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?
>> Normally, if a neuron reaches threshold, meaning voltage-sensitive Na
> channels open and the membrane hyperpolarizes due to an influx of Na, then
> we have an action potential. Bu^^^^^^^^^^^^^^?????????
A simple mistake like that does tend to make one wonder....... :-)
t, if at this time
of Na influx there is a
> large Cl conductance increase, Cl will enter the neuron as Na enters,
> thereby inhibiting an action potential (there will be no large change in
> the cells potential difference).
>> Further, at the systems level, a large decrease of synaptic transmission in
> various brain regions could have dire consequences.
>>> -Fred Livingston