Medical How does the Anasthesia work?

Did you take a look at this page already?

 

This is essentially unknown. The neuroscience of general anesthesia is almost as mysterious as everything else in neuropharmacology. Recently, understanding general anesthesia has become a focus of Dr. Emery Brown's research at MIT and MGH. Though spending a minute with google scholar, I can't seem to find any publications of his (or anyone else) on the topic. It's an important topic that has been largely neglected in neuroscience.

Here's a link to Professor Brown's webpage: http://web.mit.edu/bcs/people/brown.shtml

 

One mechanism anesthesia acts through is activation of the GABAergic signaling pathways (GABA is primarily an inhibitory neurotransmitter very common in neural function). It is not true at all that it has been neglected.

Here are some abstracts for current articles on it, you can certainly find more searching through PubMed (as an aside, Google Scholar is really inadequate for searching for such topics in my opinion; it seems better for finding books than current peer-reviewed, quality research articles).

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

As the first article in that list points out, while GABAergic mechanisms are the main focus of such research, there is some exploration into other mechanisms, such as cholinergic ones. The others are focusing in more on which GABA subtypes are responsible and in what parts of the brain.

 

I hear people say this all the time. I wonder if google scholar perhaps got better at some point and it used to not work as well? When I search for a biology topic on both I always find the exact same things. The reason I use google scholar is that it is better at finding a full-text version of an article especially if you're plugged into a university system... Also, a lot of the more theoretical literature doesn't show up on pubmed at all.

The paper on the basal forebrain and the cholinergic system is kind of interesting given the same area's supposed role in attention...

 

If you're on a university system, PubMed is even better and should give you direct links to your library's subscriptions with fulltext. I don't know what you're searching for, but then again, you made the claim you didn't find much on this topic with Google Scholar when I got quite a lot of hits on PubMed (my above list is just a tiny sampling). PubMed is where all the biomedical journals index their content, even before it's in print; it's really the first place to look for biomedical related topics.

I'm not sure what you mean by the more theoretical literature. PubMed brings up the review articles. It just doesn't bring up the junk sites that Google will (though it does still have a few odd journals it indexes that aren't terribly reputable).

 

Google Scholar found lots of hits too when I typed in "anesthesia", they were almost all clinical papers though which I didn't think were terribly interesting. The same thing happens with pubmed. In both cases, the results are a lot more interesting if you search for something like "GABA + anesthesia".

By "theoretical" I had meant computational/mathematical work. I was under the impression that pubmed doesn't index the IEEE journals, neural computation and other journals I often read. Though I just checked and that apparently isn't true.

 

The probably semi-apocryphal story an anesthesiologist once told me was that ether was first known to uh.. "get you high". They called it laughing gas for a reason!

In the mid 19th century, people used to throw parties called "ether-follies". You can imagine what would happen at such a party... The story goes, one time a dentist attending one of these things saw someone fall down and hurt himself but not seem to feel any pain.

The same dentist later performed the first painless tooth extractions using ether. From there the idea of anesthesia took off and was appropriated by other medical fields.

 

Here's an interesting article on the topic:

http://www.scienceblog.com/cms/phys...rve-impulses-say-sound-more-likely-12738.html

It suggests that nerve-impulses are mediated not by electrical signals, but by soundwaves, rendering the electrical signals rather a by-product. By altering the melting-point of the bilipid nerve membrane layer for instance ether can inhibit these. Don't know if this stuff has reached medical schools yet though, but it does explain a lot that current theory can't.

 

Don't get too excited, this theory isn't perfect either, but it has a lot of potential ;D

 

It seems my initial comment that how anesthesia works is unknown was not understood as I intended. A LOT is known about how it works on a cellular level (as moonbear pointed out). What receptors/channels it binds etc. I meant to convey the fact that very little is known about how such and such cellular processes can give rise to loss of consciousness and whatever the other effects of anesthesia are. This really is unknown.

So in some sense we know a great deal about anesthesia, but in another (in my opinion more global) sense, very little is known. As an example of the issues preventing us from this sort of understanding: many anesthetics work on the GABAergic system, so too do many epilepsy medications. So why are some compounds that target the GABAergic system anesthetics and others epilepsy drugs? This is probably not known.

The hypothesis that greghouse has posted is merely an alternative hypothesis about how anesthesia works at the cellular level. It is also a hypothesis that runs counter to a mountain of work in ion channel physiology.

For example, I don't see how this soliton theory can explain how the blocking of sodium channels by teterodotoxin can disrupt the action potential. Nor any of the myriad observations linking binding ligand binding to ion channel linked receptors (such as AMPA or NMDA) directly to membrane depolarization.

 

I understood your point.

There's so very little we know about our brains. It's the least understood object in the universe One of the greatest questions in science is right with what gravity is and how the perfect guitar riff must sound like what the scientific definition of contiousness is.

The most critical question to the solitone-theory is, how is it mediated synaptically? Here it has been proven that chemicals mediate the signal, which means that the potential must at least initiate the impulse, but if only initate, why also follow along the entire axon? Etc...

I guess that brings your mind back to the confused state it was in Phy6explorer