a question...

Other approaches to using NEURON in neuroscience education.
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a question...

Post by algofreaky » Mon Mar 27, 2006 3:56 pm

What is anode-break?

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Google for definitions/discussions of (un)common terms

Post by ted » Mon Mar 27, 2006 4:35 pm

Google finds 627 hits. At least a dozen of those should explain it fairly well. The first page
of Google's hits even includes one on this forum. There might also be something on
Wikipedia, but I didn't bother to check.


Post by algofreaky » Tue Mar 28, 2006 5:46 am

in wikipedia there is no word like anode break and if i make a serch in google i don't find the definition, i find experiments.
And another problem is that i don't understand english very well so if you can give me the definition please....please....

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Post by ted » Tue Mar 28, 2006 10:33 am

You're right, most of those Google hits don't really describe the mechanism of anode break

Anode break is an "old" term, from long before microelectrodes were invented.
Physiologists used extracellular electrodes to stimulate nerves. Stimulus electrodes were
applied to the outside of nerve trunks. An extracellular electrode is called a cathode or an
anode, depending on whether the stimulating apparatus (often just a battery in series with
an on/off switch) drives it - or +. It was observed that a cathodal stimulus would excite
the nerve when the stimulus current is turned on, but an anodal stimulus excited the nerve
when the stimulus current is turned off
(hence the term "anode break").

A cathodal stimulus excites a nerve by reducing the electrical field across the
membrane of adjacent axons ("depolarizes" them). This opens sodium channels and
triggers a spike.

What accounts for anode break excitation? It helps to know that, at rest, potassium
conductance is slightly activated, and sodium conductance is partially inactivated.
An anodal stimulus increases the transmembrane electrical field of adjacent axons
("hyperpolarizes" them), and this has two important effects: it decreases resting
potassium conductance, and it relieves sodium channel inactivation. When the anodal
stimulus is turned off, membrane potential quickly springs back from its hyperpolarized
level. Since fewer sodium channels are inactivated, more of them open up, producing
an inward (depolarizing) current. Meanwhile, potassium conductance is slower, so it
lags behind. Consequently, membrane potential overshoots the resting level, making
even more sodium channels open, generating even more inward current and producing
a spike. This is called "anode break excitation."


Post by algofreaky » Fri Mar 31, 2006 11:31 am

thank you very much Ted.

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Re: a question...

Post by PhDstudent » Mon May 23, 2011 4:46 pm


I'm interested in simulating anodal break excitation. I know it's very straightforward with the Hodgkin-Huxley model given a hyperpolarizing pulse with a suitably long duration. However, I'm looking to understand this phenomenon with a Frankenhaeuser-Huxley model.

I haven't come across any modelling publications demonstrating anodal break excitation with FH equations, but many papers examine it experimentally in various animal preparations - suggesting that it is feature common to excitable membranes, including Frankenhaeuser and Widen (1956) with a desheathed frog nerve.

Does anyone have experience using FH equations to generate anodal break excitation?

Thank you in advance for your help and insights!

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