Hyperpolarization of Neurons

Susan F Volman svolman at magnus.acs.ohio-state.edu
Sun May 1 15:19:13 EST 1994


In article <livingst-300494145201 at ts7-06.upenn.edu>,
Fred Livingston <livingst at pharm.med.upenn.edu> wrote:
>In reply to all of what I read, I just want to add my two cents, pertaining
>to Cl channels and inhibitory synapses!
>
>In many (most?) neurons, the resting potential is close to the reversal
>potential for Cl. So, through the opening of Cl channels by GABA or
>whatever, the membrane can be hyperpolarized  5-10 mV. However, this slight
>hyperpolarization is only partly responsible for the inhibition of a
>saltatory conductance.

>The main reason for the inhibition is that if the neuron's conductance is
>wickedly increased to Cl then the neuron is effectively shunted, or clamped
>near the reversal potential of Cl. Make sense? 

[Stuff deleted]

I'd like to add my $0.02, too, and a footnote on the history of
neuroscience.  All that Fred said in his post is correct, except that in
some cases the equilibrium potential for Cl is less negative than the
resting potential.  In that case, increasing the Cl conductance is
*depolarizing*, but still inhibitory, as it still has its shunting and
"clamping" effect.  The historical footnote is that this is what 
produces the inhibitory PAD -- primary afferent depolarization -- in the
spinal cord.  The PAD is a presynaptic inhibition of primary afferents that
is depolarizing (just what it's name implies).  Its inhibitory effect was
established because it reduced the size of the EPSP from primary afferents
in their postsynaptic target.  As I understand it, it is now established that
the PAD is due to an increased Cl conductance, which has the effect
of shunting the AP current at the presynaptic terminal, and thus reducing
transmitter release.  But before this was worked out, there was another 
hypothesis about how the depolarizing PAD could reduce transmitter release:
If the terminal is depolarized for a while before the AP gets there, then
more voltage sensitive K channels will be open, and some of the voltage
sensitive Na channels will have been inactivated.  This will reduce the
size of the AP as it invades the terminal.  In addition, the AP will arise
from a more depolarized baseline, and the net current will be smaller.  In
fact, this mechanism is still the only one mentioned in the latest edition
of Aidley, and it is, in my opinion, still *part* of the mechanism, because
the duration of the presynaptic inhibition can outlast the increased Cl 
conductance.  The voltage change lasts longer than the synaptic current, 
and the increased Na inactivation would last even longer.  This suggests 
that the exact relationship between the Cl equilibrium potential and the 
resting potential is finely tuned in different neurons for different effects.

Does anyone out there actually still work on this question?  It's not my
area of expertise -- I just happen to be teaching synaptic integration
right now.

Susan Volman
-- 
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