AFTERLIFE REVEALED

This essay is a 'technical upgrade' for [the afterlife] essay by David Golgotha.

WARNING: HARDCORE BRAINIAC MATERIALS CONTAINED. HIGH IQ VALUES ARE COMPULSORY TO PROCEED.

The majority will not read this article.

For Those Few who will read and understand : You are in my Dreams.

A lot of arguments concerning existence of the soul are based on the so-called afterlife experiences.

The stupidians are unaware that their highly emotional states of unity with God at the extreme life situations and receiving so-called God’s help when "there is no retreat" are explained in details on both cellular and molecular levels.

Let them be unaware. It promotes reasonable levels of suicide.

Two main biochemical mechanisms which seem to be responsible for so-called " afterlife " experience include NMDA receptors block and mu-opioid receptors activation. Another interesting transmitter that deserves mentioning is vasopressin.

Oversimplified description of these events is presented below:

1) Glutamate ( Glu ) is a major excitatory neurotransmitter in the mammalian CNS and is released by 40 - 50% of neurones in the human brain.

After the release it can act on two groups of receptors:

1.Ionotropic ( basically, ion channels that open when the transmitter, in this case Glu, binds ) and

2.Metabotropic ( after binding of Glu to which certain enzymes are activated ).

These two groups are also divided on subgroups. This division is based upon the molecular structure of receptors and their interaction with various drugs. For instance, ionotropic Glu receptors are divided on two groups: NMDA and AMPA/kainate receptors ( the names are given by the names of drugs that activate the receptors ).

The unique properties of the Ionotropic receptors ( rp ) include the ability of ALL NMDA and some AMPA to allow the entrance of Ca++ into the cell, while usually ion channels are restricted to the regulation of Na+ and K+ entrance and exit. These and other specific qualities define primary importance of these receptors in mechanisms of learning and memory. For example, long - lasting and profound effects of Ca++ infusion may lead to the establishment of LTP ( long term potentiation ). This electrophysiological event is considered to be crucial in the infrmation acquirement and retrieval processes by the majority of modern neurophysiologists. Also, the new growing connections between nerve cells can be specifically stabilised by the insertion of AMPA rp, thus providing additional hints to the events of SYNAPTIC PLASTICITY ( an ability of brain cells to adapt to the environmental changes, that eventually defines what is called IQ, emotional stability, will power, etc., in everyday life ).

Considering all this info, it is not surprising, that maximal adaptive changes are required in the life - threatening situations and enormous quantities of glutamate are released when nerve cells are in the ischaemic/hypoxic conditions (which is a clear sign for them that something is VERY, extraordinary wrong). Thus, LTP is triggered, concentration and speed of thinking are enhanced, memories of past experience retrieved and, in one word, everything necessary to plan a successful escape is provided.

But stop!

In the unexpected, extreme conditions this process cannot be properly regulated. Excessive Glu "overactivates" NMDA ( and certain AMPA ) rp., nerve cells become overloaded with Ca++ and ( I will resist temptation and will not describe death mechanisms... even if they are such a fun !!! ) simply die. So, there must be a mechanism that tries to counteract this biological " short circuit burnout ". As the release of Glu is hardly controllable and as long as Ca ++ is already overloaded the neurone it is in history, the site of the counteraction must be the gates of Ca++ entry - the NMDA itself. In fact, NMDA rp is a very finely attuned system and probably the most sophisticated receptor on this pathetic dirtball. Multiple factors can regulate its activation and inactivation and theirs detailed description can take several thousands pages, so I will spare your clouded minds from this sweet torture...

One of the factors is that the presence of another neurotransmitter amino acid - Glycine is VITAL for the NMDA activation. So, if the glycine binding site on NMDA is blocked, binding of Glu itself does no good ( or bad ). And there are endogenous compounds that can be released to block this glycine binding site, namely, derives of Kinurenate. The question to sort out yet is how much kinurenates are released in terminal situations and where are they released. But the possibility of this NMDA blocking event is VERY, VERY real ( and also logically justified ). So, what does the block of NMDA give?

Well, the PCP ( " angel dust " ) binding site is in the internal gates of the NMDA rp. while kinurenates - blocked glycine site is on the rp. surface. So ( literally !!! ) , the difference between PCP or Ketamine trip and near - death experience is basically several angstroms from the gates to the surface !!! That’s the afterlife the righteous yell for...

How pathetic.

The effects of PCP are well known - derealisation, dissociation from ones body, voices, etc., And to add insult to injury, another point: guess, where the chronic decrease of NMDA activity is usually found? YES !!! In the brains of schizophrenics...

A totally different system that also seems to be involved in near - death experiences is excessive release of opioid peptide beta - endorphin that acts on the mu - opioid receptors.

The reason for it is obvious - reaction on pain and stress.

And as it well known, opioids produce sense of pleasure.

That’s why, even if some near - death experiences can be distressing and hellish ( I suppose: in psychopaths with impaired opioid system functioning ), the majority of them are pleasant and involve heaven, angels of god, etc., In fact, I never seen someone who experienced a unity with Personal Cthulhu or visited W W I battlefields during their short "afterlife"

So, if the NMDA block raises visions and body - detachment, mu rp. activation shapes these events emotionally.

Interesting, that excessive beta - endorphin release can immobilise animals. ( Demonstration of submission in the lost fight or imitation of death in front of the predator. ) So: the majority of Xtian near death experiences indicate only one truth : Weaklings. Personally, I managed to carry on a streetfight being clinically dead... :-)))

Also interesting, that sudden rise of beta - endorphin in the brain tissue, cerebrospinal fluid and blood serum occurs in conscious dogs at the moment of cardiac arrest, but not in anaesthetised dogs. So near - death experience on the surgical table or even when death occurs during sleep must be emotionally different.

You will not meet your God when you die asleep or from the hand of the surgeon.

The last straw: enchanced secretion of vasopressin participates in the formation of long term memory of the extreme event. While the evolutionary benefits of it are clear ( I will remember it and will never do it again ), in our perverted society it becomes deeply rooted in the masochistic tendencies of masses. I will re - unite with God !

Well, suicides are welcome.

Basically, that is all considering so - called mystical afterlife experiences and the ways in which they shape real lives.

My conclusion: near - death experiences can be modelled by administration of PCP and heroine mixture on the way that the action of both drugs starts at the same time. Mixture of PCP and 7 - chlorokinurenate can prove to be even more useful.

All mystically-oriented highly spiritual hippie dorks are invited to check it out.

Lucifer bless you.

As the references are multiple, they are not listed but are available on request.