HistoryLuigi Galvani found in the 18th 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.

HistoryIn 1840, Emil Dubois-Reymond, a German

physiologist, made instruments that could measure current in nerves and muscles.

HistoryIn 1906, Dutch Physiologist, Willem Einthoven,

made the first electrocardiogram (ECG) that measured electrical impulses in the heart.

HistoryIn 1929, German

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

HistoryJulius 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’.

HistoryKenneth ‘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.

HistorySquid 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 PotentialBack 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 PotentialWhen 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 PotentialIt 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 PotentialWhen 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 PotentialSodium 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 PotentialSodium-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 PotentialDepolarization moves along the axon of the nerve cell in a wave.

Handout!

Last SlideThe 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.