We’ve talked about the general way in which neurons in the brain communicate with one another and then reviewed the ways in which cocaine messes some of the basic processes that the brain depends on.
It’s time to move on to another drug, and since the brain-addiction connection is similar for meth and cocaine, it seems the natural next step…
Methamphetamine (speed, ice, glass, crystal, meth)
Remember how we said that cocaine affects the way that dopamine is cleaned up after being released? Well, crystal meth also affects dopamine, but in a different way:
Instead of not allowing a molecule (DAT) to pull released dopamine back into the cell that released it, methamphetamine doesn’t allow the dopamine in a cell to be stored in the little packets that it’s supposed to be put away in. Like the DAT molecule, there’s another molecule that packages dopamine (and other neurotransmitters actually).
This molecule is called vesicular monoamine transporter (VMAT) because it puts a specific kind of neurotransmitter (called monoamines) into packets called vesicles.
You may be asking this right about now:
“If cocaine and crystal meth act in such similar way, why are their effects so different?”
That’s a very good question.
Even though these two ways of affecting dopamine seem very similar, they cause different changes in the levels of dopamine in the brain:
The problem with crystal meth is that the dopamine can’t be packaged at all, which means that whether the autoreceptors tell the brain to turn down dopamine output, the fact that the dopamine won’t go into it’s packages means it just keep leaking out.
Imagine having a burst pipe and trying to stop the flood by turning down the faucet… not too helpful, right?!
So what you end up with is a long lasting flood of dopamine that the brain can’t do much about… You may have already figured it out, but this is one of the many reasons why crysal meth has become the new drug epidemic; it just does its job really really well!