Potassium conductance

The inhibition of firing of catecholamine neurons resulting from amphetamine administration is likely due to activation of somatodendritic autoreceptors. This causes a hyperpolarization of the somatodendritic membrane of both locus coeruleus noradrenergic and substantia nigra dopamine neurons, probably as a consequence of an increase in potassium conductance (Lacey et al. 1987 Williams et al. 1985). 

And we believe that this fact, only recently shown by Allan North s group, is that they cause an increase in potassium conductance and as a consequence hyperpolarization of the cell body. 

ANSWER That is Lacey et al., Allan North s group. It was published in the Journal of Physiology last year. It was also an abstract in the Society 2 years ago. It is the consequence of that application of the agonists, recording intracellularly in the slice of the dopamine neuron. He gets the same thing by virtue of application of norepinephrine agonists to noradrene-gic slice preparation. That is a conventional way to create a hyperpolarization of the cell, to increase the potassium conductance, and so forth. 

Lacey, M.G. Mercuri, N.B. and North, R.A. Dopamine acts on D2 receptors to increase potassium conductance in neurons of the rat substantia nigra zona compacta. J Physiol 392 397-416, 1987. 

Williams, J.T. Henderson, G. and North, R.A.Characterization of Ctj-adrenoeeptors which increase potassium conductance in rat loeus eoeruleus neurons. Neurosci 14 95-101, 1985. 

Llinas, R. Walton, K. and Bohr, V. Synaptic transmission in squid giant synapse after potassium conductance block with external 3- and 4 - ami nopyri di nes. Bi ophvs J. 16 83-86, 1976. Mendelsohn, L.G. Kerchner, G.A. Kalra, V. Zimmerman, D.M. and Leander, J.D. Phencyclidine receptors in rat brain cortex. Biochem-Pharmacol 33-3529-3535, 1984. 

Haas, H. L. (1984). Histamine potentiates neuronal excitation by blocking a calcium-dependent potassium conductance. Agents Actions 14, 534-7. 

Grudt T, Williams JT. Kappa opioid receptors also increase potassium conductance. Proc Natl Acad Sci USA 1993 90 11429-11432. 

Triphenylmethyl sodium and triphenylmethyl potassium conduct in liquid ammonia although they slowly react with that solvent.887 888 When the liquid ammonia is allowed to evaporate from a solution of triphenylmethyl sodium in ammonia, the residue is a colorless mixture of sodamide and triphenylmethane. The sodium-tin and sodium-germanium compounds analogous to sodium triphenylmethide are also strong electrolytes in liquid ammonia. Sodium acetylide in liquid ammonia is dissociated to about the same extent as sodium acetate in water.889... 

Electrophysiological properties of histaminergic neurons show spontaneous activity of about 2 Hz. A combination of sodium, calcium and potassium conductances account... 

Trussel, L. O. and Jackson, M. B. Adenosine-activated potassium conductance in cultured striatal neurons. Proc. Natl Acad. Sci. U.S.A. 82 4857-4661,1985. 

Proarrhythmia refers to development of a significant new arrhythmia (such as VT, ventricular fibrillation [VF], or TdP) or worsening of an existing arrhythmia. Proarrhythmia results from the same mechanisms that cause other arrhythmias or from an alteration in the underlying substrate due to the antiarrhythmic agent. TdP is a rapid form of polymorphic VT associated with evidence of delayed ventricular repolarization due to blockade of potassium conductance. TdP may be hereditary or acquired. Acquired forms are associated with many clinical conditions and drugs, especially type la and type III IKr blockers. 

It blocks voltage-sensitive sodium channels, modulates the voltage-activated Ca currents, and increases potassium conductance. 

Brickley, S. G., Revilla, V., Cull-Candy, S. G Wisden, W and Farrant, M. (2001) Adaptive regulation of neuronal excitability by a voltage-independent potassium conductance. 

VanderMaelen, C. P., and Aghajanian, G. K. (1983) Evidence for a calcium-activated potassium conductance in serotonergic dorsal raphe neurons. Neurosci. Abstr., 9 500. 

Armstrong, C.M. (1969) Inactivation of the potassium conductance and related phenomena caused by quaternary ammonium ion injection in squid axons. The Journal of General Physiology, 54, 553-575. 

The clinical effects of chloroform toxicity on the central nervous system are well documented. However, the molecular mechanism of action is not well understood. It has been postulated that anesthetics induce their action at a cell-membrane level due to lipid solubility. The lipid-disordering effect of chloroform and other anesthetics on membrane lipids was increased by gangliosides (Harris and Groh 1985), which may explain why the outer leaflet of the lipid bilayer of neuronal membranes, which has a large ganglioside content, is unusually sensitive to anesthetic agents. Anesthetics may affect calcium-dependent potassium conductance in the central nervous system (Caldwell and Harris 1985). The blockage of potassium conductance by chloroform and other anesthetics resulted in depolarization of squid axon (Haydon et al. 1988). 

Haydon DA, Requena J, Simon AJB. 1988. The potassium conductance of the resting squid axon and its blockage by clinical concentrations of general anaesthetics. J Physiol 402 363-374. 

Transmembrane action potential of a sinoatrial node cell. In contrast to other cardiac cells, there is no phase 2 or plateau. The threshold potential (TP) is -40 mV. The maximum diastolic potential (MDP) is achieved as a result of a gradual decline in the potassium conductance (gK+). Spontaneous phase 4 or diastolic depolarization permits the cell to achieve the TR thereby initiating an action potential (g = transmembrane ion conductance). Stimulation of pacemaker cells within the sinoatrial node decreases the time required to achieve the TR whereas vagal stimulation and the release of acetylcholine decrease the slope of diastolic depolarization. Thus, the positive and negative chronotropic actions of sympathetic and parasympathetic nerve stimulation can be attributed to the effects of the respective neurotransmitters on ion conductance in pacemaker cells of the sinuatrial node. gNa+ = Na+ conductance. 

The parasympathetic nervous system, through the vagus nerve, inhibits the spontaneous rate of depolarization of pacemaker cells. The release of acetylcholine from cholinergic vagal fibers increases potassium conductance (gK+) in pacemaker cells, and this enhanced outward movement of K+ results in a more negative po-... 

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. 

Figure 7.2 G protein-mediated mechanisms of opioid cellular actions. Activation of the p receptor results in inhibition ofadenylyl cyclase (AC), the enzyme responsible for the formation ofcAMP, via the Gi protein, and increased potassium conductance and decreased calcium conductance, mediated via Go proteins.

The effects of digitalis on the electrical properties of the heart are a mixture of direct and autonomic actions. Direct actions on the membranes of cardiac cells follow a well-defined progression an early, brief prolongation of the action potential, followed by shortening (especially the plateau phase). The decrease in action potential duration is probably the result of increased potassium conductance that is caused by increased intracellular calcium (see Chapter 14). All these effects can be observed at therapeutic concentrations in the absence of overt toxicity (Table 13-2). 

Although the density of fibers innervating various sites differs considerably, most regions of the CNS receive diffuse noradrenergic input. All noradrenergic receptor subtypes are metabotropic. When applied to neurons, norepinephrine can hyperpolarize them by increasing potassium conductance. This effect is mediated by ct2 receptors and has been characterized... 

In the spinal cord, a2-agonists act on receptors located on the terminals of primary afferent fibers in the dorsal horn substantia gelatinosa to reduce nociceptive transmission by inhibiting the release of glutamate and substance P (Collin et al., 1994 Hamalainen and Pertovaara, 1995) (see Fig. 2). These receptors appear to be primarily of the a2A subtype which is negatively coupled to adenylate cyclase (Lakhlani et al., 1997 see Millan, 1999 but see Sawamura et al., 2000, and references therein for a discussion of the possible involvement of other a2-receptor subtypes in antinociception). Like activation of p-opioid receptors, the activation of a2-receptors increases the potassium conductance of the cells bearing these receptors, thus reducing cellular excitability. 

Everill, B. and Kocsis, J. D. Nerve growth factor maintains potassium conductance after nerve injury in adult cutaneous afferent dorsal root ganglion neurons, Neuroscience 2000, 100, 417-422. 

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