Fingolimod zmírňuje harmalinem navozenou poruchu paměti spojenou s pasivním vyhýbáním a motorické poruchy u potkaního modelu esenciálního tremoru

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Autoři: N. Dahmardeh ^1,2; M. Asadi-Shekaari ^1,2; S. Arjmand ²; M. Haghani ³; M. Shabani ²
Působiště autorů: Department of Anatomical Sciences, Afzalipour Medical Faculty, Kerman University of Medical Sciences, Kerman, Iran ¹; Intracellular Recording Lab, Kerman Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran ²; Department of Physiology, Shiraz University of Medical Sciences, Shiraz, Iran ³
Vyšlo v časopise: Cesk Slov Neurol N 2018; 81(6): 691-699
Kategorie: Původní práce
doi: https://doi.org/10.14735/amcsnn2018691

Souhrn

Předklinické údaje naznačují, že fingolimod (FTY), modulátor sfingosin-1-fosfátového receptoru, by mohl být prospěšný pro léčbu běžných neurologických poruch, včetně Parkinsonovy nemoci, RS a epilepsie. V aktuální studii byly studovány účinky FTY na harmalinem navozené motorické a kognitivní poruchy u samců potkanů kmene Wistar. Byly hodnoceny paměť spojená s pasivním vyhýbáním, průzkumné chování, chování související s úzkostí, tremor a motorické funkce. Poruchy paměti pozorované u potkanů, kterým byl podáván harmalin, byly podáním FTY do jisté míry zvráceny. Výsledky ukázaly, že FTY byl schopen obnovit šířku kroku, délku levého a pravého kroku, avšak neobnovil dobu trvání mobility. FTY zlepšil dobu strávenou v závěsu na lanku (wire grip) a na rotující tyči (rotarod). Výsledky naší studie objasnily prospěšné účinky FTY na kognici a motorické funkce u modelu esenciálního tremoru (ET) a naznačují, že modulátory sfingosin-1-fosfátového receptoru mají potenciální neuroprotektivní profil pro léčbu ET.

Klíčová slova:

esenciální tremor –⁠ fingolimod –⁠ paměť –⁠ motorické funkce

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Zdroje

1. Bermejo-Pareja F, Puertas-Martín V. Cognitive features of essential tremor: a review of the clinical aspects and possible mechanistic underpinnings. Tremor Other Hyperkinet Mov (N Y) 2012; 2: pii. doi: 10.7916/ D89W0D7W.

2. Tröster A, Woods S, Fields JA et al. Neuropsychological deficits in essential tremor: an expression of cerebello-thalamo-cortical pathophysiology? Eur J Neurol 2002; 9(2): 143– 151.

3. Nasehi M, Ketabchi M, Khakpai F et al. The effect of CA1 dopaminergic system in harmaline-induced amnesia. Neuroscience 2015; 285 : 47– 59. doi: 10.1016/ j.neuroscience.2014.11.012.

4. Bermejo-Pareja F, Louis ED, Benito-León J et al. Risk of incident dementia in essential tremor: a population-based study. Mov Disord 2007; 22(11): 1573– 1580. doi: 10.1002/ mds.21553.

5. Abbassian H, Esmaeili P, Tahamtan M et al. Cannabinoid receptor agonism suppresses tremor, cognition disturbances and anxiety-like behaviors in a rat model of essential tremor. Physiol Behav 2016; 164(Pt A): 314– 320. doi: 10.1016/ j.physbeh.2016.06.013.

6. Macdonell RA. Cortical excitability and neurology: insights into the pathophysiology. Funct Neurol 2012; 27(3): 131– 145.

7. Kralic JE, Criswell HE, Osterman JL et al. Genetic essential tremor in gamma-aminobutyric acidA receptor alpha1 subunit knockout mice. J Clin Invest 2005; 115(3): 774– 779. doi: 10.1172/ JCI23625.

8. Martin FC, Thu Le A, Handforth A. Harmaline-induced tremor as a potential preclinical screening method for essential tremor medications. Mov Disord 2005; 20(3): 298– 305. doi: 10.1002/ mds.20331.

9. Arshaduddin M, Al Kadasah S, Biary N et al. Citalopram, a selective serotonin reuptake inhibitor augments harmaline-induced tremor in rats. Behav Brain Res 2004; 153(1): 15– 20. doi: 10.1016/ j.bbr.2003.10.035.

10. Deuschl G, Elble RJ. The pathophysiology of essential tremor. Neurology 1999; 54 (11 Suppl 4): S14– S20.

11. Krahl SE, Martin FC, Handforth A. Vagus nerve stimulation inhibits harmaline-induced tremor. Brain Res 2004; 1011(1): 135– 158. doi: 10.1016/ j.brainres.2004.03.021.

12. Puschmann A, Wszolek ZK. Diagnosis and treatment of common forms of tremor. Semin Neurol 2011; 31(1): 65– 77. doi: 10.1055/ s-0031-1271312.

13. Ingwersen J, Aktas O, Kuery P et al. Fingolimod in multiple sclerosis: mechanisms of action and clinical efficacy. Clin Immunol 2012; 142(1): 15– 24. doi: 10.1016/ j.clim.2011.10.008.

14. English C, Aloi JJ. New FDA-approved disease-modifying therapies for multiple sclerosis. Clin Ther 2015; 37(4): 691– 715. doi: 10.1016/ j.clinthera.2015.03.001.

15. Hemmati F, Dargahi L, Nasoohi S et al. Neurorestorative effect of FTY720 in a rat model of Alzheimer‘s disease: comparison with memantine. Behav Brain Res 2013; 252 : 415– 421. doi: 10.1016/ j.bbr.2013.06.016.

16. Nazari M, Keshavarz S, Rafati A et al. Fingolimod (FTY720) improves hippocampal synaptic plasticity and memory deficit in rats following focal cerebral ischemia. Brain Res Bull 2016; 124 : 95– 102. doi: 10.1016/ j.brainresbull.2016.04.004.

17. Kappos L, Radue E-W, O‘connor P et al. A placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis. N Engl J Med 2010; 362(5): 387– 401. doi: 10.1056/ NEJMoa0909494.

18. Becker-Krail D, Farrand AQ, Boger AH et al. Effects of fingolimod administration in a genetic model of cognitive deficits. J Neurosci Res 2017; 95(5): 1174– 1181. doi: 10.1002/ jnr.23799.

19. Kolasiewicz W, Kuter K, Wardas J et al. Role of the metabotropic glutamate receptor subtype 1 in the harmaline-induced tremor in rats. J Neur Transm 2009; 116(9): 1059– 1063. doi: 10.1007/ s00702-009-0254-5.

20. Haghani M, Shabani M, Moazzami K. Maternal mobile phone exposure adversely affects the electrophysiological properties of Purkinje neurons in rat offspring. Neuroscience 2013; 250 : 588– 598. doi: 10.1016/ j.neuroscience.2013.07.049.

21. Shabani M, Larizadeh MH, Parsania S et al. Evaluation of destructive effects of exposure to cisplatin during developmental stage: no profound evidence for sex differences in impaired motor and memory performance. Int J Neurosci 2012; 122(8): 439– 448. doi: 10.3109/ 00207454.2012.673515.

22. Van Wijk N, Rijntjes E, Van De Heijning BJ. Perinatal and chronic hypothyroidism impair behavioural development in male and female rats. Exp Physiol 2008; 93(11): 1199– 1209. doi: 10.1113/ expphysiol.2008.042416.

23. Capoccia S, Maccarinelli F, Buffoli B et al. Behavioral characterization of mouse models of neuroferritinopathy. PloS One 2015; 10(2): e0118990. doi: 10.1371/ journal.pone.0118990.

24. Aghaei I, Arjmand S, Yousefzadeh Chabok S et al. Nitric oxide pathway presumably does not contribute to antianxiety and memory retrieval effects of losartan. Behav Pharmacol 2017; 28(6): 420– 427. doi: 10.1097/ FBP. 0000000000000311.

25. Razavinasab M, Shamsizadeh A, Shabani M et al. Pharmacological blockade of TRPV 1 receptors modulates the effects of 6-OHDA on motor and cognitive functions in a rat model of P arkinson‘s disease. Fundam Clin Pharmacol 2013; 27(6): 632– 640. doi: 10.1111/ fcp.12015.

26. Vaziri Z, Abbassian H, Sheibani V et al. The therapeutic potential of Berberine chloride hydrate against harmaline-induced motor impairments in a rat model of tremor. Neurosci Lett 2015; 590 : 84– 90. doi: 10.1016/ j.neulet.2015.01.078.

27. Abbassian H, Whalley BJ, Sheibani V et al. Cannabinoid type 1 receptor antagonism ameliorates harmaline-induced essential tremor in rat. Br J Pharmacol 2016; 173(22): 3196– 3207. doi: 10.1111/ bph.13581.

28. Arjmand S, Vaziri Z, Behzadi M et al. Cannabinoids and tremor induced by motor-related disorders: friend or foe? Neurotherapeutics 2015; 12(4): 778– 787. doi: 10.1007/ s13311-0150367-5.

29. Cheng MM, Tang G, Kuo SH. Harmaline-induced tremor in mice: videotape documentation and open questions about the model. Tremor Other Hyperkinet Mov (N Y) 2013; 3: pii. doi: 10.7916/ D8H993W3.

30. Du W, Aloyo VJ, Harvey JA. Harmaline competitively inhibits [3H] MK-801 binding to the NMDA receptor in rabbit brain. Brain Res 1997; 770(1– 2): 26– 29.

31. Kopecky BJ, Liang R, Bao J. T-type calcium channel blockers as neuroprotective agents. Pflügers Arch 2014; 466(4): 757– 765. doi: 10.1007/ s00424-014-1454-x.

32. Miwa H, Kondo T. T-type calcium channel as a new therapeutic target for tremor. Cerebellum 2011; 10(3): 563– 569. doi: 10.1007/ s12311-011-0277-y.

33. Dahmardeh N, Asadi-Shekaari M, Arjmand S et al. Modulation of sphingosine-1-phosphate receptor ameliorates harmaline-induced essential tremor in rat. Neurosci Lett 2017; 653 : 376– 381. doi: 10.1016/ j.neulet.2017.06.015.

34. Egom EE, Kruzliak P, Rotrekl V et al. The effect of the sphingosine-1-phosphate analogue FTY720 on atrioventricular nodal tissue. J Cell Mol Med 2015; 19(7): 1729– 1734. doi: 10.1111/ jcmm.12549.

35. Tariq M, Arshaduddin M, Biary N et al. 2-deoxy-D-glucose attenuates harmaline induced tremors in rats. Brain Res 2002; 945(2): 212– 218.

36. Robertson HA. Harmaline-induced tremor: the benzodiazepine receptor as a site of action. Eur J Pharmacol 1980; 67(1): 129– 132.

37. Robertson HA. The benzodiazepine receptor: the pharmacology of emotion. Can J Neurol Sci 1980; 7(3): 243– 245.

38. Riba J, Valle M, Urbano G et al. Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokinetics. J Pharmacol Exp Ther 2003; 306(1): 73– 83.

39. Asle-Rousta M, Kolahdooz Z, Oryan S et al. FTY720 (fingolimod) attenuates beta-amyloid peptide (Abeta42)-induced impairment of spatial learning and memory in rats. J Mol Neurosci 2013; 50(3): 524– 532. doi: 10.1007/ s12031-013-9979-6.

40. Balatoni B, Storch MK, Swoboda EM et al.FTY720 sustains and restores neuronal function in the DA rat model of MOG-induced experimental autoimmune encephalomyelitis. Brain Res Bull 2007; 74(5): 307– 316. doi: 10.1016/ j.brainresbull.2007.06.023.

41. Doi Y, Takeuchi H, Horiuchi H et al. Fingolimod phosphate attenuates oligomeric amyloid β– induced neurotoxicity via increased brain-derived neurotrophic factor expression in neurons. PloS One 2013; 8(4): e61988. doi: 10.1371/ journal.pone.0061988.