THC for Anxiety?
Jonah Lehrer has a piece in the New York Inquirer summarizing (at the 100,000 foot level) some research on THC and anxiety. Unfortunately, Lehrer’s article is mostly shake and stems. Here’s a toke:
Despite the fact marijuana was first cultivated almost 10,000 years ago, modern medicine has yet to find a pharmaceutical equal. No other substance melts away our fears with such slick efficiency. But that may soon change. A cadre of neuroscientists is now using the natural potency of pot—its active ingredient is Tetrahydrocannabinol (THC)—as the possible basis for a next generation anti-anxiety pill.
How does it work?
Neuroscientists now believe that a faulty endocannabinoid system might play a large part in all sorts of anxiety syndromes from post-traumatic stress disorder to irrational phobias. Furthermore, they are using this knowledge to invent new drugs. The Holy Grail is a THC compound that is targeted to the parts of our brain—like the amygdala—that modulate our sense of fear. Such a pill would give us the anti-anxiety effects of pot, but without the giddiness, stupidity and hunger. While scientists still don’t know if such a site-specific pill is possible—can we just get our amygdala high?—experiments done in the next few years should help resolve the issue.
You can pick out the seeds and inhale the rest of the piece here. The research Lehrer summarizes was published in Nature:The Endogenous Cannabinoid System Controls Extinction of Aversive Memories. Nature. 2002 Aug 1; 418 (6897):488-9. Here’s the abstract:
Acquisition and storage of aversive memories is one of the basic principles of central nervous systems throughout the animal kingdom. In the absence of reinforcement, the resulting behavioural response will gradually diminish to be finally extinct. Despite the importance of extinction, its cellular mechanisms are largely unknown.
The cannabinoid receptor 1 (CB1) and endocannabinoids are present in memory-related brain areas and modulate memory. Here we show that the endogenous cannabinoid system has a central function in extinction of aversive memories.
CB1-deficient mice showed strongly impaired short-term and long-term extinction in auditory fear-conditioning tests, with unaffected memory acquisition and consolidation. Treatment of wild-type mice with the CB1 antagonist SR141716A mimicked the phenotype of CB1-deficient mice, revealing that CB1 is required at the moment of memory extinction. Consistently, tone presentation during extinction trials resulted in elevated levels of endocannabinoids in the basolateral amygdala complex, a region known to control extinction of aversive memories.
In the basolateral amygdala, endocannabinoids and CB1 were crucially involved in long-term depression of GABA (gamma-aminobutyric acid)-mediated inhibitory currents. We propose that endocannabinoids facilitate extinction of aversive memories through their selective inhibitory effects on local inhibitory networks in the amygdala.
The full bong-hit is here.