Dopamine enhances the glial endocannabinoid signaling

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  • Ochi Hiroshi
    Department of Legal Medicine, Fujita Health University School of Medicine
  • Hirata Yukari
    Department of Legal Medicine, Fujita Health University School of Medicine
  • Hamajima Makoto
    Department of Legal Medicine, Fujita Health University School of Medicine
  • Isobe Ichiro
    Department of Legal Medicine, Fujita Health University School of Medicine
  • Igarashi Kazuo
    Association of Medicinal Analysis Department of Legal Medicine, Kinki University School of Medicine

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Abstract

<p>Endocannabinoid system (ECS) is widely distributed throughout the body and plays important roles in the physiological functions. In this study, we investigated the effect of some neurotransmitters for the expression state of ECS-related genes of C6 cells. We recognized the significant up-regulation of phospholipase c beta 4 (PLCβ4) and down-regulation of monoacylglycerol lipase (MGLL) by dopamine (DA) treatment. The similar significant expression change of PLCβ4 and MGLL were observed by selective D1 receptor agonist treatment. Because PLCβ4 and MGLL were involved in turnover of 2-arachidonylglycerol (2-AG), it was suggested that DA might affect 2-AG productivity in C6 cells. After pre-treatment with DA, C6 cells were treated with calcium ionophore to induce the 2-AG production. The amount of 2-AG significantly increased in DA pre-treatment group. It is known that endocannabinoids act as retrograde messengers and inhibit several synaptic signal transductions. In this study, we used C6 cells as a model of astrocyte. In the synapse, astrocyte forms the tripartite synapse with presynaptic neuron and postsynaptic neuron, and is known to influence the synaptic signal transductions. If astrocytes actually respond to increased DA in the same manner as C6 cells, we suppose that the increased DA at synapse induces up-regulation of 2-AG production through activation of D1 receptors, and then the 2-AG acts on the CB1 receptors existing on the presynapse and inhibit DA release from the presynaptic ends. In conclusion, our findings suggest that the glial 2-AG signaling may act as inhibitory mechanism of synaptic DA signaling.</p>

Journal

  • Medical Mass Spectrometry

    Medical Mass Spectrometry 5 (1), 2-10, 2021-06-25

    Japanese Society for Biomedical Mass Spectrometry

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