Nerve membrane potential

Narahashi, T., T. Deguchi, and E. X. Albuquerque Effects of batrachotoxin on nerve membrane potential and conductances. Nature New Biology 229, 221—222 (1971). 

The pain appears to arise from the formation of melittin pores in the membranes of nociceptors, free nerve endings that detect harmful ( noxious —thus the name) stimuli of violent mechanical stress, high temperatures, and irritant chemicals. The creation of pores by melittin depends on the nociceptor membrane potential. Melittin in water solution is tetrameric. However, melittin interacting with membranes in the absence of a membrane potential is monomeric and shows no evidence of oligomer... 

Action potentials, self-propagating. Action potentials of smooth muscle differ from the typical nerve action potential in at least three ways. First, the depolarization phases of nearly all smooth muscle action potentials are due to an increase in calcium rather than sodium conductance. Consequently, the rates of rise of smooth action potentials are slow, and the durations are long relative to most neural action potentials. Second, smooth muscle action potentials arise from membrane that is autonomously active and tonically modulated by autonomic neurotransmitters. Therefore, conduction velocities and action potential shapes are labile. Finally, smooth muscle action potentials spread along bundles of myocytes which are interconnected in three dimensions. Therefore the actual spatial patterns of spreading of the action potential vary. 

Pyrethroids, such as p,p -DDT, are toxic because they interact with Na+ channels of the axonal membrane, thereby disturbing the transmission of nerve action potential (Eldefrawi and Eldefrawi 1990, and Chapter 5, Section 5.2.4 of this book). In both cases, marked hydrophobicity leads to bioconcentration of the insecticides in the axonal membrane and reversible association with the Na+ channel. Consequently, both DDT and pyrethroids show negative temperature coefficients in arthropods increasing temperature brings decreasing toxicity because it favors desorption of insecticide from the site of action. 

Figure 1.9 Comparison of the effects of an endogenously released and exogenously applied neurotransmitter on neuronal activity (identity of action). Recordings are made either of neuronal firing (extracellularly, A) or of membrane potential (intracellularly, B). The proposed transmitter is applied by iontophoresis, although in a brain slice preparation it can be added to the bathing medium. In this instance the applied neurotransmitter produces an inhibition, like that of nerve stimulation, as monitored by both recordings and both are affected similarly by the antagonist. The applied neurotransmitter thus behaves like and is probably identical to that released from the nerve...

Other ion channels are closed at rest, but may be opened by a change in membrane potential, by intracellular messengers such as Ca + ions, or by neurotransmitters. These are responsible for the active signalling properties of nerve cells and are discussed below (see Hille 1992, for a comprehensive account). A large number of ion channels have now been cloned. This chapter concerns function, rather than structure, and hence does not systematically follow the structural classification. 

ATP certainly fulfils the criteria for a NT. It is mostly synthesised by mitochondrial oxidative phosphorylation using glucose taken up by the nerve terminal. Much of that ATP is, of course, required to help maintain Na+/K+ ATPase activity and the resting membrane potential as well as a Ca +ATPase, protein kinases and the vesicular binding and release of various NTs. But that leaves some for release as a NT. This has been shown in many peripheral tissues and organs with sympathetic and parasympathetic innervation as well as in brain slices, synaptosomes and from in vivo studies with microdialysis and the cortical cup. There is also evidence that in sympathetically innervated tissue some extracellular ATP originates from the activated postsynaptic cell. While most of the released ATP comes from vesicles containing other NTs, some... 

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. 

Fig. 6.18 Experimental arrangement for measurement of the membrane potential of a nerve fibre (axon) excited by means of current pulses (1) excitation electrodes, (2) potential probes. (According to B. 

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

Presynaptic events during synaptic transmission are rapid, dynamic and interconnected. The time between Ca2+ influx and exocytosis in the nerve terminal is very short. At the frog NMJ at room temperature, 0.5-1 ms elapses between the depolarization of the nerve terminal and the beginning of the postsynaptic response. In the squid giant synapse, recordings can be made simultaneously in the presynaptic nerve terminal and in the postsynaptic cell. Voltage-sensitive Ca2+ channels open toward the end of the action potential. The time between Ca2+ influx and the postsynaptic response as measured by the postsynaptic membrane potential is 200 ps (Fig. 10-7). However, measurements made with optical methods to record presynaptic events indicate a delay of only 60 ps between Ca2+ influx and the postsynaptic response at 38°C [21]. 

Brading But we don t know whether the nerves are synchronizing action potentials they may be bypassing them altogether and generating contraction without affecting membrane potentials. 

Hirst If you take a piece of arteriole, stimulate the purinergic nerves to evoke an excitatory junction potential, measure the diameter of the arteriole, and apply a voltage clamp, you get no contraction. If you let the membrane potential run into levels where voltage-dependent Ca2+ channels are activated, there is a contraction. 

Figure 5.3. (a) Example for a compound used in the study of membrane potentials and (b) principle of funcboning of visualizing nerve pulses in a living cell. When a nerve pulse passes, the membrane potential changes, and this induces a change in the fluorescence intensity of the probe. The temporal and spatial profile of these changes can be followed by time-resolved methods. 

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