Cell membrane expansion

Darios, F. and Davletov, B. (2006). Omega-3 and omega-6 fatty acids stimulate cell membrane expansion by acting on syntaxin 3. Nature 440, 813-817. 

The primary site of action is postulated to be the Hpid matrix of cell membranes. The Hpid properties which are said to be altered vary from theory to theory and include enhancing membrane fluidity volume expansion melting of gel phases increasing membrane thickness, surface tension, and lateral surface pressure and encouraging the formation of polar dislocations (10,11). Most theories postulate that changes in the Hpids influence the activities of cmcial membrane proteins such as ion channels. The Hpid theories suffer from an important drawback at clinically used concentrations, the effects of inhalational anesthetics on Hpid bilayers are very small and essentially undetectable (6,12,13). 

In 1954, Mullins, in a modification to the Overton hypothesis, proposed that besides the membrane concentration of the anesthetic, its volume, expressed as its volume fraction (mole fraction X partial molal volume), is important. This reasoning implied that the anesthetic, due to its solubility properties, expands the cell membrane, and that anesthesia occurs when a critical expansion value is reached, at about 0.3-0.5% of the original volume. 

Some local anaesthetics, such as benzocaine, are totally insoluble in water and cannot ionise. Consequently, there is no cation and therefore no Na+ channel block from within the cell. It is suggested that agents, such as benzocaine, which are very lipid-soluble, exert their effect in the phospholipid bilayer of the axon. This is the basis of the membrane expansion theory of local anaesthetic action. It is also possible that they diffuse laterally form the bilayer into the Na+ channel without ever accessing the axoplasm and in effect produce another variety of Na+ channel block. Repetitive depolarisation of a nerve recruits more Na+ channels and maintains them in the open state for a longer period than normal. 

Figure 30.4. Myelinating Schwann cell of PNS. The same Schwann cell is shown unwrapped (top), in longitudinal section (middle), and in cross section (bottom). Note the channels of cytoplasm (Schmidt-Lantermann clefts) and the large expanses of compacted cell membranes (myelin). (These drawings are not to scale.) (From Raine, Morphology of myelin and myelination. In P. Morell (Ed.). Myelin, 2nd ed., Plenum Press, New York, 1984.)...

DPPC is prominent in the lipid bilayer making up the cell membrane and is also a major constituent of lung surfactant ( pulmonary surfactant). The lung membrane resembles a mixed surfactant monolayer at the air/water interface. Since the temperature in a lung is below the critical temperature for DPPC monolayers, the LE-LC transition may be of significance in the continuous compression and expansion loops that this membrane undergoes during respiration. We will say more about this in sec. 3.9. 

These stages occur in the cytoplasm, at the bacterial cell membrane (probably on the cytoplasmic surface), and outside the membrane in the cell wall, respectively. The wall grows by an inside-to-outside mechanism, and new material compensates for loss of outer wall and provides for expansion for cell growth. 

Fig. 7. Reversible trapping of synaptic vesicle membrane in the plasma membrane in reticulospinal synapses. (A) Electron micrograph of a lamprey reticulospinal synapse stimulated with action potentials at 20 Hz for 20 min and then incubated for 90 min in Ca " -free solution with 10 mM EGTA. Note the reduction in the number of synaptic vesicles and the presence of large membrane expansions compared to an unstimulated synapse (inset). (B) Activation of clathrin-mediated endocytosis in reticulospinal synapses by addition of Ca +-containing extracellular solution. Spinal cord preparations were stimulated at 20 Hz for 20 min, incubated for 90 min in Ca -free solution, and then incubated in Ca -containing solution (2.6 mM) for 120 s. Electron micrograph of a synapse shows the appearance of coated pits (arrows) lateral to the active zone. Designations as in Fig. 1. Scale bar, 0.2 p.m. Modified from Gad et al. (1998) Neuron 21 601-616, with permission copyright is held by Cell Press.

Fig. 8. Effects of disruption of endophilin and amphiphysin interactions on clathrin-mediated endocytosis at the reticulospinal synapse. (A) Electron micrograph of the lateral side of the active zone in a control synapse stimulated at 5 Hz. Note the presence of clathrin-coated pits with different shapes. (B) Electron micrograph of the comparable area of a synapse in an axon that was stimulated at 5 Hz for 30 min after injection of endophilin antibodies. Note the pocket-like membrane expansions (arrows) at the margin of the synaptic area and the appearance of numerous shallow coated pits (arrows). (C) A synapse in an axon which was stimulated at 0.2 Hz for 30 min after injection of a fusion protein containing the SH3 domain of amphiphysin linked to GST. Note the accumulation of constricted coated pits around the active zone. Scale bar, 0.2 pm. B, modified from Ringstad et al. (1999), Neuron 24, 143-154, with permission copyright is held by Cell Press. C, modified from Shupliakov et al. (1997a) Science 276 259-263, with permission copyright 1997 AAAS.

Planar supported lipid membranes were first prepared and studied as simplified structural models of cell membranes [4,6, 32], and more recently as biocompatible coatings for sensor transducers and other synthetic materials [33-37], A major advantage of the planar geometry relative to vesicles, and a major contributor to the expansion of this field, is the availability of powerful surface-sensitive analyti-cal/physical techniques. Confining a lipid membrane to the near-surface region of a solid substrate makes it possible to study its structural and functional properties in detail using a variety of techniques such as surface plasmon resonance, AFM, TIRF, attenuated total reflection, and sum frequency vibrational spectroscopy [38 -2]. 

Our initial estimates of molecular transport based on electrical drift should be extended by including convection [e.g., electroosmosis (31)] and diffusion (52). The same general strategy is reasonable A dynamic pore population will be computed, in which electrical interactions are the dominant source of pore creation and expansion. In the case of a pl nar membrane with no osmotic or hydrostatic pressure gradient, the final stages of pore population expansion and collapse should also be governed by purely electrical interactions. By following the pore population over its development, the contribution of each transport mechanism can be estimated. For cell membranes, a nonzero pressure difference will usually exist. In this case, pores of... 

The membrane deformation is calculated from observed macroscopic changes in cell geometry, usually with the use of simple geometric shapes to approximate the cell shape. The membrane force resultants are calculated from force balance relationships. For example, in the determination of the area expansivity modulus of the red cell membrane or the cortical tension in neutrophils, the force resultants in the plane of the membrane of the red cell or the cortex of the white cell are isotropic. In this case, as long as the membrane surface of the cell does not stick to the pipette, the membrane force resultant can be calculated from the law of Laplace ... 

Katnik, C. and Waugh, R. 1990. Alterations of the apparent area expansivity modulus of red blood cell membrane by electric fields. Biophys. J. 57 877-882. 

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