K+ currents

The criterion of ipsocentric ring current has been used to assess aromaticity in S-N heterocycles (and related inorganic ring systems). Current density maps indicate that the ten r-electron systems [SsNs], [S4N3] " and [S4N4] ", and the fourteen r-electron system [S5N5] " support diatropic k currents, reinforced by a circulations. 

Opioids G-protein coupled p-, 5-, k-receptors l cAMP l Ca2+ currents t K+ currents l Excitability of peripheral and central neurons l Release of excitatory neurotransmitters p, 5 sedation, nausea, euphoria/re-ward, respiratory depression, constipation k dysphoria/aversion, diuresis, sedation... 

Antidepressants Noradrenaline/5-HT transporters Na+, K+ channels l Noradrenaline/ 5-HT reuptake l Na+ currents t K+ currents l Excitability of peripheral and central neurons Cardiac arrhythmia, myocardial infarction, sedation, nausea, dry mouth, constipation, dizziness, sleep disturbance, blurred vision... 

Cardiac IKi is the major K+ current responsible for stabilizing the resting membranepotential and shaping the late phase of repolarization of the action potential in cardiac myocytes. The name should not be confused with that of an Intermediate conductance calcium-activated K+ channel, which sometimes is also called IK1. 

Delayed-rectifier K+ channels activate with a delay and mediate outwardly-rectifying K+ currents. These channels may make a significant contribution to the icpolarizing phase of nervous action potentials. 

Inward Rectifier K+ Channels. Figure 1 The role of inward rectifier (Kir) channels in cardiac action potentials. Depolarization is generated and maintained by Na and Ca currents (/Na, /Ca). Voltage-gated K currents (Kv) and Kir channels contribute to repolarization and maintenance of a negative resting potential. 

This minimal K+ channel (MinK) encoded by KCNEl consists of 130 amino acid residues and has a single transmembrane segment. A slowly activating K+ current-induced MinK cRNA is expressed in Xenopus oocytes. Coexpression of KvLQTl with MinK induced a current that has characteristics similar to cardiac slowly activating delayed-rectifier K+ current, DCS, in contrast to DCR that has relative fast activation and is composed of hERG/MiRPl. 

Increases inwardly rectifying K+ current, PLC activation with increased IPs and elevated [Ca2+]j observed in recombinant systems PLC activation with increased IPs and elevated [Ca2+]j to observed in recombinant systems. PLC activation with increased IPs and elevated [Ca2+]j observed in recombinant systems. ... 

Elliott, J. K., Current Trends in VLSI Materials Part II, Semiconductor International,. 150-153 (April 1988)... 

Kang J, Chen XL, Wang H, et al Interactions of the narcotic 1-alpha-acetylmethadol with human cardiac K+ channels. Eur J Pharmacol 458 25-29, 2003 Katchman AN, McGroary KA, Kilborn MJ, et al Influence of opioid agonists on cardiac human ether-a-go-go-related gene K(+) currents. J Pharmacol Exp Ther 303 688-694, 2002... 

Figure 2.9 Hyperpolarisation-activated cation current 4 and its role in pacemaking in a guinea-pig thalamic relay neuron. (Adapted from Figs 2 and 14 in McCormick, DA and Pape, H-C (1990) J. Physiol. 431 291-318. Reproduced by permission of the Physiological Society.) (a) Records showing the time-dependent activation of the h-current by hyperpolarisation and its deactivation on repolarising, (b) Interpretation of rhythmic activity in a thalamic relay neuron. (1) The inter-spike hyperpolarisation activates 7h to produce a slowly rising pacemaker depolarisation. (2) This opens T-type Ca " channels to give a more rapid depolarisation, leading to (3) a burst of Na" spikes (see Fig. 2.8). At (4) the depolarisation has closed (deactivated) the h-channels and has inactivated the T-channels. The membrane now hyperpolarises, assisted by outward K+ current (5). This hyperpolarisation now removes T-channel in-activation and activates 7h (6), to produce another pacemaker potential...

Conti, F., and E. Neher, Single channel recordings of K+ currents in squid axons, Nature, 285, 140 (1980). 

The ion-channel blocking mechanism has been widely tested and found to be important in both pharmacology and physiology. Examples are the block of nerve and cardiac sodium channels by local anesthetics, or block of NMDA receptor channels by Mg2+ and the anesthetic ketamine. The channel-block mechanism was first used quantitatively to describe block of the squid axon K+ current by tetraethylammonium (TEA) ions. The effects of channel blockers on synaptic potentials and synaptic currents were investigated, particularly at the neuromuscular junction, and the development of the single-channel recording technique allowed channel blockages to be observed directly for the first time. 

Oringer, K. Current Practice in Polymer Recovery Operations, Chemical Engineering, Mar. 20, 1972, p. 

Stimulation of the H2 receptor leads to blockade of a Ca2+-dependent K+ current through the small K+ channel, thus causing a spike frequency adaptation (i.e. an accommodation of firing) and slow afterhyperpolarization... 

A critical cellular response to opiates is the potentiation of K+ currents [42]. Stimulation of n receptors in neurons causes an increase in K+ conductance and a reduction in cell firing. Prolonged administration of fi agonists diminishes the ability of the opiates to increase K+ conductance to inhibit neuronal firing and pain transmission is no longer attenuated. 

Parallel studies by Tallent et al. [65] have employed AtT-20 cells transfected with the fi receptor which couples to an endogenously expressed inwardly rectifying K+ channel. Prolonged application of DAMGO to these cells also desensitizes the ability of opiates to potentate the K+ current. The desensitization of the fi receptor in AtT-20 cells did not involve changes in the ability of the K+ channel to be activated since GTP analogs perfused into the opiate-treated cells increased K+ currents to a similar extent as in drug naive cells. 

The desensitization of the fi receptor was heterologous. In oocytes cotransfected with ft and serotonin receptors, chronic morphine treatment abolished morphine and serotonin potentiation of the K+ current [63]. Similarly, in AtT-20 cells transfected with the cloned fi receptor, chronic DAMGO treatment abolished the ability of opiates and somatostatin, acting via endogenous somatostatin receptors in these cells, to stimulate K+ conductance [65]. 

Fig. 22 (a) Model system able to perform six different logic functions depending on its structural parameters e and k. Current intensity passing through this system for e = k = 0 eV, v = 5 meV, and a and [1 going from 0 to 1 eV. The variation of the current respects the XOR truth table a strong current is obtained for = 0=1 and =1 = 0 and a weak one for = 0 = 0 and =1 = 1. Due to the stable plateaux at the comers of the map, this device naturally corrects small deviations in the inputs that lead to even smaller deviations in the output... 

I88-E89. The answers arc 188-g 189-b. (Hardman, pp 858-859, 864-865.) It is widely accepted that anti arrhythmic drugs are best classified according to their electro physio logic attributes. This is best accomplished by relating the effects of the different drugs to their actions on Na and Ca channels, which are reflected by changes in the monophasic action potential. Amiodarone blocks Na, Ca, and K currents and markedly prolongs repolarization, particularly in depolarized cells. Hecainide is related... 

From the earliest measurements of tissue calcium, it was clear that total calcium is largely a measure of stored calcium. Through the years, scientists have used a variety of indirect measures of [Ca2+]j. These include shortening of or tension in muscles secretion from secretory cells the activity of Ca2+-dependent enzymes, most notably glycogen phosphorylase and flux of K+, or K+ currents, as a reflection of Ca2+-activated K+ channels. In addition, investigators often use the radioactive calcium ion [45Ca2+] as an indirect indicator of Ca2+ concentrations and Ca2+ movements. 

Dick GM, Kong ID, Sanders KM (1999) Effects of anion channel antagonists in canine colonic myocytes comparative pharmacology of Cl" Ca2+ and K+ currents. Br J Pharmacol 127 1819-1831... 

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