Change by Catalytic Protonation and the Implications for Synaptic Transmission

In cholinergic synapses, the neurotransmitter acetylcholine (ACh) is rapidly hydrolyzed by esterases to choline and acetic acid (AH). It is believed that this reaction serves the purpose of deactivating ACh once it has exerted its effect on a receptor protein (AChR). The protons liberated in this reaction, however, may by themselves excite the postsynaptic membrane. Herein, we investigated the response of cell membrane models made from phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidic acid (PA) to ACh in the presence and absence of acetylcholinesterase (AChE). Without a catalyst, there were no significant effects of ACh on the membrane state (lateral pressure change &le;0.5 mN/m). In contrast, strong responses were observed in membranes made from PS and PA when ACh was applied in presence of AChE (&gt;5 mN/m). Control experiments demonstrated that this effect was due to the protonation of lipid headgroups, which is maximal at the pK (for PS: pKCOOH&asymp;5.0; for PA: pKHPO4&minus;&asymp;8.5). These findings are physiologically relevant, because both of these lipids are present in postsynaptic membranes. Furthermore, we discussed evidence which suggests that AChR assembles a lipid-protein interface that is proton-sensitive in the vicinity of pH 7.5. Such a membrane could be excited by hydrolysis of micromolar amounts of ACh. Based on these results, we proposed that cholinergic transmission is due to postsynaptic membrane protonation. Our model will be falsified if cholinergic membranes do not respond to acidification