Depolarization action potential spread

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. 

Succinylcholine, similar to acetylcholine, interacts with the cholinergic receptors at the end plate region of the muscle, resulting in depolarization of the chemically excitable membrane. This, in turn, creates local action potentials, spreading them to and depolarizing the adjacent excitable membranes, finally culminating in a muscle contraction, or fasciculation, which is an uncoordinated muscle contraction. However, unlike acetylcholine, succinylcholine is not metabolized by acetylcholinesterase, and hence causes persistent depolarization of the end plate. The continuous presence of succinylcholine leads to inexcitability of the membrane adjacent to the end plate, resulting in... 

Voluntary muscle contraction is initiated in the brain-eliciting action potentials which are transmitted via motor nerves to the neuromuscular junction where acetylcholine is released causing a depolarization of the muscle cell membrane. An action potential is formed which is spread over the surface membrane and into the transverse (T) tubular system. The action potential in the T-tubular system triggers Ca " release from the sarcoplasmic reticulum (SR) into the myoplasm where Ca " binds to troponin C and activates actin. This results in crossbridge formation between actin and myosin and muscle contraction. 

The action potential is propagated by local spread of depolarization 99 Membranes at nodes of Ranvier have high concentrations of Na+ channels 99... 

The action potential is propagated by local spread of depolarization. How does the action potential propagate smoothly down an axon, bringing new channels into play ahead of it Any electrical depolarization or hyperpolarization of a cell membrane spreads a small distance in either direction from its source by a purely passive process often called cable or electrotonic spread. The spread occurs because the intracellular and extracellular media... 

Figure 4.2 Cartoon representation of an ECC trace and ventricular cardiac action potential, (a) A representation of an ECC trace with its five typical deflections (PQRST) arising from the spread of electrical activitythrough the heart. The QRS wave denotes the ventricular depolarization, while the T wave represents ventricular repolarization. The QT interval therefore estimates the duration of a ventricular action potential, (b) Schematic of the five phases of a ventricular action potential. Phase 0 is the rapid depolarization phase due to a large influx of Na+ ions (Ina). Phase 1 occurs with the inactivation of Na+ channels and the onset of transient outward (repolarizing) currents (/to)...

Once an action potential is initiated at the hillock, it continues in a self-propagating fashion to the end of the axon. Voltage-sensitive ion channels are opened by the depolarization, allowing further influx of Na+ and a spread of the action potential. Thus, the action potential is a self-regenerating spread of membrane depolarization. 

Once you get an action potential generated, it will flow down the neuronal axon. Remember that an action potential is a sequence of membrane depolarization and repolarization events mediated by voltage-gated sodium ion and potassium ion channels. The basic idea is provided in figure 21.3. The initial depolarization will spread to adjacent voltage-gated ion channels, which will open, ions will flow, and so forth. Thus, the wave of depolarization moves down the axon. It is the means by... 

Generally, it is always only a very small part of the membrane that is depolarized during an action potential. The process can therefore be repeated again after a short refractory period, when the nerve cell is stimulated again. Conduction of the action potential on the surface of the nerve cell is based on the fact that the local increase in the membrane potential causes neighboring voltage-gated ion channels to open, so that the membrane stimulation spreads over the whole cell in the form of a depolarization wave. 

The worker heart muscle cells (as opposed to the cells in the conduction system, which are also specialized muscle cells) are peculiar in using both Na and Ca in the depolarization phase of the action potential (Figure 5.8b, bottom). While they do not normally create action potentials themselves, under pathological conditions some of them may show spontaneous discharge. This depolarization may then spread across the entire heart (or parts of it) and interfere with normal and regular activity. While both calcium and sodium channel blockers have their applications in treating heart arrhythmias, the beauty of the sodium channel blockers is that they will not interfere with the activity of the regular pacemakers (since those essentially don t use sodium channels). Another beneficial feature was pointed out above Lidocaine extends the duration of the inacti-... 

In myelinated neurons, voltage-gated Na channels are concentrated at the nodes of Ranvler. Depolarization at one node spreads rapidly with little attenuation to the next node, so that the action potential jumps from node to node (see Figure 7-40). 

After the initial transduction of odor space into neural space by the olfactory receptors, a second messenger cascade amplifies the response in each cell, leading to activation of a cyclic nucleotide gated (CNG) ionic channel. The resulting ion flows depolarize the membrane, generating the receptor potential, which spreads to the site of action potential initiation [19]. 

As shown in Fig. 31 the effects of GABA and 5-HT applied consecutively to the same neuron, at a concentration of 0.1 mM, were quite different. In contrast to the action of 5-HT, the decrease in resistance evoked by GABA was very much faster and was associated with a substantial depolarization. Recovery was also very much faster. The reversal potential for 5-HT lay between - 85 and — 90 mV, and replacement of chloride in the medium by propionate did not change the effectiveness of 5-HT since a hyperpolarization evoked by the 5-HT and a low chloride medium was shorter. It should perhaps be mentioned that propronate may not be the ideal chloride replacement in studies of cortical neurons. Indeed, a number of workers have suggested that propionate will pass through the chloride channel activated during the ipsp (Dreifuss et al, 1969) or by spreading depression (Nicholson, 1979). 

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