History Luigi Galvani found in the 18 th century that the muscle of a dead frog would twitch if electricity passed through it. These experiments lead to tons of research in the field of electrical conductivity of muscle tissue and the body.

History In 1840, Emil Dubois-Reymond, a German physiologist, made instruments that could measure current in nerves and muscles.

History In 1906, Dutch Physiologist, Willem Einthoven, made the first electrocardiogram (ECG) that measured electrical impulses in the heart.

History In 1929, German physiologist, Hans Berger, measured the electrical changes associated with brain activity, the electroencephalograph (EEG) was born.

History Julius Bernstein, who worked under Dubois- Reymond, suggested that nerve impulses were an electrochemical message created by the movement of ions through the nerve cell membrane. This was called his ‘Membrane Hypothesis’.

History Kenneth ‘Kacy’ Cole and Howard Curtis in 1939 came up with the evidence that backed up Bernstein’s theory. They found a rapid change in the potential (voltage) across a squid neuron when it was excited.

History Squid axons became popular lab equipment for neurobiologists because of their diameter and their length. Alan Hodgkin and Andrew Huxley won the Nobel Prize for physiology in 1963 for explaining the action potential sequence we are about to go over. FYI… they involved more mathematical modeling than we are going to do.

Action Potential Back to Cole and Curtis… they found that the resting potential of the nerve was -70 mV. This means that there are more positive charges on the outside of the nerve cell than on the inside.

Action Potential When the nerve became excited, the potential went up to 40 mV and this was termed the action potential. The action potential did not last long and the nerve cell went back to its resting potential.

Action Potential It has been found that it is the movement of positive ions that causes the potential to change in a nerve cell, not the negative ions. The highly concentrated potassium ions want to diffuse out of the nerve cell while the highly concentrated sodium ions want to diffuse in.

My Brain hurts… So as potassium diffuses out, sodium diffuses in… why does the potential change since they both have the same charge?

Action Potential The resting membrane is more permeable to potassium diffusion than sodium diffusion. This means more potassium is moving out than sodium moving in and consequently the outside of the nerve cell is more positive than the inside. This leads to why the resting potential is -70 mV. There are fewer positive ions inside the nerve cell than outside. The resting membrane is said to be charged or polarized.

Action Potential When the nerve cell becomes excited, it becomes more permeable to sodium than potassium. Scientists believe that sodium and potassium gates open and close opposite of one another. As one type of gate opens, the other closes.

Action Potential Sodium rushes into the cell which causes a reversal of charge called a depolarization. Once the voltage becomes positive, the sodium gates close. That is why the max action potential under normal situations is only 40 mV.

Action Potential Sodium-potassium pumps actively restore the original resting potential by moving sodium out and potassium back in. This is called repolarization. Nerve cells cannot transport a second message until the resting potential is reset. This is called the refractory period, the time it takes the nerve cell to be repolarized.

Action Potential Depolarization moves along the axon of the nerve cell in a wave.

Handout!

Last Slide The critical amount of electricity that is required from a nerve cell to fire is known as the threshold level. Stimuli below this level do not initiate a response. Any amount of stimulus above the threshold level gets the same response from the nerve cell. Nerve firing is an all-or-none response. It fires maximally or not at all.