Decreased activity of brain phospholipid metabolic enzymes in human users of cocaine and methamphetamine

Ross, Brian M.; Moszczynska, Anna; Peretti, Frank J.; Adams, Vernard I.; Schmunk, Gregory A.; Kalasinsky, Kathryn S.; Ang, Lee Cyn; Mamalias, Nikolaos; Turenne, Sylvie; Kish, Stephen J.

doi:10.1016/s0376-8716(02)00022-4

Cited by 39 publications

(31 citation statements)

References 22 publications

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“…A recent study by Kita et al (2000) revealed that treatment with METH induced cyclooxygenase-2 protein expression in the mice striatum; and in turn, ketoprofen prevented against METH-induced striatal neurotoxicity (Asanuma et al, 2003). Furthermore, more recent study indicated a decreased striatal activity of Ca-stimulated phospholipase A2 in autopsied brain of chronic cocaine and METH users (Ross et al, 2002). The latter finding is in line with an earlier result showing that pretreatment with citicoline, which increases the rate of membrane phospholipids synthesis, for two weeks attenuated some measures of craving in cocainedependent subjects (Renshaw et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

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

Anggadiredja

Nakamichi

Hiranita

et al. 2004

Neuropsychopharmacol

111

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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.

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Section: Discussionmentioning

confidence: 99%

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

Anggadiredja

Nakamichi

Hiranita

et al. 2004

Neuropsychopharmacol

111

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“…The reduced activity of cPLA2 may be associated with over-stimulation of striatal dopamine receptors because dopamine D2 receptors stimulate cPLA2 activity in CH101 cells [21]. Moreover, the activity of phosphocholine cytidylyltransferase, the rate-limiting enzyme of phosphatidylcholine synthesis, is also reduced in cocaine users [20]. Although the biological significance of each phospholipid species is largely unclear, it has been suggested that the cellular localization of phospholipid species is necessary for functional compartmentalization of the plasma membrane of neurons.…”

Section: Phospholipidsmentioning

confidence: 99%

“…The altered phospholipid metabolism likely resulted from the changes in the activity of brain phospholipid metabolic enzymes following psychostimulant exposure. Reduced activity of calciumstimulated phospholipase A2 (cPLA2) was reported in the striatum of human cocaine and methamphetamine users [19,20]. The reduced activity of cPLA2 may be associated with over-stimulation of striatal dopamine receptors because dopamine D2 receptors stimulate cPLA2 activity in CH101 cells [21].…”

Section: Phospholipidsmentioning

confidence: 99%

Psychostimulants, Brain Membrane Lipids and Dopamine Transmission

Chen¹

2016

J Biomol Res Ther

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Membrane lipids in the brain play important roles in regulation of the membrane compartmentalization, function and signaling of neurotransmitter transporters and receptors. This review summarizes findings on changes in the composition and metabolism of brain membrane lipids such as phospholipids, cholesterol and sphingolipids following chronic exposure to psychostimulants. We also discussed the mechanisms by which membrane lipids regulate the membrane compartmentalization and function of dopamine transports and receptors in animal brain tissues and cultured cell lines. This review indicates that chronic psychostimulant exposure causes the remodeling of brain membrane lipid, which may contribute to psychostimulant-induced functional alterations in dopamine transporters and receptors. Brain membrane lipids could be exploited as a new avenue for pharmacological interventions of abnormal brain dopamine transmission and dopamine-related addiction behavior.

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“…In addition to the actions of psychostimulants on mesolimbic and mesocortical dopamine circuitry (Berman et al , 2008), recent preclinical and clinical studies suggest that these drugs may cause alterations in phospholipid metabolism (Reid et al , 1996; Ross et al , 1996, 2002; Ross and Turenne, 2002). Dopaminergic receptor-mediated phospholipase A2 activation and increased phospholipid hydrolysis has also been suggested by in vitro studies (Hussain and Lokhandwala, 1997; McAllister et al , 1993; Vial and Piomelli, 1995).…”

Section: Introductionmentioning

confidence: 99%

Neurochemical Alterations in Methamphetamine-Dependent Patients Treated with Cytidine-5′-Diphosphate Choline: A Longitudinal Proton Magnetic Resonance Spectroscopy Study

Yoon

Lyoo

Kim

et al. 2009

Neuropsychopharmacol

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Cytidine-5 0 -diphosphate choline (CDP-choline), as an important intermediate for major membrane phospholipids, may exert neuroprotective effects in various neurodegenerative disorders. This longitudinal proton magnetic resonance spectroscopy ( 1 H-MRS) study aimed to examine whether a 4-week CDP-choline treatment could alter neurometabolite levels in patients with methamphetamine (MA) dependence and to investigate whether changes in neurometabolite levels would be associated with MA use. We hypothesized that the prefrontal levels of N-acetyl-aspartate (NAA), a neuronal marker, and choline-containing compound (Cho), which are related to membrane turnover, would increase with CDP-choline treatment in MA-dependent patients. We further hypothesized that this increase would correlate with the total number of negative urine results. Thirty-one treatment seekers with MA dependence were randomly assigned to receive CDP-choline (n ¼ 16) or placebo (n ¼ 15) for 4 weeks. Prefrontal NAA and Cho levels were examined using 1 H-MRS before medication, and at 2 and 4 weeks after treatment. Generalized estimating equation regression analyses showed that the rate of change in prefrontal NAA (p ¼ 0.005) and Cho (p ¼ 0.03) levels were greater with CDP-choline treatment than with placebo. In the CDP-choline-treated patients, changes in prefrontal NAA levels were positively associated with the total number of negative urine results (p ¼ 0.03). Changes in the prefrontal Cho levels, however, were not associated with the total number of negative urine results. These preliminary findings suggest that CDP-choline treatment may exert potential neuroprotective effects directly or indirectly because of reductions in drug use by the MA-dependent patients. Further studies with a larger sample size of MA-dependent patients are warranted to confirm a long-term efficacy of CDP-choline in neuroprotection and abstinence.

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Decreased activity of brain phospholipid metabolic enzymes in human users of cocaine and methamphetamine

Cited by 39 publications

References 22 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

Psychostimulants, Brain Membrane Lipids and Dopamine Transmission

Neurochemical Alterations in Methamphetamine-Dependent Patients Treated with Cytidine-5′-Diphosphate Choline: A Longitudinal Proton Magnetic Resonance Spectroscopy Study

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