After the delivery of the significant stimulus, the resting membrane potential of -70 mV rapidly increases and this rapid change is called an action potential or in other words a nerve impulse, which acts as a signal in the neurone. This rapid increase is caused by ionic currents crossing the membrane through voltage-gated channels.
The stimulus brings about the change in membrane potential and the slow rising phase, were some voltage gated sodium ion channels open and sodium ions move into the cell down their concentration gradient until threshold potential is reached at -55mV, after which they all rapidly open and depolarisation of the axon occurs. This increases the charge inside the cell membrane and decreases is outside. As threshold potential was reached, a nerve impulse(action potential) is initiated at the axon hillock were there are many voltage gated sodium ion channels. It is propagated down the axon length via current loops. Voltage change activates voltage-gated sodium ion channels in the neighbouring plasma membrane, and then the next area becomes depolarised that is adjacent to the area already depolarised on the axon.
After the membrane potential has reached +30 mV (its peak), repolarisation of that axon area occurs. Here the voltage-gated sodium ion channels become inactivated so the membrane is no longer permeable to sodium ions, however instead the voltage-gated potassium channels open which means potassium ions begin to leave the cell down their concentration gradient. This is all occurring during the absolute refractory period during which no stimulus, no matter how powerful, can initiate another nerve impulse. When this section of the axon reaches the relative refractory period, the activation gates of the sodium voltage-gated channels are still closed but the inactivation gates, though most are shut, are about to open. The gates for the potassium voltage-gated channels are still open. This is important for the sodium voltage-gated channels as they have to pass the ‘closed’ stage after inactivation in order for them to open again, for the potassium channels it is less so, as they just move from open to closed. During the relative refractory period, if the stimulus is sufficiently strong and exceed the threshold, another nerve impulse can be initiated. As more potassium ions leave the cell than had during the resting phase, the membrane potential drops to -80 mV which is the hyperpolarisation stage. To return the membrane potential back to the normal -70 mV resting potential, the sodium/potassium ion pump pumps two potassium ions in for three sodium ions out very rapidly using ATP. These processes constantly occur down the whole length of the axon in loops after the stimulus is applied to propagate the nerve impulse.
- ↑ Molecular Biology of the Cell, 4th edition Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter. New York: Garland Science; 2002. Chapter 11: Membrane Transport of Small Molecules and the Electrical Properties of Membranes. Voltage-Gated Cation Channels Generate Action Potentials in Electrically Excitable Cells. P621
- ↑ Molecular Biology of the Cell, 4th edition Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter. New York: Garland Science; 2002. Chapter 11: Membrane Transport of Small Molecules and the Electrical Properties of Membranes. The Use of Channelrhodopsins Has Revoluntionized the Study of Neural Circuits. P624