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Action potentials threshold potential

A shift of the voltage-dependence of inactivation to a hyperpolarizing direction, resulting in a lower fraction of channels available for activation at action potential threshold. [Pg.127]

Na+ Channel inactivation leading to Elevated action potential threshold Decreased nerve conduction and velocity Decreased Na+ leak and decreased likelihood of Na+ gradient collapse Stabilized Na+ gradient-linked transporters (glucose, creatine, Ca2+, H+, transmitters)... [Pg.126]

Braitman (1989) found that CN (10-200 pM) rapidly depressed synaptic transmission between Schaffer collateral-commissural fibres and pyramidal cells. Analysis of input/output curves revealed both a decrease in excitatory postsynaptic potential generation and an increase in action potential threshold these suggested that the rapidity of action was due to a direct effect on CNS neurones. However, most studies emphasize a role for biochemical mechanisms as being mainly responsible for neurotoxicity. [Pg.509]

Ion Channels Modulating Action Potential Threshold and Rate of Discharge. 137... [Pg.129]

Both disodium cromoglycate and nedocromil sodium have antitussive effects in humans. In this instance, their activity occurs by increasing the depolarisation of sensory nerves, which increases the threshold for an action potential and therefore inhibits the activity of these neurons. [Pg.397]

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)... 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)...
ACh can sometimes inhibit neurons by increasing K+ conductance and although it has been found to hyperpolarise thalamic neurons, which would normally reduce firing, strong depolarisation may still make the cell fire even more rapidly than normal. This appears to be because the hyperpolarisation counters the inactivation of a low-threshold Ca + current which is then activated by the depolarisation to give a burst of action potentials (McCormick and Prince 1986b). [Pg.128]

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... [Pg.109]


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See also in sourсe #XX -- [ Pg.185 ]




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