variability in recorded action potential amplitudes
rsnorman at mediaone.net
Thu May 11 08:14:24 EST 2000
What you ask is not possible for the very reason indicated in the
paper you cite. That is an invertebrate preparation and, typically,
the cell body and the single neurite leading out of it are not
electrically excitable. The action potention is produced somewhere
in the neuropil amid the profusion of branches of axons and dendrites
(which look all the same). The recording seen in the soma is only
a fraction of the "true" action potential.
The fact that the action potential early in the refractory period is
substantially different from that in the "rested" cell is clear from the
first intracellular records. For examply, see the original Hodgkin and
The variation in amplitude and duration of the action potential in the
axonal terminal is an important aspect of synaptic modulation,
regulating transmitter release. However, these changes are almost
never recordable with intracellular techniques.
And there certainly is no uniformity in the action potentials measured
in different mammalian cells -- skeletal muscle, cardiac muscle, or
CNS neurons. Then when you throw in lower vertebrates, crustaceans,
insects, gastropods and cephalopod molluscs, even the sensitive
mimosa plant and some algae like Chara and Nitella you find an
enormous diversity of potentials.
People don't mention these facts because they are "well known",
especially to comparative physiologists. The validity of one's own
experimental data is determined by experience, the consistency
and reliability of getting similar data time after time, the stability of
recording over time. And the peer review process is the final step
of ensuring that your own judgement of what is acceptable accords
with that of others in the field.
So, sorry, I won't specify that "a resting potential < -72.3 mV is
and the peak overshoot of the action potential must exceed +24.6 mV"
Graham Zemunik <graham at psy.uwa.edu.au> wrote in message
news:391A33E5.75B32B83 at psy.uwa.edu.au...
> Thanks for the replies.
> I had always assumed (for intracellular recordings) that damage to the
> was the most likely candidate, although the odd paper does explicitly
> mention the effect due to recording site.
> For example, in recordings from antennal lobe neurons in the moth Manduca
> sexta, Matsumoto and Hildebrand (Proc R Soc Lond B 213, 249-277 (1981))
> the comment:
> "Action potentials recorded from the cell bodies typically had amplitudes
> between 40 and 60mv and were non-overshooting (the resting potential was
> usually -65 to -70mV) suggesting that action potentials did not actively
> invade the cell bodies"
> I quote this because this is probably the most informative comment I have
> seen in any paper :)
> That's not to say that some other gems remain undiscovered. To this end,
> does anyone know of any papers/books that quantify the variability in
> recorded amplitudes due to damage to the cell? - ie some sort of critique
> the technique.
> I realise, of course, that with damage there will be a continuum from
> nothing to very high, but, for all practicle purposes, is there some
> (amplitude) threshold above which neurophysiologists say "yep this one's
> I think some statistics of this sort would be important to know, because
> only then would one be able to say, with some confidence, that variability
> in the size of action potentials, from one neuron type to another, is due
> intrinsic channel variations (density, kinetics), as opposed to
> in the recording technique.
> It may well be that there are too many factors at play - my gut feeling is
> that there may be. Either way, the answer is informative.
> Graham Zemunik
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