Hyperpolarization, cell membrane

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... 

Recent work using confocal microscopy has found localized increases of [Ca2+]j named Ca2+ sparks which are due to the release of Ca2+ from one or a small number of RyRs (Jaggar et al 2000). These localized releases of Ca2+ activate Ca2+-dependent channels in the surface membrane (Perez et al 2001). Activation of the Ca2+-activated K+ current will hyperpolarize the membrane potential (Herrera et al 2001) and thereby decrease Ca2+ entry into the cell on voltage-dependent Ca2+ channels. This provides a mechanism whereby Ca2+ release from the SR can decrease contraction. It is therefore important, in different smooth muscles, to consider to what extent SR Ca2+ release activates rather than decreases contraction. It is, of course, possible that, in the same smooth muscle, SR release may sometimes directly activate contraction and, at other times, decrease it by activating K+ channels. 

During the action potential in vas deferens or urinary bladder the rise in [Ca2+] close under the cell membrane is responsible, in combination with the depolarization, for the repolarization phase as it causes the opening of Ca2+-activated K+ channels through which a large repolarizing outward current flows (Arnaudeau et al 1997, Imaizumi et al 1998, Ohi et al 2001). This may lead to a transient period of hyperpolarization (an afterhyperpolarization ) following the action potential (Imaizumi et al 1998). 

The SR may contribute to excitation-contraction (EC) coupling in two ways firstly, by the release of Ca2+ for contraction as described above, but secondly by modulating membrane excitability. As will be described elsewhere in this book, the SR is an important mediator of surface membrane ion channel activity, and hence, excitability. Spontaneous Ca2+ release from the SR can activate Ca2+-sensitive ion channels. Both K+ (Kca) and Cl- (Clsmooth muscle cell membrane can be activated by SR Ca2+. If Kca channels are activated there will be a hyperpolarization, as K+ ions leave the cell and spontaneous transient outward currents (STOCs) can be recorded (Carl et al 1996, Nelson Quayle... 

K+ channels selectively transport K+ across membranes, hyperpolarize cells, set membrane potentials and control the duration of action potentials, among a myriad of other functions. They use diverse forms of gating, but they all have very similar ion permeabilities. All K+ channels show a selectivity sequence of K+ Rb+ > Cs+, whereas the transport of the smallest alkali metal ions Na+ and Li+ is very slow—typically the permeability for K+ is at least 104 that of Na+. The determination of the X-ray structure of the K+-ion channel has allowed us to understand how it selectively filters completely dehydrated K+ ions, but not the smaller Na+ ions. Not only does this molecular filter select the ions to be transported, but also the electrostatic repulsion between K+ ions, which pass through this molecular filter in Indian file, provides the force to drive the K+ ions rapidly through the channel at a rate of 107-108 per second. (Reviewed in Doyle et al., 1998 MacKinnon, 2004.)... 

Because the membrane is partially depolarized in the dark, its neurotransmitter glutamate is continuously released. Glutamate inhibits the optic nerve bipolar cells with which the rod cells synapse. By hyperpolarizing the rod cell membrane, light stops the release of glutamate, relieving inhibition of the optic nerve bipolar cell and thus initiatii a signal into the brain. 

The transient change in the transmembrane potential upon excitation. An action potential cycle consists of a transient depolarization of the cell membrane of an excitable cell (such as a neuron) as a result of increased permeability of ions across the membrane, followed by repolarization, hyperpolarization, and finally a return to the resting potential. This cycle typically lasts 1-2 milliseconds and travels along the axon from the cell body (or, axon hillock) to the axonal terminus at a rate of 1-100 meters per second. See Membrane Potential... 

In this equation, x is the ion in question, [x]j is the concentration inside the cell, and [x] is the concentration outside the cell. For potassium, using a [K]j of 140 mM and a [K]o of 4 mM, the Ek is equal to -94 mV, which is almost identical to the normal resting membrane potential of -90 mV. The contribution of other ionic species to the resting membrane potential is smaller because of the low transmembrane permeability at hyperpolarized resting membrane potentials. 

Other vasodilators, such as diazoxide and minoxidil, cause dilation of blood vessels by activating potassium channels in vascular smooth muscle. An increase in potassium conductance results in hyperpolarization of the cell membrane, which will cause relaxation of vascular smooth muscle. 

Uterine relaxation is mediated in part through inhibition of MLCK. This inhibition results from the phosphorylation of MLCK that follows the stimulation of myometrial (3-adrenoceptors relaxation involves the activity of a cyclic adenosine monophosphate (cAMP) mediated protein kinase, accumulation of Ca++ in the sarcoplasmic reticulum, and a decrease in cytoplasmic Ca. Other circulating substances that favor quiescence of uterine smooth muscle include progesterone, which increases throughout pregnancy, and possibly prostacyclin. Progesterone s action probably involves hyperpolarization of the muscle cell membrane, reduction of impulse conduction in muscle cells, and increased calcium binding to the sarcoplasmic reticulum. 

Ivermectin binds selectively and with high affinity to glutamate gated chloride ion channels in invertebrate nerve and muscle cells. This leads to an increase in the permeability of cell membrane to chloride ions with hyperpolarization of nerve of muscle cell, resulting in paralysis and death of the parasite. 

Upon occupation of biotin receptors, the cell membrane becomes hyperpolarized. This hyperpolarization causes an increase in the posteriorly directed beating of the cell s propulsive cilia, and the cells move smoothly up the concentration gradient. Importantly, the hyperpolarization also decreases the likelihood of membrane depolarization, and if mild, slows the ciliary beat frequency and slows the cells, while if large, brings about a calcium action potential that reverses the ciliary... 

In the CNS, receptors at most synapses are coupled to ion channels, that is, binding of the neurotransmitter to the postsynaptic membrane receptors results in a rapid but transient opening of ion channels. Open channels allow ions inside and outside the cell membrane to flow down their concentration gradients. The resulting change in the ionic composition across the membrane of the neuron alters the postsynaptic potential, producing either depolarization or hyperpolarization of the postsynaptic membrane, depending on the specific ions that move and the direction of their movement. 

Stimulation of inhibitory neurons causes movement of ions that results in a hyperpolarization of the postsynaptic membrane. These inhibitory postsynaptic potentials (IPSP) are generated by the following (1) Stimulation of inhibitory neurons releases neurotransmitter molecules, such as Y-aminobutyric acid (GABA) or glycine, which bind to receptors on the postsynaptic cell membrane. This causes a transient increase in the permeability of specific ions, such as, potassium and chloride ions. (2) The influx of chloride (Cl ) and efflux of potassium (K+) cause a weak hyperpolarization or inhibitory post-... 

---