Channel closing

Bulk microstructure Continuous channels Between fibers Complex foam to vertically oriented channels Closed cell to open cell foam None... 

Measured quenching distance as a function of equivalence ratio for propane/air mixture (top), and pictures of (a) downward and (b) upward propagating flames in channels, close to quenching. Channel widths as in the graph. Frame numbers correspond to the numbers of experimental points. 

In the sarcoplasm of resting muscle, the concentration of Ca + is 10 to 10 mol/L. The resting state is achieved because Ca + is pumped into the sarcoplasmic reticulum through the action of an active transport system, called the Ca + ATPase (Figure 49-8), initiating relaxation. The sarcoplasmic reticulum is a network of fine membranous sacs. Inside the sarcoplasmic reticulum, Ca + is bound to a specific Ca -binding protein designated calsequestrin. The sarcomere is surrounded by an excitable membrane (the T tubule system) composed of transverse (T) channels closely associated with the sarcoplasmic reticulum. 

Using the cell-attached patch clamp technique on frog muscle fibers (79), one can observe only two conditions the open, conducting state of the receptor and a nonconducting state of unknown identity. The transitions behave according to stochastic principles the lifetimes of any particular condition are distributed exponentially. The open state has a mean duration that is the inverse of the rate of channel closing. Because channel open time depends only upon a conformational shift, agonist concentration does not influence the parameter. It is, however, influenced... 

The primary characteristic of a sequential blocker, as observed with the patch clamp technique, is that the reciprocal of the mean duration of the lifetime equals the normal channel closing rate plus the rate constant of channel blockade times the drug concentration. Therefore, increasing the drug concentration shortens the mean channel open time. 

From Eq. (6.2), the mean open time is predicted to be the reciprocal of the rate constant for channel closing (xopen = 1/a). For bursts recorded at very low agonist concentrations, the mean closed time within bursts, xg, is equal to 1/( 3 + 2k 2), and the mean number of gaps per burst, N, is equal to 3/2 2. Using these two simultaneous equations, it is then possible to calculate (3 and k 2. 

Notice that the problem states that the distribution of open times is a single exponential. This tells you that a mechanism containing a single open state of the receptor can describe the data. Using the above hint, the channel closing rate (call this a) is therefore the reciprocal of the mean open time. Thus, at -60 mV, a = 1/5 msec, or 200 sec-1 at -120 mV, a = 1/10 msec, or 100 sec-1. This indicates that the channel closing conformational change is affected by the electric held across the membrane. 

Phase 3 begins at the peak of the action potential. At this point, the Ca++ channels close and K+ channels open. The resulting efflux of K+ ions causes the repolarization phase of the action potential. 

Phase 3 Repolarization occurs as Ca2+ channels close and K+ channels open. Efflux of K+ from within the cell repolarizes the cell fairly rapidly compared with Ca2+-dependent depolarization. 

Phase 1 Repolarization begins to occur as Na+ channels close and K+ channels open. Phase 1 is short in duration and does not cause repolarization below 0 mV. 

Phase 3 The L-type Ca2+ channels close and K+ efflux now causes repolarization as seen before. The relative refractory period (RRP) occurs during phases 3 and 4. 

Immediately after the passage of an action potential, the Na ion channels close spontaneously and cannot be re-opened for a period of time. This is the refractory period. An action potential therefore cannot proceed in the opposite direction, i.e. it is unidirectional, which imposes a direction on propagation of the whole action potential. This is analogous to the means by which directionality is achieved in a metabolic pathway or a signalling sequence of reactions within either process there is at least one irreversible (non-equilibrium) reaction which provides directionality (Chapter 2). 

The excitable membrane of nerve axons, like the membrane of cardiac muscle (see Chapter 14) and neuronal cell bodies (see Chapter 21), maintains a resting transmembrane potential of -90 to -60 mV. During excitation, the sodium channels open, and a fast inward sodium current quickly depolarizes the membrane toward the sodium equilibrium potential (+40 mV). As a result of this depolarization process, the sodium channels close (inactivate) and potassium channels open. The outward flow of potassium repolarizes the membrane toward the potassium equilibrium potential (about -95 mV) repolarization returns the sodium channels to the rested state with a characteristic recovery time that determines the refractory period. The transmembrane ionic gradients are maintained by the sodium pump. These ionic fluxes are similar to, but simpler than, those in heart muscle, and local anesthetics have similar effects in both tissues. 

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