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      Interactions between the Kynurenine and the Endocannabinoid System with Special Emphasis on Migraine

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          Abstract

          Both the kynurenine and the endocannabinoid systems are involved in several neurological disorders, such as migraine and there are increasing number of reports demonstrating that there are interactions of two systems. Although their cooperation has not yet been implicated in migraine, there are reports suggesting this possibility. Additionally, the individual role of the endocannabinoid and kynurenine system in migraine is reviewed here first, focusing on endocannabinoids, kynurenine metabolites, in particular kynurenic acid. Finally, the function of NMDA and cannabinoid receptors in the trigeminal system—which has a crucial role in the pathomechanisms of migraine—will also be discussed. The interaction of the endocannabinoid and kynurenine system has been demonstrated to be therapeutically relevant in a number of pathological conditions, such as cannabis addiction, psychosis, schizophrenia and epilepsy. Accordingly, the cross-talk of these two systems may imply potential mechanisms related to migraine, and may offer new approaches to manage the treatment of this neurological disorder.

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          Molecular characterization of a peripheral receptor for cannabinoids.

          S. MUNRO, K L Thomas, M. Abu-Shaar … (1993)
          The major active ingredient of marijuana, delta 9-tetrahydrocannabinol (delta 9-THC), has been used as a psychoactive agent for thousands of years. Marijuana, and delta 9-THC, also exert a wide range of other effects including analgesia, anti-inflammation, immunosuppression, anticonvulsion, alleviation of intraocular pressure in glaucoma, and attenuation of vomiting. The clinical application of cannabinoids has, however, been limited by their psychoactive effects, and this has led to interest in the biochemical bases of their action. Progress stemmed initially from the synthesis of potent derivatives of delta 9-THC, and more recently from the cloning of a gene encoding a G-protein-coupled receptor for cannabinoids. This receptor is expressed in the brain but not in the periphery, except for a low level in testes. It has been proposed that the nonpsychoactive effects of cannabinoids are either mediated centrally or through direct interaction with other, non-receptor proteins. Here we report the cloning of a receptor for cannabinoids that is not expressed in the brain but rather in macrophages in the marginal zone of spleen.
          Article 0 comments Cited 901 times – based on 0 reviews     Review now
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            Structure of a cannabinoid receptor and functional expression of the cloned cDNA.

            L Matsuda, S Lolait, M J Brownstein … (1990)
            Marijuana and many of its constituent cannabinoids influence the central nervous system (CNS) in a complex and dose-dependent manner. Although CNS depression and analgesia are well documented effects of the cannabinoids, the mechanisms responsible for these and other cannabinoid-induced effects are not so far known. The hydrophobic nature of these substances has suggested that cannabinoids resemble anaesthetic agents in their action, that is, they nonspecifically disrupt cellular membranes. Recent evidence, however, has supported a mechanism involving a G protein-coupled receptor found in brain and neural cell lines, and which inhibits adenylate cyclase activity in a dose-dependent, stereoselective and pertussis toxin-sensitive manner. Also, the receptor is more responsive to psychoactive cannabinoids than to non-psychoactive cannabinoids. Here we report the cloning and expression of a complementary DNA that encodes a G protein-coupled receptor with all of these properties. Its messenger RNA is found in cell lines and regions of the brain that have cannabinoid receptors. These findings suggest that this protein is involved in cannabinoid-induced CNS effects (including alterations in mood and cognition) experienced by users of marijuana.
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              Pathophysiology of Migraine: A Disorder of Sensory Processing.

              Peter J Goadsby, Philip Holland, Margarida Martins-Oliveira … (2017)
              Plaguing humans for more than two millennia, manifest on every continent studied, and with more than one billion patients having an attack in any year, migraine stands as the sixth most common cause of disability on the planet. The pathophysiology of migraine has emerged from a historical consideration of the "humors" through mid-20th century distraction of the now defunct Vascular Theory to a clear place as a neurological disorder. It could be said there are three questions: why, how, and when? Why: migraine is largely accepted to be an inherited tendency for the brain to lose control of its inputs. How: the now classical trigeminal durovascular afferent pathway has been explored in laboratory and clinic; interrogated with immunohistochemistry to functional brain imaging to offer a roadmap of the attack. When: migraine attacks emerge due to a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment. In the first, premonitory, phase that precedes headache, brain stem and diencephalic systems modulating afferent signals, light-photophobia or sound-phonophobia, begin to dysfunction and eventually to evolve to the pain phase and with time the resolution or postdromal phase. Understanding the biology of migraine through careful bench-based research has led to major classes of therapeutics being identified: triptans, serotonin 5-HT1B/1D receptor agonists; gepants, calcitonin gene-related peptide (CGRP) receptor antagonists; ditans, 5-HT1F receptor agonists, CGRP mechanisms monoclonal antibodies; and glurants, mGlu5 modulators; with the promise of more to come. Investment in understanding migraine has been very successful and leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.
              Article 0 comments Cited 574 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 30 July 2017
                Publication date Collection: August 2017
                Volume: 18
                Issue: 8
                Electronic Location Identifier: 1617
                Affiliations
                [1 ]MTA-SZTE Neuroscience Research Group, University of Szeged, H-6725 Szeged, Hungary; gabor.balazs.nagy@ 123456gmail.com (G.N.-G.); zsuzsanna.bohar@ 123456gmail.com (Z.B.)
                [2 ]Faculty of Health Sciences and Social Studies, University of Szeged, H-6726 Szeged, Hungary
                [3 ]Institute of Biochemistry, Biological Research Center, Hungarian Academy of Sciences, H-6726 Szeged, Hungary; zador.ferenc@ 123456gmail.com (F.Z.); dvoracsko.szabolcs@ 123456brc.mta.hu (S.D.); benyhe.sandor@ 123456brc.mta.hu (S.B.); tomboly.csaba@ 123456brc.mta.hu (C.T.)
                [4 ]Department of Neurology, Faculty of Medicine, Albert Szent-Györgyi Clinical Center, University of Szeged, H-6725 Szeged, Hungary; apardutz@ 123456yahoo.com
                Author notes
                [* ]Correspondence: vecsei.laszlo@ 123456med.u-szeged.hu ; Tel.: +36-62-545-351
                [†]

                These authors contributed equally to this work.

                Article
                Publisher ID: ijms-18-01617
                DOI: 10.3390/ijms18081617
                PMC ID: 5578009
                PubMed ID: 28758944
                SO-VID: d95ec753-ffbf-4fe6-b713-15d5afb178fc
                Copyright © © 2017 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 30 June 2017
                Date accepted : 21 July 2017
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: cannabinoids,endocannabinoids,cannabinoid receptors,kynurenines,opioids,migraine
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: cannabinoids, endocannabinoids, cannabinoid receptors, kynurenines, opioids, migraine

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