2023, Number 1
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Arch Neurocien 2023; 28 (1)
Intra-striatum lodoxamide produced conditioning place preference in rats via GPR35 independent mechanisms
Díaz-Barba A, Guerrero-Alba R, Quintanar JL, Marichal-Cancino BA
Language: Spanish
References: 30
Page: 20-24
PDF size: 256.21 Kb.
ABSTRACT
The function of the protein-coupled receptor 35 (GPR35) in the central nervous system (CNS) remains
largely unknown. Due to its expression in the ventral striatum, a key area in the brain reward system,
the function of GPR35 in reinforcing actions is questioning. To analyze if activation of GPR35 in the
ventral striatum is related to reinforcing actions, male Wistar rats (250-300 g) received stereotaxic
surgery to place guide cannulae in the ventral striatum. Lodoxamide (a full rat-GPR35 agonist) or
vehicle (DMSO 10%) were injected (intra-ventral-striatum) in the absence and during the pretreatment
with ML-194 (a selective GPR35 antagonist). Lodoxamide (100 pmol) induced a significant increment
in preference for the drug-conditioning chamber (p ‹ 0.05), but not vehicle or ML-194 per se (p ›
0.05). On the other hand, the pretreatment with ML-194 did not prevent lodoxamide’s reinforcing
effects. Thus, the reinforcing actions of lodoxamide (intra-ventral-striatum) involve mechanisms likely
independent of GPR35 which remains to be identified; and a role for GPR35 in the brain reward
systems (at least in ventral striatum) seems improbable.
REFERENCES
O'Dowd BF, Nguyen T, Marchese A, Cheng R, Lynch KR, Heng HH,et al. Discovery of three novel G-protein-coupled receptor genes.Genomics. 1998;47(2):310-3.doi: 10.1006/geno.1998.5095
Fallarini S, Magliulo L, Paoletti T, de Lalla C, Lombardi G. Expressionof functional GPR35 in human iNKT cells. Biochem Biophys ResCommun. 2010;398(3):420-5. doi: 10.1016/j.bbrc.2010.06.09
Guo J, Williams DJ, Puhl HL, 3rd, Ikeda SR. Inhibition of N-typecalcium channels by activation of GPR35, an orphan receptor,heterologously expressed in rat sympathetic neurons. J PharmacolExp Ther. 2008;324(1):342-51. doi: 10.1124/jpet.107.127266
Jenkins L, Alvarez-Curto E, Campbell K, de Munnik S, Canals M,Schlyer S, et al. Agonist activation of the G protein-coupled receptorGPR35 involves transmembrane domain III and is transduced viaGα₁₃ and β-arrestin-2. Br J Pharmacol. 2011;162(3):733-48. doi:10.1111/j.1476-5381.2010.01082.x
Wang J, Simonavicius N, Wu X, Swaminath G, Reagan J, Tian H, etal. Kynurenic acid as a ligand for orphan G protein-coupled receptorGPR35. J Biol Chem. 2006;281(31):22021-8. doi: 10.1074/jbc.M603503200
Amori L, Wu HQ, Marinozzi M, Pellicciari R, Guidetti P,Schwarcz R. Specific inhibition of kynurenate synthesis enhancesextracellular dopamine levels in the rodent striatum. Neuroscience.2009;159(1):196-203.
Pocivavsek A, Wu HQ, Potter MC, Elmer GI, Pellicciari R,Schwarcz R. Fluctuations in endogenous kynurenic acid controlhippocampal glutamate and memory. Neuropsychopharmacology.2011;36(11):2357-67. doi: 10.1038/npp.2011.127
Wonodi I, Schwarcz R. Cortical kynurenine pathway metabolism: anovel target for cognitive enhancement in Schizophrenia. SchizophrBull. 2010;36(2):211-8.
Ohshiro H, Tonai-Kachi H, Ichikawa K. GPR35 is a functionalreceptor in rat dorsal root ganglion neurons. Biochem Biophys ResCommun. 2008;365(2):344-8.
Mok MH, Fricker AC, Weil A, Kew JN. Electrophysiologicalcharacterisation of the actions of kynurenic acid at ligand-gated ionchannels. Neuropharmacology. 2009;57(3):242-9.
Morales-Puerto N, Giménez-Gómez P, Pérez-Hernández M, Abuin-Martínez C, Gil de Biedma-Elduayen L, Vidal R, et al. Adicción yvía de la cinurenina: ¿Una nueva pareja de baile? Pharmacol Ther.2021;223:107807. doi: 10.1016/j.pharmthera.2021.107807
Taniguchi Y, Tonai-Kachi H, Shinjo K. Zaprinast, a well-known cyclicguanosine monophosphate-specific phosphodiesterase inhibitor, isan agonist for GPR35. FEBS Letters. 2006;580(21):5003-8. doi:10.1016/j.febslet.2006.08.015
Shrimpton AE, Braddock BR, Thomson LL, Stein CK, Hoo JJ.Molecular delineation of deletions on 2q37.3 in three cases withan Albright hereditary osteodystrophy-like phenotype. Clin Genet.2004;66(6):537-44. doi: 10.1111/j.1399-0004.2004.00363.x
Sengupta P. The laboratory rat: relating its age with human's. Int JPrev Med. 2013;4(6):624-30.
McGrath JC, Drummond GB, McLachlan EM, Kilkenny C, WainwrightCL. Guidelines for reporting experiments involving animals: theARRIVE guidelines. Br J Pharmacol. 2010;160(7):1573-6.
Bayne K. Revised Guide for the Care and Use of LaboratoryAnimals available. Sociedad Americana de Fisiología. Physiologist.1996;39(4):199, 208-11.
Paxinos G, Watson C. El cerebro de rata en coordenadasestereotáxicas. 7th ed. Nueva York: Academic Press; 2014.
Vázquez-León P, Miranda-Páez A, Calvillo-Robledo A, Marichal-Cancino BA. El bloqueo de GPR55 en el gris periacueductaldorsal produce comportamientos similares a la ansiedad y evocarespuestas agresivas defensivas en ratas preexpuestas al alcohol.Neurosci Lett. 2021:136218.
Vázquez-León P, Ramírez-San Juan E, Marichal-Cancino BA,Campos-Rodríguez C, Chávez-Reyes J, Miranda-Páez A. NPY-Y(1)receptors in dorsal periaqueductal gray modulate anxiety, alcoholintake, and relapse in Wistar rats. Pharmacol Biochem Behav.
2020;199:173071.20. Liu J, Tao X, Liu F, Hu Y, Xue S, Wang Q, et al. Comportamiento yseñalización Epac hipocampal a la nicotina CPP en ratones. TranslNeurosci. 2019;10:254-9.
Díaz-Barba A, Calvillo-Robledo A, Vázquez-León P, Gallegos-VieyraE, Quintanar JL, Marichal-Cancino BA. Central GPR55 may preventnicotine reinforcing actions: a preliminary study. Acta Neurobiol Exp(Wars). 2022;82(3):304-14. doi:10.55782/ane-2022-029
Sun Y, Chen G, Zhou K, Zhu Y. A Conditioned Place PreferenceProtocol for Measuring Incubation of Craving in Rats. J VisExp.2018(141).
Bespalov A, Dumpis M, Piotrovsky L, Zvartau E. Excitatory aminoacidreceptor antagonist kynurenic acid attenuates rewarding potential ofmorphine. Eur J Pharmacol. 1994; 264(3):233-9.
Bespalov A. The expression of both amphetamine-conditioned placepreference and pentylenetetrazol-conditioned place aversion isattenuated by the NMDA receptor antagonist (±)-CPP. Drug AlcoholDepend. 1996;41(1):85-8.
Avunduk AM, Avunduk MC, Dayanir V, Tekelioğlu Y, Dayioğlu YS.Pharmacological mechanism of topical lodoxamide treatmentinvernal keratoconjunctivitis: a flow-cytometric study. OphthalmicRes. 1998; 30(1):37-43. doi: 10.4062/biomolther.2018.227
Kim MJ, Park SJ, Nam SY, Im DS. Lodoxamide AttenuatesHepaticFibrosis in Mice: Involvement of GPR35. Biomol Ther(Seoul).2019; 28(1):92-97. doi: 10.4062/biomolther.2018.227.Epub ahead of print.
Sharmin O, Abir AH, Potol A, Alam M, Banik J, Rahman AFMT,Tarannum N, Wadud R, Habib ZF, Rahman M. Activationof GPR35protects against cerebral ischemia by recruiting monocyte-derivedmacrophages. Sci Rep. 2020; 10(1):9400. doi: 10.1038/s41598-020-66417-8.
Navratilova E, Xie JY, King T, Porreca F. Evaluation of reward frompain relief. Ann N Y Acad Sci. 2013; 1282:1-11. doi:10.1111/nyas.12095
Parenteau GL, Clark RE. Prevention of ischemia-reperfusion injury bythe allergy drug lodoxamide tromethamine. Ann ThoracSurg. 1991;52(4):832-8.
MacKenzie AE, Caltabiano G, Kent TC, Jenkins L, McCallum JE,Hudson BD, Nicklin SA, Fawcett L, Markwick R, CharltonSJ, MilliganG. The antiallergic mast cell stabilizers lodoxamide and bufrolin asthe first high and equipotent agonists of human and rat GPR35. MolPharmacol. 2014; 85(1):91-104. doi: 10.1124/mol.113.089482.