Innovations In Clinical Neuroscience

JAN-FEB 2017

A peer-reviewed, evidence-based journal for clinicians in the field of neuroscience

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[ V O L U M E 1 4 , N U M B E R 1 – 2 , J A N U A R Y – F E B R U A R Y 2 0 1 7 ] Innovations in CLINICAL NEUROSCIENCE 49 intermediates that eventually leads to n euronal degeneration. Therefore, the role that the IF diet plays in protecting CA1 neurons after MDMA administration is important in our study and requires further investigation to determine how R OS is involved in IF diet-induced neuroprotection. 9,17 The mechanisms whereby caloric restriction enhances cognitive functions and memory and resistance to aging and neurodegenerative disease are studied extensively. 24,39,49,64 Animal studies suggest that CR and specifically IF diets may benefit the brain by reducing levels of oxidative stress and enhancing cellular stress resistance mechanisms. Mild metabolic stress associated with CR stimulates secretion of neuroprotective factors, such as BDNF, by cells to produce proteins that increase cellular resistance to disease processes. 28,41,64 Interestingly, it has been reported that the mouse brain exhibits a greater increase in the number of injured neurons in some brain regions, especially in cerebellum, cortex, and hippocampus after MDMA treatment compared to that in rats. 21 This finding highlights the importance of interspecies variation in neuroprotective mechanisms after MDMA administration and requires further investigation into the role the IF diet plays. Some neurotransmitters, including 5- HT and dopamine, play roles in the regulation of hippocampal neurogenesis. 5-HT depletion decreases hippocampal neurogenesis, and, similarly, dopamine depletion affects neuronal proliferative activity, although the specific effects of dopamine on neurogenesis are still arguable. 22 It will be interesting to study the effects of the IF diet on various aspects of these neurotransmitter systems in MDMA-treated mice. CONCLUSION In conclusion, the results of this study show that an IF diet leads to significantly less anxiety-like behavior and promotes faster recovery in mice when compared to an AL diet. Additionally, the IF diet exerted neuroprotective effects on neurons of the CA1 area of hippocampus. We suggest that the behavioral and histological effects of the IF diet be f urther explored in rodent experimental models for its possible role in the treatment of MDMA-induced neurotoxicity in humans. ACKNOWLEDGMENT The authors wish to thank Dr. Firuzi for providing access to lab facilities for our behavioral work; the Section of Applied Research and Tehran Antinarcotics Police for providing the study drug; Dr. Ali Reza Khajeamiri, Mrs. Keshavarzi, and Mrs. Ghalavandi for their assistance with stereological work; and Mrs. Aghazadeh and Ms. Khalilian for their editorial assistance. This work was part of a MSc thesis of Z. Ebrahimian, supervised jointly by MJ Khoshnoud and MR Haidari. REFERENCES 1. Freye E, Levy J. Pharmacology and Abuse of Cocaine, Amphetamines, Ecstasy and Related Designer Drugs. 1st ed. New York: Springer Netherlands; 2009:143–172. 2. Kalant H. The pharmacology and toxicology of "ecstasy" (MDMA) and related drugs. CMAJ. 2001;165(7):917–928. 3. Capela JP, Carmo H, Remiao F, et al. Molecular and cellular mechanisms of ecstasy-induced neurotoxicity: an overview. Mol Neurobiol. 2009;39(3):210–271. 4. Green AR, Mechan AO, Elliott JM, et al. The pharmacology and clinical pharmacology of 3,4- methylenedioxymethamphetamine (MDMA, "ecstasy"). Pharmacol Rev. 2003;55(3):463–508. 5. Controlled Substance Schedules. United States Department of Justice Drug Enforcement Agency [website]. Diversion Control Division. December 2016. https://www.deadiversion.usdoj.gov/sc hedules/#define. Accessed February 2017. 6. Yazar-Klosinski BB, Mithoefer MC. Potential psychiatric uses for MDMA. Clin Pharmacol Ther. 2017;101(2):194–196. 7. Song BJ, Moon KH, Upreti VV, et al. Mechanisms of MDMA (ecstasy)- induced oxidative stress, mitochondrial dysfunction, and organ damage. Curr Pharm Biotechnol. 2010;11(5):434–443. 8. Busceti CL, Biagioni F, Riozzi B, et al. Enhanced tau phosphorylation in the hippocampus of mice treated with 3,4- methylenedioxymethamphetamine ("Ecstasy"). J Neurosci. 2008;28(12):3234–3245. 9. Colado MI, Camarero J, Mechan AO, et al. A study of the mechanisms involved in the neurotoxic action of 3,4-methylenedioxymethamphetamine (MDMA, 'ecstasy') on dopamine neurones in mouse brain. Br J Pharmacol. 2001;134(8):1711–1723. 10. Ferraz-de-Paula V, Stankevicius D, Ribeiro A, et al. Differential behavioral outcomes of 3,4- methylenedioxymethamphetamine (MDMA-ecstasy) in anxiety-like responses in mice. Braz J Med Biol Res. 2011;44(5):428–437. 11. O'Shea E, Esteban B, Camarero J, et al. Effect of GBR 12909 and fluoxetine on the acute and long term changes induced by MDMA ('ecstasy') on the 5-HT and dopamine concentrations in mouse brain. Neuropharmacology. 2001;40(1):65–74. 12. Lin HQ, Burden PM, Christie MJ, Johnston GA. The anxiogenic-like and anxiolytic-like effects of MDMA on mice in the elevated plus-maze: a comparison with amphetamine. Pharmacol Biochem Behav. 1999;62(3):403–408. 13. Lyles J, Cadet JL. Methylenedioxymethamphetamine (MDMA, ecstasy) neurotoxicity: cellular and molecular mechanisms. Brain Res Brain Res Rev. 2003;42(2):155–168. 14. Sprague JE, Nichols DE. Neurotoxicity of MDMA (ecstasy): beyond metabolism. Trends Pharmacol Sci. 2005;26(2):59–60. 15. Stone DM, Hanson GR, Gibb JW. Differences in the central serotonergic effects of methylenedioxymethamphetamine (MDMA) in mice and rats. Neuropharmacology. 1987;26(11):1657–1661. 16. Liang X, Nagai A, Sheikh AM, et al. Increased vulnerability of hippocampal CA1 neurons to hypoperfusion in

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