Negatively charged chloride ions however would not, hence a net negative charge would develop across the membrane. At equilibrium the electrical force pulling potassium ions back into the cell would be exactly counterbalanced by the concentration gradient pulling potassium ions out of the cell.
This model helps us to understand the following points about the development of an equilibrium potential:. Ionic concentration gradients exist across cell membranes, these are mainly established by the ion pumps discussed earlier.
With knowledge of the relative concentrations of different ions across a cell membrane, the Nernst equation can be used to calculate the equilibrium potentials for different ions. The equation can easily be understood by referring back to some of the principles already discussed. And the electrical gradient, where an increase in the electrical charge of an ion z will decrease the potential difference required to balance diffusion.
The rate at which a given ion moves along its concentration gradient will be governed by diffusion, the rate of this being increased by an increase in temperature T. As at rest and body temperature the cell membrane is mostly permeable to potassium, it is not surprising that the calculated equilibrium potential of mV for this ion is not much different from the resting membrane potential of mV that we see in many excitable cells.
The actual resting membrane potential can be predicted using the Goldman constant field equation Goldman- Hodgkin-Katz equation. This formula takes into account the relative permeability of the membrane to other ions. As clinicians we are familiar with the importance of maintaining potassium concentrations within normal limits in order to avoid cardiac complications.
At rest the excitable cell membrane is mostly permeable to potassium. Because of this, changes in extracellular potassium concentration have a marked effect on the resting membrane potential. That is, it depolarises the cell. In cardiac tissue for example this will markedly increase the likelihood of action potential generation and therefore increases the risk of arrhythmias.
In neuronal tissue Potassium homeostasis is very well maintained by neuroglia, particularly Astrocytes. The sequence of events resulting in the generation of an action potential can be summarised as follows:.
In other nerves the stimulus for generator potential production may be, for example, secondary to ion channel activation by neurotransmitters released at the synapse.
The trace then rapidly reverses and falls back towards the resting level. This is called the spike potential. This is after depolarisation. After reaching the previous resting level, the trace overshoots. This is known as after hyperpolarisation. This period coincides with the refractory period. If a small current is applied to a neurone the minimal intensity of stimulating current threshold current that, acting for a given time, will produce an action potential can be determined.
A short intense current , or weak, but long, stimulus will both result in an action potential, providing threshold is reached. If the threshold current is not reached then an action potential will not be generated. If the stimulating current rises too slowly then an action potential will not be generated as the neuron will adapt. This is known as accommodation. Once threshold has been reached then further increases in stimulating current will not cause any increment in the action potential.
In short, unless threshold is reached, no action potential will be generated. Furthermore, any further increases in stimulation intensity will not result in any change in the action potential. Multiple Action Potentials will be produced if a stimulating current is applied to a neuron. The frequency of firing will increase in proportion to the magnitude of the stimulus current until a maximum firing frequency is reached usually around Hz.
Once voltage gated sodium channels are opened, at threshold, sodium ions move into the neuron in a direction that takes V m towards the equilibrium potential for sodium 65 mV.
The membrane is depolarised. Threshold can therefore be explained as the membrane potential at which enough voltage gated sodium channels are opened that the relative ionic permeability of the membrane favours sodium over potassium. The Falling phase now needs explaining. This can be described in terms of the action of two types of channel. First, the voltage gated sodium channels start to close. Secondly, voltage gated potassium channels open triggered by membrane depolarization.
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