Article by WashingtonStateWire. Published on Tuesday, May 03, 2011 EST.

Slow down, legislators of all stripes. You are so busy you missed it. Yes, today, write it down, a new bill of the week. Senator Carrell has introduced a bill that makes possession of make-believe-pot a crime. Not a make-believe-crime, but possession of a class 1 controlled substance. Uh huh, jail and everything. This pot-want-to-be is called synthetic (that means someone other than God made it) cannabimimietics. Yep, you see the part of the word that sounds like mimic? That means “act like”.

So there you have it. Now these ungodly mimics will go in the law book right between the butene cousins, diethylthiambutene, and his sister Ethel, as in ethylmethylthiambutene.

Knowing our reading audience demands much more technical and medical detail I have put together a little abstract for you (whatever that is)

Abstract (from PubMed.gov)

Cannabinoids (CB) can act as retrograde synaptic mediators of depolarization-induced suppression of inhibition or excitation in hippocampus. This mechanism may underlie the impairment of some cognitive processes produced by these compounds, including short-term memory formation in the hippocampus. In this study, we investigated several compounds known to interact with CB receptors, evaluating their effects on K(+)-evoked release of [3H]D-aspartate ([3H]D-ASP) and [3H]GABA from superfused synaptosomes isolated from the rat hippocampus. [3H]D-ASP and [3H]GABA release were inhibited to different degrees by the synthetic cannabinoids WIN 55,212-2; CP 55,940, and arachidonyl-2′-chloroethylamide/N-(2-chloroethyl)-5Z,8Z,11Z,14Z-eicosatetraenamide (ACEA), as well as by the endocannabinoids, anandamide (AEA), and 2-arachidonoylglycerol (2-AG). Both types of release were also inhibited by capsaicin. The inhibition produced by each of the cannabinoid compounds and capsaicin was unaffected by capsazepine or by the CB1-receptor antagonists AM-251 and SR141716A. The mechanism underlying AEA- and synthetic CB-induced inhibition of the release of [3H]GABA and [3H]D-ASP from rat hippocampal synaptosomes might not involve activation of presynaptic CB1 receptors.

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