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  • AADD Moderators: swilow | Vagabond696

How does nitrous work?

cancle

Bluelighter
Joined
Jan 26, 2001
Messages
597
Has anyone got any detailed info on how N20 affects the brain. I remember reading somewhere that it dissolves the lipid fat membrane. But I have no idea what this really means.
Thanks.
 
FAQ: Nitrous Oxide, N2O, whippits, johnny gas, laughing gas FAQ - Written by pinger
'Ave a read of that - the answers in there somewhere from memory (it's quite long, which is a good thing)...
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Nah Pleo, I checked.
What i'm looking for is a 'this is your brain on nitrous' sort of thing.
 
I just checked erowid and there appears to be some good verbal explanatinos there. Not a big nitrious expert so didm't want to try and explain myself.
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Dancing, the eternal quest to mash my ankles into dust.
 
n2o is a disassociative anesthetic, similar in many ways to ketamine and dxm...yes?
I've had a hard time finding good info on nang juice, but there is a fair bit on the other disso's.
I'm interested too if anyone can come up with good n2o specific info. Even Erowid has been little help with this one.
 
Erowid has a bit but it dosn't really say what the physiological effects are.
I was hoping for diagrams and stuff. What part/s of the brain are effected and so on.
 
Well I was kind of interested in this, because I didn’t know how nitrous worked… so I had a look around and as far as I can tell this is how it works:
(There’s a lot missing, and it may not all be completely correct, so please pick me up if I’m wrong, and just use this as a step in the ladder).
N2O and NMDA receptors
From the lungs, nitrous oxide starts to reach the brain (and other organs) within 15 seconds. Nitrous oxide dissolves in synaptic lipid membranes (of the brain) and alters the binding of neurotransmitter to specific receptor proteins. I think the thing with it dissolving the synaptic lipid (fat) membrane is just necessary for it to reach the receptors – because the receptor is positioned in the lipid bilayer – in the membranes of the cells.
N-methyl-D-aspartate (NMDA) receptors are thought to play a key role in learning, memory and the perception of pain. In the brain, NMDA receptors are activated by a signalling chemical called glutamate, and blocked by nitrous oxide. So it makes sense that nitrous oxide and other aesthetic drugs are in a class called ‘NMDA antagonists’ or ‘NMDA receptor blockers’ – a group of drugs that inhibit excitatory transmissions (prevent the transfer of signals that activate nerves (& raise their membrane potential)).
(^^ Therefore, Nitrous oxide blocks the NMDA receptors and stops some of the signals between nerves in the brain.)
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Ok, so that’s pretty general saying that it stops some signals in the brain... believe it or not I’m finding it pretty hard to find other stuff on the actual effect of blocking NMDA receptors. Therapeutic uses are being developed because blockage of the NMDA receptors may help in a stroke – where there is a huge increase of glutamate production in the brain – and this kills many neurons by promoting apoptosis (suicide of cells) – and by blocking NMDA receptors, you can prevent the release of glutamate. However, that’s not what we want. We want to know what the NMDA receptors do usually, and what happens if they’re blocked when there’s not a huge influx of glutamate. Hrmph.
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Evidence for N2O involvement with NMDA receptors
The researchers came up with several lines of evidence suggesting that nitrous oxide blocks NMDA receptors. The gas prevented brain damage in rats that would have been caused by high NMDA doses. In addition, electrical measurements from rat brain cells in culture showed that nitrous oxide cuts NMDA-type signalling in half, but has only a small effect on GABA-type signalling, the other common pathway affected by anaesthetics. Finally, high doses of the drug damaged the same brain cells as the hallucinogenic drug phencyclidine (PCP) and the aesthetic ketamine, both known NMDA-blockers.
Role of Glutamate & association with N20
Drugs of abuse that block NMDA receptors include phencyclidine (PCP or "angel dust"), ketamine (special "K") and nitrous oxide (laughing gas). These all prevent brain cells from picking up glutamate, a chemical messenger that cells use to communicate with each other. L-Glutamic acid – glutamate – is the most prevalent excitatory neurotransmitter in the vertebrate nervous system. Upon stimulation of a nerve, glutamate is released. It is an important neuro-transmitter in the brain. Here’s a pretty show of how it’s released from the nerves etc: http://www.bioanim.com/CellTissueHumanBody6/S3dPages/kanalGlutam2wa.html
I can’t find any more exact information on this right now (and plus I want to do other stuff..) but very generally, if the neuronal transmissions in the brain are disrupted, then your brain function will be disrupted. A lack of motor control is a good example. Pain receptors are also effected quite a lot (that’s why it’s used as an anaesthetic). Oxygen deprivation probably has a lot to do with the passing out thing too.
N2O and Alcohol
It is known that alcohol can interfere with certain transmitter systems in the brain. The systems use chemical molecules, such as glutamate and GABA, to activate nerve cell receptors and transmit messages from one cell to another. NMDA antagonists interfere with glutamate transmission in the same way that alcohol does, and thus have a similar cell-killing effect in the brain (when given as a single high dose). Investigators also found that drugs that excessively activate GABA receptors, as alcohol does, also can kill nerve cells in the brain.
(^^^ ha ha, so it is just a gutter drug like alkemehol!!)
Some papers thought that nitrous oxide produced withdrawal symptoms (usually in the cases of doctors and dentists who haves chronic exposure to it, but they thought that: Nitrous oxide exposure induces increase in GABA-A receptor a1 subunit mRNA expression in the cingulate cortex, hippocampus, ventral tegmental area and medial septum of mice. These results are also consistent with the hypothesis that ethanol and nitrous oxide produce dependence and withdrawal through common mechanisms. This mechanism of action corresponds closely to the action of ethanol, which also acts on these receptors.
(^^ Yep, getting more & more like alcohol)
N2O & vitamin B-12
Regular use of nitrous oxide can cause reproductive problems and may interfere with the ability of the body to use vitamin B-12. A 1992 study published in the New England Journal of Medicine found that women exposed to high levels of nitrous oxide in their jobs (they were dental assistants) had a greater risk of infertility.
Due to this, it was speculated the gas might interfere with the secretion of reproductive hormones. Long-term use of nitrous oxide can make it more difficult for the body to process vitamin B-12. This can damage the bone marrow and the nervous system. Loss of sensation and other nervous system malfunctions may develop.
(^^ alcohol results in significant B-12 loss too!)
N2O & memory
It was written in a couple of places the effect of Nitrous Oxide on NMDA receptors and memory. Basically: blocking NMDA receptors keeps Ca++ from entering the postsynaptic cell during simultaneous firing (the cell that the information/energy is being passed to). This would stop the synapse strengthening effects of Ca++ and therefore stop new memories from forming.
(^^ not really related, but maybe interesting).
N2O and Pregnancy
But I must add at the bottom here, that if you are PREGNANT, I know everyone knows that it’s bad to drink or do ANY form of drugs – but it REAALLLy is. You kill nerves such as developing sensory nerves of the foetus that CANNOT be replaced. Glutamate-induced excitation of neurons is believed to be crucial in the early development of the brain. Interference in the activity of the transmitters of the brain (especially glutamate) during the synaptogenesis period (the last trimester of pregnancy and the first several years after birth in humans) causes millions of developing neurons to commit suicide (die by apoptosis). This interference can be caused by drugs – especially ethanol and nitrous oxide – to which the human foetal brain may be exposed during the third trimester by drug-abusing mothers. Ethanol triggers massive apoptotic neurodegeneration in the developing brain by interfering with both the NMDA and GABAA receptor systems, and this can explain the reduced brain mass and lifelong neurobehavioral disturbances associated with intrauterine exposure of the human foetus to ethanol (foetal alcohol syndrome).
So just a word of warning – that those old wives tales about being good when you’re pregnant are really, really valid and true; don’t drink, don’t smoke and don’t do drugs (esps. alcohol and NO2) if you’re pregnant and care about your baby. It may just be one drink or one nang for you, but it might result in a % loss of sensory perception for your child, or a irreversible disruption of behavioural and psychiatric well-being. [/ranting mother image].
I don’t think I really answered your question, but I found it harder than I thought. This is what I got anyway:
- Nitrous oxide blocks NMDA receptors.
- The blockage of the NMDA receptors interrupts the transmission of glutamate between nerves.
- Glutamate is a vital neurotransmitter in the brain.
- The reduced neuronal signals in the brain causes a decrease in brain function.
The step missing is what glutamate is really used for in the brain – what effects it causes, and what inhibition of it results in. Anyone??
- Alcohol and N2O work in very similar ways, both acting on the NMDA receptors, and GABA receptors in the brain.
- N2O causes a loss of Vitamin B-12 in the body.
- N2O may effect memory (although I have a feeling this is only associated with chronic use).
- N2O is VERY bad for foetus and newborn babies.
Hope that helps
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That's exactly the stuff I've been looking for. Thank you very, very much. where did you find it?
Any voluteers to make an ammendment to the FAQ. Mabye we can get a dance safe 'this is your brain on ecstasy' but, 'this is your brain on nitrous oxide' slideshow going. There dosn't seem to be enough n2o info avaliable.
 
Try Here ... Information on the glutamate amino acid....
Basically states that the glutamate amino acid is extrected which helps communication between some neurons, I haven't really read the article in great detail but yes
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ruski, thanx dude! ^^^^
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I've copied the relevant bit and pasted it here so it's all together - but there is a cool picture of a neuron on the actual page for anyone interested
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A category of glial cells [in the brain], termed astrocytes, play an active role in brain function by affecting the activity of neurons.
Several studies indicate that following the rise of calcium, astrocytes release the amino acid glutamate, which helps them talk to the neurons. The communication flows both ways, with neurons also being able to talk to the astrocytes through their own glutamate release.
Adding glutamate to cell samples of astrocytes prompts them to produce special molecules that nourish neurons, known as trophic factors. Other research has found that these molecules are key to memory function.
This all may mean that glutamate release from neurons triggers astrocytes to produce trophic factors, which then help neurons process information for memory.
Cancle - no problem
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I found the info all over the place, but if you're looking up any science stuff on the net, I suggest you use google as your search engine.. it'll save you a lot of troubles. I think half the reason there's not much info on N2O is because they don't all that much about it. Research appears to just be taking off now in response to a possible treatment for strokes, and the withdrawal doctors, nurses and dentists are having. That's what it seems like to me anyhew... You can't look up 'Nitrous Oxide' and get the same kind of comprehensive explanation that you get when you type ‘Ecstasy’... but I'm sure it will come with time
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nice one fifi
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... "wisest is he who knows that he does not know" ... "someone prove i exist" ... asparagus? ...
 
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