What cocktail of drugs go into anesthetics and what do those drugs actually do?
In: Biology
It depends.
For local anæsthetics, typically a single compound (usually ending in -caine e.g. lidocaine, benzocaine, cocaine) is injected near the site. These work by blocking voltage-gated sodium channels (VGSCs), which acts to prevent action potentials from propagating.
(Compound blocks the channel that sodium ions flow through. These ions moving is what creates actions potentials — the nerve signals. Because they’re blocked, no sodium can flow, no action potential is sent, and the nerve is effectively temporarily cut.)
For general anæsthetics the situation is a little more complicated. There is no single answer here. Certain drugs, like propofol, benzodiazepines, and barbiturates work as positive allosteric modulators on the GABA_A pathway. I’ll break this down:
GABA_A receptors control chloride channels. When a GABA molecule binds to a GABA_A receptor, its Cl^- channel opens and chloride ions flood into the neuron. This causes a state called hyperpolarization, which makes the neuron less likely to fire. This makes GABA a very important inhibitory neurotransmitter (GABA inhibits neurons firing out of control).
Many drugs are what are called agonists, meaning they bind to the receptor and the receptor thinks it’s the neurotransmitter, and does whatever the receptor does.
This isn’t the case with positive allosteric modulators (PAMs) however. PAMs don’t bind to the active receptor site, instead they bind somewhere else. But this binding serves to increase the relative effect of the normal neurotransmitter. In our GABA_A example, this means that when a GABA_A PAM binds to the GABA_A receptor, the GABA binding site is still unfilled. When one of your normally-present GABA molecules eventually does bind to the site, the receptor will perform its normal action (in this case, opening the chloride channel). The difference is that it will either open the channel *more often* or for *a longer time* whenever this happens. Essentially, they potentiate the effect of GABA.
So for this class of drugs, the mechanism is essentially making your normally present negative feedback mechanism (GABA) stronger than normal (through PAM), which acts to basically inhibit things way more intensely than normal. The surface level effect is sedation of varying level.
Some other GAs, like ketamine, work in even different ways. There is yet another receptor, the NMDA receptor, which controls calcium channels (also for a form of signal transduction). Ketamine literally plugs the hole in this channel, so no signal can pass. This is also how chloroform and nitrous oxide work.
NMDAR also has two binding sites, one for glycine, and another for glutamate. Both must be bound for the channel to be open. Xenon is an antagonist at the glycine site, basically competing for control. Although rare (it’s very expensive), you can use xenon for GA.
There are many more examples with different mechanisms, but I think that should be enough.
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**TL;DR** Your body uses nerves to send signals. These nerves send signals using ion channels. There are lots of types of ion channels. There are lots of things called receptors which control the lots of types of ion channels. You can use drugs which block these receptors and channels to effectively stop signals from being sent down nerves, providing anæsthesia.
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