Behavioral pharmacokinetics of marijuana

Barnett, Gene; Ličko, Vojtech; Thompson, Travis

doi:10.1007/bf00427321

Cited by 71 publications

(33 citation statements)

References 7 publications

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“…The effects of THC on ERK phosphorylation in mice, reported here, were observed at doses (1 mg/kg) that are low for experimental studies in animals and may correspond to the amounts of THC absorbed by human subjects during heavy intoxication (Barnett et al, 1985). This dose of THC has minimal aversive effects in mice, and, given after a priming injection in the home cage, is capable of inducing conditioned place preference .…”

Section: Functional Implications Of the Regulation Of Erk And Immediamentioning

confidence: 62%

Regulation of Extracellular Signal-Regulated Kinase by Cannabinoids in Hippocampus

et al. 2003

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Endocannabinoids form a novel class of intercellular messengers, the functions of which include retrograde signaling in the brain and mediation or modulation of several types of synaptic plasticity. Yet, the signaling mechanisms and long-term effects of the stimulation of CB1 cannabinoid receptors (CB1-R) are poorly understood. We show that anandamide, 2-arachidonoyl-glycerol, and ⌬9-tetrahydrocannabinol (THC) activated extracellular signal-regulated kinase (ERK) in hippocampal slices. In living mice, THC activated ERK in hippocampal neurons and induced its accumulation in the nuclei of pyramidal cells in CA1 and CA3. Both effects were attributable to stimulation of CB1-R and activation of MAP kinase/ERK kinase (MEK). In hippocampal slices, the stimulation of ERK was independent of phosphatidyl-inositol-3-kinase but was regulated by cAMP. The endocannabinoid-induced stimulation of ERK was lost in Fyn knockout mice, in slices and in vivo, although it was insensitive to inhibitors of Src-family tyrosine kinases in vitro, suggesting a noncatalytic role of Fyn. Finally, the effects of cannabinoids on ERK activation were dependent on the activity of glutamate NMDA receptors in vivo, but not in hippocampal slices, indicating the existence of several pathways linking CB1-R to the ERK cascade. In vivo THC induced the expression of immediate-early genes products (c-Fos protein, Zif268, and BDNF mRNAs), and this induction was prevented by an inhibitor of MEK. The strong potential of cannabinoids for inducing long-term alterations in hippocampal neurons through the activation of the ERK pathway may be important for the physiological control of synaptic plasticity and for the general effects of THC in the context of drug abuse.

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Section: Functional Implications Of the Regulation Of Erk And Immediamentioning

confidence: 62%

Regulation of Extracellular Signal-Regulated Kinase by Cannabinoids in Hippocampus

et al. 2003

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“…It should be noted, however, that some studies have reported data showing diminished performance on the DAT (Casswell and Marks 1973;Barnett et al 1985;Perez-Reyes et al 1988;Marks and MacAvoy 1989), the DSST (Heishman et al 1989(Heishman et al , 1997Kelly et al 1993: Wilson et al 1994Haney et al 1997Haney et al , 1999, and the RAT (Heishman et al 1989;Foltin et al 1993;Kelly et al 1993;Haney et al 1997) following similarly tested concentrations of ⌬ 9 -THC. One possible reason we did not observe any performance decrement on these tasks is because the MicroCog TM , which required 30-45 min for completion, was administered during peak marijuana intoxication and participants' post-marijuana performance on the DAT, DSST, and RAT occurred under less than peak marijuana-related subjective and physiological effects.…”

Section: Discussionmentioning

confidence: 98%

Effects of Acute Smoked Marijuana on Complex Cognitive Performance

Hart

Gorp

Haney

et al. 2001

Neuropsychopharmacology

227

175

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“…For example, there is a consistent body of evidence showing that individuals who are acutely intoxicated display impaired memory, slowed information processing speed, and poor attention. 28,29 What defines acute intoxication in the literature is somewhat arbitrary, with studies using 4 to 24 hours as the cutoff period. 28,29 Of note, however, is that pharmacokinetic studies have shown that the acute cognitive effects of cannabis attributable to the initial rapid rise in serum THC begin tapering off 3 to 5 hours after consumption.…”

Section: Discussionmentioning

confidence: 99%