@article{ref1,
title="Carisoprodol: Update on abuse potential and mechanism of action",
journal="Molecular and Cellular Pharmacology",
year="2015",
author="Kumar, M. and Dillon, G.H.",
volume="7",
number="1",
pages="1-10",
abstract="Carisoprodol is a centrally-acting skeletal muscle relaxant frequently prescribed for acute musculoskeletal conditions. Recreational use of carisoprodol is an increasing problem. Tolerance to carisoprodol develops quickly and abusers often take 10-20 times the normal dose, leading to intoxicating effects. Also, abrupt cessation of carisoprodol results in severe withdrawal syndrome including delusions, seizures and even death. Considering its alarming rate of abuse and subsequent consequences, carisoprodol was scheduled (schedule IV) at the federal level effective January 11, 2012. Until recently, it was widely accepted that the sedative and muscle relaxant effects of carisoprodol were due predominantly to its metabolite, meprobamate. However, it is now clear that carisoprodol itself modulates and directly gates γ-aminobutyric acid type A receptors (GABAARs), the predominant inhibitory neurotransmitter receptors in mammalian brain. Recent work has provided additional insight into carisoprodol's interaction with GABAARs. This may underlie the ability of carisoprodol in enhancing the sedative effects of CNS depressants, contributing to its potential for abuse. In this review, we discuss current understanding with regard to the abuse potential of carisoprodol, therapeutic and abuse-related actions of this drug, and possible molecular actions that underlie these effects. © 2015, LumiText Publishing. All rights reserved.<p /><p>Language: en</p>",
language="en",
issn="1938-1247",
doi="10.4255/mcpharmacol.15.01",
url="http://dx.doi.org/10.4255/mcpharmacol.15.01"
}