In this review (PMID: 15471589, section 2.4), it saids the "action potential-induced calcium-dependent fluorescence transient" at axonal boutons is related to membrane potential. NO matter de- or hyper-polarization, the fluorescence is decreased. It did not explain the detail why (maybe the did but I dont get the meaning), but indicated there is a by-physical relationship.
I am interested in what the "by-physical" really means here. Can any one give any suggestion? or any paper that give a more clear explaination?
thank you.
p.s.
this paper described several possibility in the end of the review. but I am confused with one statement.
"Depolarisation may lead to a decrease in Ca2+ influx because of inactivation of Na+ and/or Ca2+ channels"
does it mean depolarization leads to inactivation of Na+ channel?
Hello Geng,
I will try to explain what I know about Ca2+ channels, I hope I got your question right.
”GABAA receptor activation both increased the resting Ca2+-dependent fluorescence and decreased the incremental fluorescence upon action potential propagation.”
Their point is that GABAA depolarizes the bouton through a K+ efflux in the cell, so it will depolarizes locally the bouton. This will have 2 effects on 2 different sets of Ca2+ channels:
* Low threshold calcium channels will open, thus increasing the basal calcium concentration in the cell.
* As there is more Ca2+ ions in the cell, their driving force will decrease. Thus during the AP propagation, less Ca2+ will enter the cell through High-threshold Ca2+ channels.
This is a “classic” effect of the membrane potential on basal and dynamic calcium entry.
Blocking the tonic GABA or hyperpolarizing the cell should indeed have the opposite effect, and thus increase the AP-induced CA2+ entry, but they observe the opposite. They do not really explain why, but they put some ideas in the following paragraphs:
“What about the decrease in action potential-evoked Ca2+ influx with hyperpolarisation? The explanation for this is not obvious, but a possibility is that hyperpolarisation leads to de-inactivation of K+ channels, leading to a narrowing of the action potential waveform.”
To understand this hypothesis, you have to know that High-threshold Ca2+ channels will open around 0 mV during an AP, but at this potential there will NOT be any calcium influx: the driving force is too weak. The calcium influx will happen during the repolarizing phase of the AP. And as so, the important factor is the time needed to repolarize from the AP, thus the width of the AP. A large / slow AP will produce a big Ca2+ entry; a really quick and narrow one will produce a small Ca2+ entry.
And the width of the AP is roughly produced by the activation state of K+ channels. If we depolarize the cell, we inactivate K+ channels. This will produce wider APs, increasing the Ca2+ entry during its propagation.
This is how you can produce a wide range of calcium influx by playing on the membrane potential: potential will modify the basal concentration and driving force of Ca2+, but will modify the AP shape as well, leading to potential opposite effects.
And seeing your 2nd comment: yes absolutely, depolarization will inactivates Na+ and Ca2+ channels as well. And this will modify calcium entry and even presynaptic release. If you want to read more, here are some references:
https://www.ncbi.nlm.nih.gov/pubmed/25461842
https://www.ncbi.nlm.nih.gov/pubmed/27994539
I hope I was clear enough, good luck for the rest of your studies!
To see a different view in explaining ionic shifts, please read these papers:
- DOI:
- 10.3233/JIN-170012
- DOI:
- 10.1155/2016/7192427
- In a nutshell, both extracellular and intracellular enviro ments are charged gells not diluted solutions, hence it is not possible either with electrophysiological or optical means to decide about cross memebrane from release of screening charges in the gels. Hope it iwas helpfull to you
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