I just started using cocaine about a week ago, and since starting I have herd the term "crack". At first I thought it was funny that someone could become addicted to a drug. After a week, I now understand, but here is my question, Why is cocaine so addictive? Is it just that we have no other way to get high, or is it a government conspiracy? Let’s hear some theories and other nonsense comments.
(Sorry Stryker, couldn't resist. And I in no way advocate the use of drugs.
Posted by Alexa (Member # 6285) on :
Of course you advocate the used of drugs. What we do is a witness to what we believe and gives comfort and encouragement to those who choose to go down the same path.
Posted by Maccabeus (Member # 3051) on :
Focus Factor! They're giving the stuff away free and they say outright that they're doing it because they're sure that once you start you won't want to stop! If that's not an indication of addiction, what is?
Posted by Bob the Lawyer (Member # 3278) on :
Well, cocaine works by blocking the reuptake receptors of norepinephrine, dopamine and serotonin. This increases the concentration of neurotransmitters in the synaptic cleft (the space between the cell sending the signal and the cell getting the signal) and, therefore, increases the stimulatory effect on the cell receiving the signal. So, instead of one cell tapping the other it effectively punches it and you get a rush. However, the cell that receives the signal doesn’t like getting punched so it responds by reducing the number of receptors that receive the signal (you can’t feel something you never received). So to get the same feeling you’re going to need even more neurotransmitters in the cleft, which means you’re going to have to take even more cocaine. It also means that while cocaine isn’t in your system the signals you normally send won’t be as strong, because the cocaine has already reduced the number of receptors. It takes time for the body to replace them and usually you’ve already taken another shot of cocaine before this can happen (hello withdrawal symptoms). It actually makes the lows even lower because it jacks up the negative feedback on the cell that releases the neurotransmitters, so they release them even slower than normal and reduces the amount of enzyme that can make them. So, not only are subsequent signals not as strong because there aren’t as many receptors to respond to them, but the signals are slower which reduces the stimulatory effect even further. Interestingly enough, because the intracellular pools of transmitter get depleted tyrosine hydroxylase (makes transmitter) gets disinhibited, so while there’s less of it in the cell the actual turnover of transmitter synthesis is increased. Basically it works as a sort of ultra-powered anti depressant. Normal anti depressants use the same mechanism, but they aren’t so broad with their specificity (generally blocking only one of the big three) and don’t bind so tightly (so there’s a reduced effect).
Hey, I know you weren’t actually looking for an answer, but that’s no excuse to not learn something, right?