- The transmitter system (How it all works [last bio post will help])
Specifically in the last bio post you'll need to know how the exocytosis works (the sending, blocking and re-uptake between the pre and post synaptic receptors on the axon bulbs).
What do bio chemicals do to your body?
The natural body's chemical signals (neurotransmitters) are made by nuclei around the brain.
NT have different effects on the body because they ARE the commands that are send across the brain and through the nervous system by the action potential.
Different neurotransmitters have different effects on other neurotranmitters, for example Dopamine levels (a neurotransmitter) can be effected by Catechlamines (a neurotransmitter) which are a type of Monoamines (a neurotransmitter). Hence you get different levels of NT.
Monoamines ---
-----------> Indolamines ----------> Serotonin
This is one example of the silly amount of neurotransmitters, of which you don't need to know them all, just how they work. Here wiki's page on NT, the main ones and how they effect chemical levels etc.
The drugs can effect the storage of NT in vesicles, and the pre and post synaptic and auto receptors.
You can have 'Leaky' vesicles, a 'Release' from vesicles or no 'Release' from vesicles (the pic above explains the vesicles situation if you can't remember what they are). For example if L-DOPA a natural dietary supplement, blocks the release of Fenclonine (PCPA) which indirectly decreases the amount of serotonin released.
A more natural example may be the venom of the black widow spider. It's venom a NT releases acetylcholine (ACh) which tells the muscles to contract paralyzing their victim!
No release from the vesicles is the effect of the NT Botulinum Toxin (BoTox), as it blocks the docking of the ACh vesicles, which in turn blocks the release of ACh. So you don't have the wrinkles (that you would have if the muscles in your forehead contract) for 3 or 4 months. This effectively paralyses your forehead lol.
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The NT can also stimulate or block the post-synaptic receptor, and stimulate the pre-synaptic auto-receptor. The later being part of the re-uptake of NTs still in the synaptic cleft.
Nicotine stimulates the pre-synaptic receptors to release more dopamine, which is related to the reward circuits of the brain. Whereas atropine blocks the post-synaptic receptors, which I think relaxes the person, but I got confused and tired (I'll check this out some other time). Any by blocking the post-synaptic receptors you end up with either loads of NT floating around in the excellular fluid in the cleft or if the pre-synaptic auto receptor is still working, loads of NT in the pre-synaptic bulb/vesicles. However apomorphone stimulates the pre-synatpic autoreceptor to stop the uptake of NT back into the pre-synaptic bulb (again didn't quite understand it, so I'll come back to it late when I'm not so tired).
Chronic drug effects such as the upregulation of receptors: more receptors or receptors are more sensitive. As nicotine receptorsonly let through so many nicotine NT, a smoker's brain adds more nictine receptor to solve the problem.
Next Post
2) Neurotransmitter pathways (NTs are projected across the brain through pathways)
Something fun for your trouble
This website has funny mouth pictures
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