PneuroHD

"Increased ECF calcium also raises the threshold potential, again making it harder to create an action potential, but, when an action potential is reached, a greater number of neurotransmitter vesicles are released." Partly true. ECF can and does raise Action Potential Threshold making it "more difficult" for an action potential to be stimulated. But when the action potential is reached it does NOT increase or decrease the amount of neurotransmitter released at the axon terminal or increase or mitigate the desired signal in the case of cardiac rhythmic cells. Action Potentials are all or nothing. They either fire or they don't. when fired they propogate the signal that particular cell is programmed to release/trasmit. no more. no less. it the accumulation of all the cells' signals together that increase or decrease a particular response. "Increased ECF calcium will bind to Sodium gates, making it harder for sodium to bind to the sodium voltage gated channel, and create a conformational change that opens the channel, therefore it takes longer for enough sodium influx to reach threshold potential." False. calcium does bind to a variety of substrates/receptors etc but it does not bind to sodium channels. Nor does sodium bind to voltage-gated sodium channels. If you check your semantics in that paragraph you can see where the discrepancy falls. they're voltage-gated sodium channels, not sodium voltage gated channels. ie- as a specific, sufficient voltage is passed onto the region wherein the voltage-gated sodium channels reside these channels open allowing sodium to travel down the channel, further propogating the signal. ie- VOLTAGE induces a conformational change that opens the channel to allow sodium to travel into the cell and ultimately depolarize the cell or the region of the axon, in the cases of a neuron, in which those channels resided. "open voltage gated calcium channels, allowing the in-flow of calcium which directly causes neurotransmitter vesicles to undergo exocytosis." True. once voltage-gated calcium channels are opened by the action potential propogation to the axon terminal, calcium rushes in and binds to proteins that induce release of neurotransmitter vesicles to targeted axons dendrites.

Volatile, Ca++ does not bind to Potassium channels receptors, in this case of this discussion at least. in the focus of this discussion it is the opening of Ca++ channels that causes activation of the membrane by the ability of Calcium to flow through the opened channel thus causing depolarization of the membrane and subsequent activation of the cell. YOu are right that this is indeed dependent on/influenced by Potassium channel activation/Potassium gradient flow. quanitative presense (or absence) has nothing to do with a membrane receptors ability to make "it is easier to cause a conformational change to open these channels". activation of the channel, ie-your "conformational change" is based solely on the presense of an agonist or strong voltage change to initiate the receptors operation. the quanitative involvement has to do with the number of receptors that are activated and the amount of Ca++ present to flow down the channel to cause a voltage change in order to overcome the Activation Potential and fire the cell. WIthout adequate Calcium there will be insufficient or no gradient and Calcium will not "flow" and thus will not create the necessary action potential to cause the cell to fire.

"HeartICU", you're mostly correct. Increasing extra or intra cellular concentrations of ions doesn't change action potential thresholds. AP thresholds don't change; at least not due to quantitative changes of ion presence or absence. In the case of hypercalcemia, the resting membrane potential would be hyperpolarized (made more negative in this case), drawing the membrane potential away from the AP threhold, NOT lowering the cell's AP threshold away from an absolute membrane potential. You are absolutely correct that this makes the cell "less excitable" (although it would be better to say that it requires a greater depolarizing stimulus than calling it "less excitable"; this is a semantical point that my fellow scientists and i are always arguing about; just what we need to defeat that nerd stigma, huh? ) as it requires a more intense depolarizing stimulus to reach the Action Potential threshold and initiate cellular action: nerve impulse, muscle contraction, rhythmic signal, whatever... To numerically display it. Most excitable mammalian cells under normal homeostatic have a resting membrane potential of -70mV and action potential threshold of -55mV. (Please note that i said most, not all.) In a state of hypercalcemia, the excessive extracellular positive charge brought about by the above normal presence of calcium (2+ ionic charge) would increase the gradient between the interior and exterior of the cell. This would change the resting membrane potential to, for example, -80 mV. In the homeostatic case you only have a 15 mV bridge to gap in order to reach threshold and ellicit an action potential. But in the hypercalcemic case you now require a stronger depolarizing, 25 mV, stimulus to initiate the Action Potential.