Study hints at brain chemistry of cocaine withdrawal pain

slimvictor

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U.S. researchers have uncovered part of what’s happening, on a cellular level, to make cocaine addicts going cold turkey feel so bloody awful, according to a study.

The results provide a better understanding of what’s creating that crashing low of withdrawal—and may offer a clue for researchers looking to mitigate the symptoms and keep the user from relapsing.

Studying genetically-engineered mice, the researchers focused on a molecule—called cannabinoid receptor 1, or CB1—that slows communication between nerve cells.

The molecule is particularly important in what is called the nucleus accumbens region of the brain, which governs emotion and motivation.

It was already well-known that cocaine produces strong effects on that part of the brain. But this is the first study of cocaine’s impact on CR1 production, and what that means for the nucleus accumbens during and after a cocaine high.

When a person is high on cocaine, “it speeds everything up, pushing you to a highly rewarding emotional state,” said lead author, Bradley Winters.

The cocaine caused the mice to produce an excess of CB1, effectively slamming the brakes on the brain’s hyper-activity in the nucleus accumbens.

“It is kind of like going down a steep hill so you have to start riding that brake really hard,” Winters explained in a statement.

The problem is that the brain doesn’t seem to know to let up on the brakes, after the cocaine high wears off.

cont at
http://www.japantoday.com/category/...at-brain-chemistry-of-cocaine-withdrawal-pain
 
I believe this is the paper.

As usual there is no actual link or proper citation and the issue is grossly oversimplified.

article abstract said:
Furthermore, the membrane excitability of [CB1-expressing neurons] in the NAc was up-regulated after withdrawal from cocaine exposure, an effect that might increase [indirect] inhibition. Taken together with our previous findings that the membrane excitability of NAc [medium spiny neurons] is decreased during cocaine withdrawal, the present findings suggest that the basal functional output of the NAc is inhibited during cocaine withdrawal by multiple mechanisms.

From what I can glean, this paper says the cannabinoid 1-expressing neurons in the NAcc are coupled to GABAergic inhibitory neurons that act as feedback regulators. In cocaine withdrawal, the CB1 expressing neurons in the NAcc become hypersensitive and as a result they inhibit the natural activity in the NAcc responsible for pleasure.

I hate when non-educated people try to write stories about drugs, genetics, or biochemical pathways.
 
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