Inhibition by arachidonic acid and other fatty acids of dopamine uptake at the human dopamine transporter

Chen, Nianhang; Appell, Michael; Berfield, Janet L.; Reith, Maarten E. A.

doi:10.1016/j.ejphar.2003.08.045

Cited by 32 publications

(36 citation statements)

References 29 publications

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“…In this study, DA uptake was inhibited by AEA and AA with IC 50 values of about 10 and 30 µM, respectively. In both of these investigations, AA mimicked the effects of AEA on dopamine and 5-HT transporter, but AEA was more potent inhibitor than AA [106,107]. In another recent study, the effects of AEA and AA were investigated on the glycine transporter subtype 1 (GLYT) [108].…”

Section: E Other Membrane Proteins Directly Affected By Endocannabinmentioning

confidence: 96%

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Receptor-Independent Effects of Endocannabinoids on Ion Channels

Öz¹

2006

CPD

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Endogenous cannabinoids (endocannabinoids), produced from membrane-bound precursors via calcium and/or G-protein dependent processes, mimic the effects of cannabinoids by activating cannabinoid CB(1) and/or CB(2) receptors. Several reports however, also indicate that endocannabinoids can produce effects that are independent of cannabinoid receptors. Thus, in pharmacologically relevant concentrations, endocannabinoids have been demonstrated to modulate the functional properties of voltage-gated ion channels including Ca(2+) channels, Na(+) channels and various types of K(+) channels, and ligand-gated ion channels such as 5-HT(3), and nicotinic ACh receptors. In addition, the functional modulations by endocannabinoids of other ion-transporting membrane proteins such as transient potential receptor-class channels, gap junctions, and neurotransmitter transporters have also been reported. These findings indicate that additional molecular targets for endocannabinoids exist and that these targets may represent important sites for cannabinoids to alter either the excitability of the neurons or the response of the neuronal systems. This review focuses on the results of recent studies indicating that beyond their receptor-mediated effects, endocannabinoids alter the function of ion channels directly.

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Section: E Other Membrane Proteins Directly Affected By Endocannabinmentioning

confidence: 96%

“…In a recent study, AEA and AA reduced the dopamine uptake activity in HEK-293 cells expressing the human dopamine transporter [106]. In another study, the effects of AEA and AA were investigated on 5-HT and dopamine (DA) uptake into rat neocortical synaptosomes [107].…”

Section: E Other Membrane Proteins Directly Affected By Endocannabinmentioning

confidence: 98%

Receptor-Independent Effects of Endocannabinoids on Ion Channels

Öz¹

2006

CPD

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“…The N-methyl-D-aspartate-evoked presynaptic DA release in striatal neurons has been shown to be under the facilitatory control of endogenously formed AA (L'hirondel et al 1999). The degree of unsaturation of hydrocarbon tails appears to determine, in a concentration-dependent fashion, the relative potency in reducing DA uptake, with AA producing more inhibition that saturated acids (i.e., arachidic and stearic acids) and oleic and linoleic acids (cisunsaturated acids) also producing important inhibition as compared to vehicle incubation in cellular line (HEK-293) expressing the DA transporter (Chen et al 2003). In striatum-derived cell lines (X61) expressing a dopaminergic phenotype, the exposure to a variety of LCFAs and, particularly OA and AA, produced a linear and timedependent positive stimulation of the cellular DA content (Heller et al 2005).…”

Section: Discussionmentioning

confidence: 98%

Effects of the increase in neuronal fatty acids availability on food intake and satiety in mice

et al. 2010

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“…Drugs of abuse and intra cranial self stimulation produce reinforcing effects through the same reward circuitry (122), and also increase dopamine neurotransmission in a dopaminergic reward-related area of such circuitry (1,2,3,78,129,130) that has been related to their reinforcing effects (5,79,80). Thus, it is not apparently clear why cocaine and cannabinoid CB1 receptor agonists, which share the ability to stimulate the brain reward circuitry, may have different and antagonistic effects in this procedure.…”

Section: Cannabinoid Modulation Of the Effects Of Cocaine On Thresholmentioning

confidence: 98%

Modulation of the endocannabinoid system: Therapeutic potential against cocaine dependence

Tanda

2007

Pharmacological Research

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Dependence on cocaine is still a main unresolved medical and social concern, and in spite of research efforts, no pharmacological therapy against cocaine dependence is yet available. Recent studies have shown that the endocannabinoid system participates in specific stages and aspects of drug dependence in general, and some of this evidence suggests an involvement of the cannabinoid system in cocaine effects. For example, cocaine administration has been shown to alter brain endocannabinoid levels, and the endocannabinoid system has been involved in long-term modifications of brain processes that might play a role in neuro/behavioral effects of psychostimulant drugs like cocaine. Human studies show that marijuana dependence is frequently associated with cocaine dependence, and that the cannabinoid receptor CNR1 gene polymorphism might be related to cocaine addiction. This article will review the main papers in the field showing how a modulation of different components of the cannabinoid system might interact with some of the neurobiological/behavioral effects of cocaine related to its reinforcing effects, evaluated in preclinical models or in clinical settings. The goal of this review will be to provide insights into the complex picture of cocaine abuse and addiction, and to extrapolate from such endocannabinoid-cocaine interactions useful information to test the therapeutic potential of cannabinoid ligands and endocannabinoid-level enhancers against cocaine dependence for future preclinical/clinical trials.

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Inhibition by arachidonic acid and other fatty acids of dopamine uptake at the human dopamine transporter

Cited by 32 publications

References 29 publications

Receptor-Independent Effects of Endocannabinoids on Ion Channels

Receptor-Independent Effects of Endocannabinoids on Ion Channels

Effects of the increase in neuronal fatty acids availability on food intake and satiety in mice

Modulation of the endocannabinoid system: Therapeutic potential against cocaine dependence

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