Nerve cell permeability

Calcium ions also regulate nerve cell permeability to sodium and potassium, and in turn affect nerve transmission (48). Further, calcium enhances the release of acetylcholine at the neuromuscular junctions (49). Figure 5 presents a schematic summary of the events... 

The membranes of nerve cells contain well-studied ion channels that are responsible for the action potentials generated across the membrane. The activity of some of these channels is controlled by neurotransmitters hence, channel activity can be regulated. One ion can regulate the activity of the channel of another ion. For example, a decrease of Ca + concentration in the extracellular fluid increases membrane permeability and increases the diffusion of Na+. This depolarizes the membrane and triggers nerve discharge, which may explain the numbness, tinghng, and muscle cramps symptomatic of a low level of plasma Ca. ... 

The electricity-producing system of electric fishes is built as follows. A large number of flat cells (about 0.1 mm thick) are stacked like the flat unit cells connected in series in a battery. Each cell has two membranes facing each other. The membrane potentials of the two membranes compensate for each other. In a state of rest, no electrostatic potential difference can be noticed between the two sides of any cell or, consequently, between the ends of the stack. The ends of nerve cells come up to one of the membranes of each cell. When a nervous impulse is applied from outside, this membrane is excited, its membrane potential changes, and its permeability for ions also changes. Thus, the electrical symmetry of the cell is perturbed and a potential difference of about 0.1 V develops between the two sides. Since nervous impulses are applied simultaneously to one of the membranes in each cell, these small potential differences add up, and an appreciable voltage arises between the ends of the stack. 

Table 3.1 Concentration and Permeability of Ions Responsible for Membrane Potential in a Resting Nerve Cell...

Essentially all nerve cells have one or more projections termed dendrites whose primary function is to receive information from other cells in their vicinity and pass this information on to the cell body. Following the analysis of this information by the nerve cell, bioelectrical changes occur in the nerve membrane that result in the information being passed to the nerve terminal situated at the end of the axon. The change in membrane permeability at the nerve terminal then triggers the release of the neurotransmitter. 

The specific situation we wish to consider is the osmotic equilibrium that develops in an apparatus that has a semipermeable membrane impermeable to the macroion only. That is, the membrane is assumed to be permeable not only to the solvent but also to both of the ions of the low molecular weight electrolyte, but not to the colloidal ion Pz+. At equilibrium the low molecular weight ions will be found on both sides of the membrane, but not in equal concentrations, because of the presence of the macroions on one side of the membrane. We have already come across an example of such a situation in the vignette at the beginning of this chapter on the role of Donnan equilibrium on the so-called resting states of nerve cells. 

Figure 4.10. Overview of nerve impulse transmission in chemical synapses. The action potential in the presynaptic nerve cell induces release of the nemotransmitter (e.g., acetylcholine) into the synaptic cleft. The transmitter binds to its receptor, e.g. the nicotinic acetylcholine receptor (NAR). The NAR is a hgand-gated channel it will open and become permeable to both and Na. This will move the membrane potential toward the average of the two respective equilibrium potentials however, in the process, the firing level of adjacent voltage-gated sodium charmels will be exceeded, and a full action potential will be triggered (inset).

A healthy immune system is able to destroy most antigens. During that time the patient experiences signs of inflammation (see 12.2 Signs of Inflammation). The inflammatory response is brought about by prostaglandins that cause vasodilatation, relax smooth muscles, and make capillaries permeable and sensitize nerve cells within... 

Bone and tooth formation blood clotting, cell permeability nerve stimulation muscle contraction enzyme activation... 

Osmotic pressure water balance acid-based balance nerve stimulation muscle contraction cell permeability... 

The membrane spontaneously becomes less permeable to sodium ions and more permeable to potassium ions. Consequently, potassium ions flow outward, and so the membrane potential returns to a negative value. I he resting level of —60 mV is restored in a few milliseconds as the K conductance decreases to the value characteristic of the unstimulated state. I he wave of depolarization followed by repolarization moves rapidly along a nerve cell. The propagation of these waves allows a touch at the tip of your toe to be detected in your brain in a few milliseconds. 

Pardaxin P-2 is a 33 amino acid peptide isolated from the mucc al secretion of the Pacific sole, Pardachirus pavoninus, that exhibits surfactant properties. Pardaxin has been shown to interfere with ion transport in both epithelium and nerve cells. At concentration below 10 mmol T, pardaxin forms voltage-dependent, ion-permeable channels in artificial liposomes. The structure of pardaxin P2 in aqueous trifluoroethanol solution has been determined using the NOE distance restrained/molecular dynamics method. This study showed that the peptide adopts an amphiphilic helix over residues 7-11, a bend at residues 12-13 and another helix over residues 14-26. 

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