Where is the end of life?

We're not sure about it, even though all the vital impulses are apparently ceased, the appearance deceives us and can not take the full assurance of the existence of death.

Brain death or absence of neurological activity leads to the thought that the widespread failure of other organs is inevitable. But there are cases where such failure does not occur, or at least not as "fast" as reported.

Therefore, the phenomenon of death is still indecipherable and subject to idiosyncratic review, because that always happens by case and not by the majority

You have explained why signalling might stop, but not why it is irreversible.

Is it really irreversible? How to explain because it is irreversible if not really irreversible?

A simple (perhaps too simple) answer would be to say that the "communication" between the cells or neurons in the brain (and central nervous system) falls below the threshold for sending vital messages.

The "bandwidth" for the communication channels in the body is shrinking so that the capacity for coding and decoding physical activities corresponding to conscious perceptions and more generally for life supporting functions, decline irreversibly.

If "brain death" (a Flat EEG but brain cells still alive) is reversible, this possibility would help to explain Near-Death Experiences

Dear Francesca, although - as a Monist - I do not believe that the soul survives the death of the body, I found important insights in your message. The relation of consciousness with body activity seems to be more complex than most researchers realize. It is trivially possible for the body to be alive while consciousness disappears; but it seems also possible for consciousness to remain somehow active while neurons stop sending their pulses (action potentials) to each other. This is no doubt an altered state of consciousness, when normal functions (as being at the center of egocentric space) seem to be deactivated, but the person is still aware of herself and the environment - according to reports. Twelve years ago I briefly reviewed - with Johnson - experiments with ketamine inducing near-death experiences (see attached paper).

I have to think this through logically.  the reason we have action potentials is because the inside of the neuron is negative relative to the outside of the neuron.  The extra cellular fluid is more positive than the inside.  You suggest that extra cellular potassium increases. which you said would make the action potentials impossible.  Potassium ions are positive,  so if the problem is that the glial cells release more K+, that does not make sense. More positive would not stop the APs.

I think what research shows is that the glial cells release more glutatmate, which is stored in them.  The NMDA receptor for glutamate  causes the ligand gated channel to stick open (with help from the non-NMDA receptors) and calcium then enters the cells. the cells then become edematous (full of fluid), and the cells are often killed.  Other than that, I don't know.

Dear Gayle, please take a look at the attached picture. During the REPOLARIZATION phase, potassium efflux from the neuron depends on the difference of potential. If potassium at the extracellular medium is too high, the neurons does not repolarize.

Dear Gayle, please also take a look at the attached paper. Astrocytes do not release K+ as you mentioned, but when they are activated by Ca++ they capture extracellular K+

Failure of potassium homeostasis causes neuronal depolarization and concomitant failure of neuronal function. This phenomenon is referred to as spreading depression/depolarization (SD) or anoxic depolarization. You may be interested in our recent review on SD, and publications in my thesis on potassium homeostasis during hypoxia (with some references to papers linking this to NDE as well, although this is not my expertise) https://www.researchgate.net/profile/Bas-Jan_Zandt/contributions?ev=prf_act

Why this is in some cases irreversible could be a matter of system dynamics, and this is under active investigation (work of Dahlem, for example)

Another cause for a flat EEG, while cells are still viable, is that synapses become permanently damaged, e.g. during an ischemic insult, e.g:

Hofmeijer and van Putten: https://www.researchgate.net/publication/51971138_Ischemic_cerebral_damage_an_appraisal_of_synaptic_failure

Furthermore, cells can indeed remain alive and be even harvested from dead brains, as long as hours post mortem:

Swaab et al: http://onlinelibrary.wiley.com/doi/10.1111/j.1582-4934.2002.tb00522.x/pdf

Article Ischemic Cerebral Damage An Appraisal of Synaptic Failure

A nice model:

Conf Proc IEEE Eng Med Biol Soc. 2014 Aug;2014:4880-3.

doi: 10.1109/EMBC.2014.6944717.

Effects of astrocytic mechanisms on neuronal hyperexcitability.

Grigorovsky V, Bardakjian BL.

Abstract

While originally astrocytes have been thought to only act as support to neurons, recent studies have implicated them in multiple active roles, including the ability to moderate or alter neuronal firing patterns and to possibly be involved in both the prevention and propagation of epileptic seizures. In this study we propose a new model to incorporate pyramidal cells and interneurons (a common neural circuit in CA3 hippocampal slices) as well as a model of astrocyte. As both potassium and calcium ions have been shown to potentially affect neuronal hyperexcitability, the astrocytic model has both mechanisms - the clearance of potassium through potassium channels (such as KIR, KDR and sodium-potassium pump), and the influence of astrocyte in the synapse (forming the tripartite synapse with calcium-glutamate interactions). Preliminary findings of the model results show that when potassium conductances in the astrocyte are decreased, it results in the accumulation of extracellular potassium, leading to both spontaneous discharges and depolarization block, while the alteration of normal calcium response in the astrocyte can lead to just hyperexcitable conditions without the depolarization block.