Why Nerve Cells Work Faster Than The Theory Allows

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Why Nerve Cells Work Faster Than The Theory Allows

http://www.medicalnewstoday.com/medicalnews.php?newsid=41972

With accuracy unknown until now, researchers from the Max Planck

Institute for Dynamics and Self-Organization and the Bernstein Center

for Computational Neuroscience in Göttingen together with the

neurophysiologist Maxim Volgushev from the Ruhr-Universität Bochum

have analyzed, by which rules, the nerve cells in the cerebral cortex

decide to send out impulses. They surprisingly found, that the high

flexibility and speed with which these cells work cannot be explained

using the present, central model of neurophysiology, the Hodgkin-

Huxley model. Their findings suggest that the sodium channels, which

open in the cell membranes during a nerve impulse, do not work

independently of each other, as assumed so far, but support each

other during the opening process. This new type of mechanism appears

to help the cells transmit fast changing signals and suppress slow

signals.

(Nature, Volume 440, Number 7087, 2006)

Every living cell maintains a voltage difference across its cell

membrane. Nerve cells distinguish themselves from other cells in that

they use this voltage difference to process and transmit messages.

When a nerve cell receives an impulse, the voltage across the cell

membrane is reversed. This " action potential " spreads out through the

long appendages of the cell with high speed. At the end of the

appendages it is transmitted to other cells. In 1952, Alan Lloyd

Hodgkin and Fielding Huxley described in a mathematical model

how such an action potential originates on the basis of measurements

on neurons of the squid. The Hodgkin-Huxley model, for which the

scientists later received the Nobel Prize, has since then served to

explain the signal processes in all neurons.

According to the Hodgkin-Huxley model, an action potential is

initiated when the voltage across the membrane of the nerve cell

reaches to a certain threshold value. Voltage gated sodium channels

react to this voltage change by opening up and triggering an

avalanche-like reaction. Positively charged sodium ions flow through

the open channels into the cell, which leads to a further increase of

the membrane potential and the opening of additional sodium channels.

The threshold and the speed with which the action potential

originates vary from cell to cell - for any individual cell however,

these parameters are specified for the most part by the

characteristics of its sodium channels.

An interdisciplinary team of physicists and neurophysiologists from

the Max Planck Institute for Dynamics and Self-Organization in

Göttingen and the Ruhr-Universität Bochum has now examined more

closely the speed and threshold of action potentials in nerve cells

of the cerebral cortex of the mammal brain. They were able to show

that action potentials are initiated extremely rapid here. Although a

single action potential lasts a millisecond, a stronger influx of

sodium already sets in during the first 200 microseconds. The sodium

channels appear to open almost simultaneously, so that sodium ions

can flow into the cells very quickly and in large amounts. At the

same time, however, the researchers found in their measurements that

the threshold values at which the action potentials were initiated

were very variable.

In order to understand what causes this unusual behavior, the

scientists tried to recreate the behavior of the cells in computer

simulations of Hodgkin-Huxley-type models. To their surprise, it

turned out that a high variability of the threshold value and a rapid

onset of the action potential cannot be unified in this model. Both

characteristics behave like both sides of a seesaw. To obtain a high

variability of the threshold value, the model requires a low speed of

initiation of the action potential. A rapid onset is only obtained,

when the variability of the threshold value is low.

In order to recreate the observed behavior of the nerve cells in

computer simulations, Wolf and his colleagues postulated a new

mechanism, which explains how the sodium channels not always open at

the same threshold value, but nevertheless open almost

simultaneously. When a sodium channel opens, it influences, according

to the new model, other sodium channels in the immediate

neighborhood - the channels open " cooperatively " and not - as

according to Hodgkin-Huxley - independently of each other and only

dependent on the voltage across the membrane. To test this

hypothesis, the scientists used a trick: If it would be possible to

measurably stop the cooperative mechanism, then that would be a good

argument for its existence. They achieved this by blocking a part of

the sodium channels with the nerve poison tetrodoxin, so that the

channels that still functioned lay so scattered in the membrane, that

they were not able to cooperate.

Furthermore, the researchers were able to show that the cells

probably used this novel mechanism to differentiate between the

received signals and only answer to certain ones. Bjoern Naundorf

summarizes these results, „The cells function like a high-pass

filter; fast signals are transmitted well, slow signals are

suppressed " . Both aspects of the initiation of the action potential

play different roles. The large variability of the threshold

potentials allows the cells to ignore slowly varying stimuli. The

cells continuously increase their threshold so that in many cases no

impulse is initiated at all. The fast activation of action

potentials, on the other hand, helps the cells to transmit fast

changing signals, even with high precision. According to the Hodgkin-

Huxley model, the cells would lack the ability to do this.

" Many scientists - including us - saw the Hodgkin-Huxley model up to

now no longer as a hypothesis, but believed that it was principally

applicable to all neurons " , says Fred Wolf, who led the study at the

Max Planck Institute for Dynamics and Self-Organization in

Göttingen. He and his colleagues have now shown that this is not so.

The better cognitive ability of higher animals, such as cats or

humans compared to squid or snails, is not only attributed to the

higher number of neurons in the brains of these animals, but also to

the manner in which the neurons process signals. To do so, these

higher animals presumably use molecular mechanisms which the lower

animals do not possess.