Membrane potential threshold

Automa-ticity. Special cardiac cells, such as SA and AV nodal cells, His-bundle cells, and Purkinje fibers, spontaneously generate an impulse. This is the property of automaticity. Ectopic sites can act as pacemakers if the rate of phase 4 depolarization or resting membrane potential is increased, or the threshold for excitation is reduced. 

An inhibitory input increases the influx of Cl to make the inside of the neuron more negative. This hyperpolarisation, the inhibitory postsynaptic potential (IPSP), takes the membrane potential further away from threshold and firing. It is the mirror-image of the EPSP and will reduce the chance of an EPSP reaching threshold voltage. 

Figure 1.4 Ionic basis for excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Resting membrane potential ( — 70 mV) is maintained by Na+ influx and K+ efflux. Varying degrees of depolarisation, shown by different sized EPSPs (a and b), are caused by increasing influx of Na. When the membrane potential moves towards threshold potential (60-65 mV) an action potential is initiated (c). The IPSPs (a b ) are produced by an influx of Cl. Coincidence of an EPSP (b) and IPSP (a ) reduces the size of the EPSP (d)...

Ordinarily, when the current pulse is over, the excess charges will be drained through the passive transport channels, and by operation of the sodium-potassium pumps the original values of membrane potential and of the concentration gradients will be reestablished. However, when in the case of depolarization the negative value of cp has dropped below a certain threshold value, which is about -50 mV, the picture changes drastically Excitation of the membrane occurs. When the current is turned off, the membrane potential not only fails to be restored but continues to... 

FIGURE 30.3 Changes in membrane potential cp of a cell membrane occurring upon application of depolarizing current pulses of different amplitude / (a,b) below threshold (c) excitation of the membrane during an above-threshold pulse. 

The ventricular action potential is depicted in Fig. 6-2.2 Myocyte resting membrane potential is usually -70 to -90 mV, due to the action of the sodium-potassium adenosine triphosphatase (ATPase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane increases to a threshold potential, usually -60 to -80 mV. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to rapidly enter the cell. This rapid influx of positive ions... 

Na+ channels to depolarize the membrane all the way to threshold however, it brings the membrane potential closer toward it. This increases the likelihood that subsequent stimuli will continue depolarization to threshold and that an action potential will be generated by the postsynaptic neuron. 

Figure 5.3 Spatial summation. Multiple excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs) produced by many presynaptic neurons simultaneously may add together to alter the membrane potential of the postsynaptic neuron. Sufficient excitatory input (A and B) will depolarize the membrane to threshold and generate an action potential. The simultaneous arrival of excitatory and inhibitory inputs (A and C) may cancel each other out so that the membrane potential does not change.

A pacemaker potential involves gradual depolarization of the cell membrane to threshold. The subsequent generation of an action potential causes smooth muscle contraction. This type of spontaneous depolarization is referred to as a "pacemaker potential" because it creates a regular rhythm of contraction. 

Slow-wave potentials also involve gradual depolarization of the cell membrane, but these depolarizations do not necessarily reach threshold. Therefore, the depolarization may simply be followed by repolarization back to the initial membrane potential. These slow "wave-like" potentials occur rhythmically and do not lead to smooth muscle contraction. The peak-to-peak amplitude of the slow-wave potential is in the range of 15 to 30 mV. Therefore, under the appropriate conditions, the depolarization phase of the slow-wave potential may, in fact, reach threshold. When this occurs, a burst of action potentials is generated, resulting in muscle contraction. 

The sinoatrial (SA) node is located in the wall of the right atrium near the entrance of the superior vena cava. The specialized cells of the SA node spontaneously depolarize to threshold and generate 70 to 75 heart beats/ min. The "resting" membrane potential, or pacemaker potential, is different from that of neurons, which were discussed in Chapter 3 (Membrane Potential). First of all, this potential is approximately -55 mV, which is less negative than that found in neurons (-70 mV see Figure 13.2, panel A). Second, pacemaker potential is unstable and slowly depolarizes toward threshold (phase 4). Two important ion currents contribute to this slow depolarization. These cells are inherently leaky to sodium. The resulting influx of Na+ ions occurs through channels that differ from the fast Na+ channels that cause rapid depolarization in other types of excitable cells. Toward the end of phase... 

Phase 0 begins when the membrane potential reaches threshold (-40 mV). Recall that the upstroke of the action potential in neurons is due to increased permeability of fast Na+ channels, resulting in a steep, rapid depolarization. 

However, in the SAnode, the action potential develops more slowly because the fast Na+ channels do not play a role. Whenever the membrane potential is less negative than -60 mV for more than a few milliseconds, these channels become inactivated. With a resting membrane potential of -55 mV, this is clearly the case in the SA node. Instead, when the membrane potential reaches threshold in this tissue, many slow Ca++ channels open, resulting in the depolarization phase of the action potential. The slope of this depolarization is less steep than that of neurons. 

Parasympathetic stimulation causes a decrease in heart rate. Acetylcholine, which stimulates muscarinic receptors, increases the permeability to potassium. Enhanced K+ ion efflux has a twofold effect. First, the cells become hyperpolarized and therefore the membrane potential is farther away from threshold. Second, the rate of pacemaker depolarization is decreased because the outward movement of K+ ions opposes the effect of the inward movement of Na+ and Ca++ ions. The result of these two effects of potassium efflux is that it takes longer for the SA node to reach threshold and generate an action potential. If the heart beat is generated more slowly, then fewer beats per minute are elicited. 

This is the time from the absolute refractory period until the cell s membrane potential is less than the threshold potential. It corresponds to the period of increased K+ conductance. 

Thus, a 10 1 transmembrane gradient of a single monovalent ion, say potassium, will generate a membrane potential of 58 mV. See Resting Potential Action Potential Depolarization Threshold Potential Nernst Equation Goldman Equation Patch-Clamp Technique... 

PERMEABILITY PERMEABILITY CONSTANT MEMBRANE POTENTIAL ACTION POTENTIAL DEPOLARIZATION GOLDMAN EQUATION NERNST EQUATION RESTING POTENTIAL THRESHOLD POTENTIAL PATCH-CLAMP TECHNIQUE Membrane protein dynamics,... 

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