Nerve cell Potential, spike

Fig. 6.24 A hypothetic scheme of the time behaviour of the spike linked to the opening and closing of sodium and potassium channels. After longer time intervals a temporary hyperpolarization of the membrane is induced by reversed transport of potassium ions inside the nerve cell. Nernst potentials for Na+ and K+ are also indicated in the figure. 

The structure of a nerve is not simple. In the following account, the stress is upon a single aspect of the mechanism of the action of a nerve, the origin of the spike potential in sections of the nerve called nodes in which the axon is in contact on the outside with the extracellular fluids. The relevant properties of a nerve cell free of a myelin sheath can be seen in Table 14.1. 

Section (4) refers to the restrictions imposed on cation movement by membranes. The relative ease of movement of potassium through a nerve membrane at rest generates a potassium potential. Imposition of a perturbation upon the membrane changes its properties so that it is more permeable to sodium, and the activated membrane shows a sodium potential of reversed sign to the potassium potential. Thereupon a self-propagating spike of depolarization which is rapidly followed by recovery to the rest state fiows along the nerve cell and is the nerve message. 

Although phosphatidylserine is in general asymmetrically distributed in cell membranes with the bulk of this lipid in the cytoplasmic leaflet of the bilayer, some phosphatidylserine appears to reside in the outer lipid monolayer of the axonal membrane. Furthermore, this phosphatidylserine is involved in the nerve action potential. Treatment of an axon with extracellular serine decarboxylase converts phosphatidylserine to -ethanolamine, which results in a decrease in the action potential spike height. Catalysis of the reversed reaction by this enzyme in the presence of excess L-serine converts phosphatidylethanolamine to -serine. This produces an average of 28% increase in the action potential amplitude. It is worth noticing that several anaesthetic compounds have been shown to bind phosphatidylserine in vitroThe role of phosphatidylserine phase behavior in the nerve action potential will be discussed in somewhat more detail in Section 7. 

When the nerve cell is stimulated, certain channels in the membrane open, allowing Na" ions to rush into the cell and causing the potential to temporarily rise to about +30 mV (Figure 18.13 t). Other channels that allow K ions to rush out of the cell open in turn, bringing the potential back down to near its resting potential. The result is a spike in the electrochemical potential across the membrane, which provides the... 

A FIGURE 18.14 Potential Changes across the Nerve Cell Membrane The changes in ion concentrations that take place when a nerve cell is stimulated result in a spike in the electrochemical potential across the membrane. 

Stimulation or inhibition of autonomic effector cells by ACh results from interaction of ACh with muscarinic ACh receptors. In this case, the effector is coupled to the receptor by a G protein (see Chapter 1). In contrast to skeletal muscle and neurons, smooth muscle and the cardiac conduction system (sinoatrial [SA] node, atrium, atrioventricular [AV] node, and the His-Purkinje system) normally exhibit intrinsic activity, both electrical and mechanical, that is modulated but not initiated by nerve impulses. At some smooth muscle, ACh causes a decrease in the resting potential (i.e., the membrane potential becomes less negative) and an increase in the frequency of spike production, accompanied by a rise in tension. A primary action of ACh in initiating these effects through muscarinic receptors is probably partial depolarization of the cell membrane brought about by an increase in Na and, in some instances, Ca conductance activation of muscarinic receptors can also activate the G -PLC-IP pathway leading to the mobilization of stored Ccf. Hence, ACh stimulates ion fluxes across membranes and/or mobilizes intracellular Ca to cause contraction. 

The waveform of the oscillations predicted by the model for cytosolic Ca (fig. 9.7) resembles that of the spikes observed for a number of cells stimulated by external signals. In particular, the rise in cytosolic Ca is preceded by a rapid acceleration that starts from the basal level although it originates from a different, nonelectrical mechanism, this pattern, which is reminiscent of the pacemaker potential that triggers autonomous spiking in nerve and cardiac cells (DiFrancesco, 1993), has been observed (Jacob et al, 1988) in epithelial cells stimulated by histamine (see fig. 9.3). As in the model by Meyer Stryer (1988), the oscillations of Ca " in the intracellular store have a saw-tooth appearance (see the dashed ctirve in fig. 9.7). Here, however, the phenomenon does... 

The central nerv ous system of insects consists essentially of a double nerve cord situated ventrally and punctuated by segmental ganglia from which the peripheral ner es arise. The axon of such a nerve measures up to 10 /xm in diameter and is enclosed in a thin non-myelinated lipoprotein sheath. These axons are bundled into nerves which are surrounded by dove-tailed layers of neuroglial cells, and the whole is enclosed by a protein lamella. The polarization of a resting nerve is very similar to that of vertebrate nerve (see Section 7.5.1). On electrical stimulation, successive spikes can be obtained at intervals of a millisecond but the action potentials are propagated only at about 2 m s , i.e. some 50 times slower than in the larger myelinated axons of vertebrates. 

Tetrodotoxin (TTX) is a good example of a compound that has recently assumed a prominent rdle in biophysical investigations of nerve and muscle function it selectively prevents the opening of membrane channels for Na-ions that would normally occur during depolarization. TTX has become an important tool in the dissection of the excitation process of electrically excitable cell-membranes into phases involving separate and successive activation of ion-selective channels. Use of TTX has already helped establish that there are many types of nerve and muscle cells in which spike potentials are not accompanied by an inward current of sodium ions but of calcium ions. TTX has been successfully employed in studies on nerve and muscle cells of many arthropods and molluscs as well as of vertebrates —its mechanism of action was found to be identical in all cases. 

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