Prostaglandin E2 attenuates SR141716A-precipitated withdrawal in tetrahydrocannabinol-dependent mice

Anggadiredja, Kusnandar; Yamaguchi, Taku; Tanaka, Hiroyuki; Shoyama, Yukihiro; Watanabe, Soichi; Yamamoto, Tsuneyuki

doi:10.1016/s0006-8993(02)04169-0

Cited by 27 publications

(18 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We recently demonstrated that cannabinoid-induced behavioral suppression is due to the activation of the arachidonic acid cascade (Yamaguchi et al, 2001b), which is mediated by the prostanoid EP3 receptor (Yamaguchi et al, 2004). Moreover, we have shown that prostaglandin E 2 attenuated the expression of the SR141716A-precipitated withdrawal syndrome in THCdependent mice (Anggadiredja et al, 2003). This evidence suggests that the arachidonic acid cascade regulates the intracellular action of cannabinoids, and consequently, takes the role of the endocannabinoid in the brain reward system.…”

mentioning

confidence: 80%

Endocannabinoid System Modulates Relapse to Methamphetamine Seeking: Possible Mediation by the Arachidonic Acid Cascade

Anggadiredja

Nakamichi

Hiranita

et al. 2004

Neuropsychopharmacol

Self Cite

113

View full text Add to dashboard Cite

We clarified the modulating action of the endocannabinoid system, and its possible mediation by the arachidonic acid cascade, on the reinstatement of methamphetamine (METH)-seeking behavior, using the intravenous self-administration paradigm in rats. Following 12 days of self-administration of METH, the replacement of METH with saline resulted in a gradual decrease in lever press responses (extinction). Under extinction conditions, METH-priming or re-exposure to cues previously paired with METH infusion markedly increased the responses (reinstatement of drug-seeking). The cannabinoid CB1 receptor antagonist, SR141716A, blocked this behavior. Although the cannabinoid agonist, D 8 -tetrahydrocannabinol (THC), had no effects by itself, coadministration of the agonist and METH at small doses reinstated the drug-seeking behavior. THC attenuated the effects of the reinstatement-inducing dose of METH, but enhanced the effect of cues. Either given repeatedly during the extinction or singly, 24 h before the first METH-priming or cues challenge, THC suppressed the reinstatement. In another set of experiments, we found that diclofenac, a cyclooxygenase inhibitor, also attenuated the reinstatement induced by exposure to cues or drug-priming. These results suggest that the endocannabinoid system, through possible mediation by the arachidonic acid cascade, serves as a modulator of the reinstating effects of METH-priming and cues. Extending the current view on the treatment of drug dependence, these results indicate that endocannabinoid-activating substances as well as cyclooxygenase inhibitors may be promising as antirelapse agents.

show abstract

mentioning

confidence: 80%

Endocannabinoid System Modulates Relapse to Methamphetamine Seeking: Possible Mediation by the Arachidonic Acid Cascade

Anggadiredja

Nakamichi

Hiranita

et al. 2004

Neuropsychopharmacol

Self Cite

113

View full text Add to dashboard Cite

show abstract

“…6). Other studies have highlighted a loss of weight as a clear sign of cannabinoid withdrawal (Jones et al, 1981;Budney et al, 2001;Anggadiredja et al, 2003). In addition, spontaneous cannabinoid withdrawal has been described for 72 hr after CP-55,940 treatment in mice (Oliva et al, 2003), producing alterations in gene transcription such as increased proopiomelanocortin (POMC) gene expression.…”

Section: Discussionmentioning

confidence: 99%

Long-Lasting Increase of Alcohol Relapse by the Cannabinoid Receptor Agonist WIN 55,212-2 during Alcohol Deprivation

López-Moreno

González-Cuevas²,

Fonseca³

et al. 2004

J. Neurosci.

View full text Add to dashboard Cite

“…Clonidine, a nonspecific α 2 -receptor agonist that attenuates certain opioid withdrawal symptoms (Uhde et al, 1980), also reverses symptoms of precipitated THC withdrawal in mice (Lichtman et al, 2001). Similarly, the decrease in precipitated withdrawal in THCdependent mice by prostaglandin is hypothesized to be mediated by decreased noradrenergic activity (Anggadiredja et al, 2003). Lofexidine, which is approved for the treatment of opioid withdrawal in the United Kingdom (Strang et al, 1999) and is undergoing clinical trials in the U.S., has been shown to be as effective as clonidine in attenuating opioid withdrawal symptoms, but has a more favorable side effects profile regarding hypotension and sedation (Bearn et al, 1996;Lin et al, 1997;Kahn et al, 1997).…”

mentioning

confidence: 99%

Effects of THC and lofexidine in a human laboratory model of marijuana withdrawal and relapse

et al. 2007

View full text Add to dashboard Cite

Individuals seeking treatment for their marijuana use rarely achieve sustained abstinence.Objectives-To determine if THC, a cannabinoid agonist, and lofexidine, an α 2 -adrenergic receptor agonist, given alone and in combination, decreased symptoms of marijuana withdrawal and relapse, defined as a return to marijuana use after a period of abstinence.Methods-Nontreatment-seeking, male volunteers (n=8), averaging 12 marijuana cigarettes/day, were maintained on each of four medication conditions for 7 days: placebo, THC (60 mg/day), lofexidine (2.4 mg/day), and THC (60 mg/day) combined with lofexidine (2.4 mg/day); each inpatient phase was separated by an outpatient washout phase. During the first 3 inpatient days, placebo marijuana was available for self-administration (withdrawal). For the next 4 days, active marijuana was available for self-administration (relapse). Participants paid for self-administered marijuana using study earnings. Self-administration, mood, task performance, food intake and sleep were measured.Results-THC reversed the anorexia and weight loss associated with marijuana withdrawal, and decreased a subset of withdrawal symptoms, but increased sleep onset latency, and did not decrease marijuana relapse. Lofexidine was sedating, worsened abstinence-related anorexia, and did not robustly attenuate withdrawal, but improved sleep and decreased marijuana relapse. The combination of lofexidine and THC produced the most robust improvements in sleep, and decreased marijuana withdrawal, craving and relapse in daily marijuana smokers relative to either medication alone.Conclusions-These data suggest the combination of lofexidine and THC warrant further testing as a potential treatment for marijuana dependence. KeywordsMarinol; Britlofex; dependence; withdrawal; treatment; cannabinoid; norepinephrine Marijuana use is prevalent in American society, and the number of individuals who currently meet DSM-IV criteria for cannabis abuse or dependence has steadily increased since the 1990s (Compton et al., 2004). Although marijuana is less likely to produce dependence than drugs such as nicotine, alcohol or heroin (Anthony et al., 1994), the sheer number of marijuana smokers combined with the increasing potency of marijuana has NIH Public AccessAuthor Manuscript Psychopharmacology (Berl). Author manuscript; available in PMC 2012 June 12.Published in final edited form as:Psychopharmacology (Berl). 2008 March ; 197(1): 157-168. doi:10.1007/s00213-007-1020-8. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript resulted in a significant number of individuals developing cannabis use disorders, i.e., approximately 1.5% of the U.S. population (Compton et al., 2004).A number of studies have demonstrated that there is a personal (i.e., not court-mandated) demand for marijuana treatment, particularly when marijuana-specific treatment programs are offered (Roffman et al., 1988;Stephens et al., 1993;Lang et al., 2000). Treatmentseekers report distress about their marijuana use, and repeatedly ...

show abstract

Prostaglandin E2 attenuates SR141716A-precipitated withdrawal in tetrahydrocannabinol-dependent mice

Cited by 27 publications

References 34 publications

Endocannabinoid System Modulates Relapse to Methamphetamine Seeking: Possible Mediation by the Arachidonic Acid Cascade

Endocannabinoid System Modulates Relapse to Methamphetamine Seeking: Possible Mediation by the Arachidonic Acid Cascade

Long-Lasting Increase of Alcohol Relapse by the Cannabinoid Receptor Agonist WIN 55,212-2 during Alcohol Deprivation

Effects of THC and lofexidine in a human laboratory model of marijuana withdrawal and relapse

Contact Info

Product

Resources

About