Action of potassium and sodium ions play an important role in the propagation of change in membrane potential during nerve conduction. Membrane potential is determined by the ratio of the concentration of potassium ions inside to the ratio outside the nerve cells. This is termed as resting potential. When ligand-gated sodium ion channels at the synapse combine neurotransmitters, sodium ion transports from the outside to inside of the nerve cell. The transport initiates a change in the membrane potential from the resting to the action potential that is based on the ratio of concentration of sodium ions inside to that outside the cell.
This action potential is normally propagated along the axon towards the terminal by opening the voltage-gated sodium channels having approximately 1ms lifespan. The membrane then goes back to the resting potential through the hyperpolarization considering that the delayed potassium ion channels open successively. For this reason, the propagation of the change in the membrane potential is conducted towards the axon terminal along the axon.
It appears challenging to explain the hyperpolarization incase the ratio of potassium ion concentration inside to that outside the cell becomes higher than the previous value at the resting potential. This disrupts the potassium ion outflow from inside to outside the nerve cell in an excited state. Therefore, researchers led by Dr. Osamu Shirai at Kyoto University in Japan constructed a model for nerve conduction implementing liquid-membrane cells that imitate the function of potassium and sodium ions channels. They proposed an improved mechanism for the propagation of the action potential determined by the electrochemical assessment of the model that imitates the ligand-gated sodium ion channels at the synapse and voltage-gated sodium ion channels at the Ranvier nodes. Their work is now published in Physical Chemistry Chemical Physics.
The authors adopted a liquid membrane cell with two aqueous and one nitrobenzene phases. The cell was separated into eight liquid membrane cells and the potential for each determined against the reference electrode. The two aqueous phases mimicked the extracellular and intracellular phases. The authors recorded the current flowing across each cell as the local current. The cell with the eight liquid membrane cells was divided into the receiving and the sending sites of the change in membrane potential in a bid to imitate the mechanism that the change in membrane potential is propagated from the synapse to an adjacent node in the axon.
When the authors connected the receiving cells to the resting potential cell, the membrane potential remained relatively the same as the resting potential for all the cells. Low currents, on the other hand were negligibly low. After switching the sending site from the resting potential to the active potential, local current was generated and each cell membrane potential changed. Sodium ions shifted from the aqueous phase 2 to 1 in the active potential cell. Potassium ions, similarly, moved from phase 1 to 2 in the Rec cells. Every cell was connected in parallel, therefore, the sum of current flowing through the receiving cells was equal to the that flowing through the active potential cell.
The authors developed a new interpretation of the hyperpolarization. Based on the functions of the voltage-gated sodium channels and ligand-gated sodium channels at the Ranvier nodes and synapse, respectively, a new mechanism for propagation of the active potential basing on the relationship between the circulating current and the membrane potential. The ligand-gated channels function as power supply gadgets to initiate the action potential along the axon while the voltage-gated channels act as supporting power supply gadgets that help in directional propagation of the active potential.
Y.Takano, O. Shirai, Y. Kitazumi and K. Kano. Proposal of a new mechanism for the directional propagation of the action potential using a mimicking system. Phys. Chem. Chem. Phys., 2017, 19, 5310—5317.Go To Phys. Chem. Chem. Phys.