The brain addiction connection : Crystal meth, and our friend dopamine

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:

This flood is similar to the effect of crystal meth on the brain. By interrupting the way the brain packages dopamine, speed causes an unstoppable flood of this neurotransmitter.While cocaine doesn’t allow the neurons to take dopamine back up (reuptake), the brain has these small monitoring devices called autoreceptors. These receptors detect the levels of dopamine in the brain and adjust the output. When cocaine increases dopamine levels, these autoreceptors decrease the amount of dopamine being released.

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!

Dopamine function in a non-drug-using, meth addict after quitting, and a meth addict after 1 year of staying cleanThe long lasting effects on the brain are similar to those of cocaine, but can be even more devestating. Meth is very neurotoxic meaning that at high levels, it can actually kill neurons by over exciting them. In fact, for both cocaine and methamphetamine, but especially for meth, it can take a very long time (a year or more) for dopamine function to look like anything close to a non-user’s brain (look for the decrease in red in the middle figure showing less overall activity in this area).

Check out this video about meth’s effects:

The brain-addiction connection : Neurons and neurotransmitters

As I’d mentioned in an earlier post, while many people experiment with, or use, drugs at some point in their lives, only a small percentage (between 10%-15%) develop chronic drug abuse and dependence¬†problems. While some of the specifics of what makes one person more likely to move from recreational use to addiction are still being investigated and hotly debated, we do know quite a lot about what happens in the brain when drug are used.

Before I can go into the specifics of the brain-addiction connection…

We need a little background on the way the brain works:

The neuron

The brain is in essence a very complex network of interconnected fibers (neurons) and their maintenance and support structures. The brain contains about 10,000,000,000,000 (10 trillion) of these cells, and they each make many connections.

The left end of the neuron in the picture on the right is called the dendrite; this is the neuron’s main information receiving hub. The long part extending to the right is called an axon, and it ends in axon terminals that eventually connect to other neurons’ dendrites.

This is the basic way in which everything that happens in the brain is communicated, including our thoughts, feelings, movements, and memories!!! Dendrite to axon, to axon terminals, to dendrites, and back to step 1. How this transmission is achieved within the neuron is not necessary for this discussion; let’s just say that you should eat your bananas and make sure you always have some potassium, sodium, and calcium in your body…

How do the neurons talk to one another?

Neurotransmitters

What is important for us is the way these neurons transfer information across the gap between the axon terminals and their connecting dendrites. This is achieved by chemicals called neurotransmitters. There are quite a few of these, but the main ones we’re going to be concerned with are serotonin, adrenaline, GABA, and dopamine as these are some of the major players in drug addiction (especially dopamine).

When a neuron wants to send a signal to its neighbor, it releases packets of a neurotransmitter (most axon terminals release only one specific neurotransmitter), and these are received by specialized receptors at the dendrites of the receiving neuron. If enough neurotransmitter is released and enough receptors are activated, the signal starts again and the cycle continues…

Neurotrasnmitters and drug use

Most abused drugs disrupt some combination of factors within this mechanism to produce both the intended, and unintended, effects they are known for.

Alright, that’s probably enough to absorb for now, more on what specific drugs do to interrupt this process soon!

Question:
How many of you knew about the ways in which drugs affect the brain? Would you mind sharing the things you’ve learned and where you’d learned them?