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Saeed, Mohammad, Ghadiri, Ameneh, Hadizadeh, Farzin, Attaranzadeh, Armin, Alavi, Mohaddeseh Sadat, Etemad, Leila. (1397). Cinnamaldehyde improves methamphetamine-induced spatial learning and memory deficits and restores ERK signaling in the rat prefrontal cortex. , 21(12), 1316-1321. doi: 10.22038/ijbms.2018.35368.8427
Mohammad Saeed; Ameneh Ghadiri; Farzin Hadizadeh; Armin Attaranzadeh; Mohaddeseh Sadat Alavi; Leila Etemad. "Cinnamaldehyde improves methamphetamine-induced spatial learning and memory deficits and restores ERK signaling in the rat prefrontal cortex". , 21, 12, 1397, 1316-1321. doi: 10.22038/ijbms.2018.35368.8427
Saeed, Mohammad, Ghadiri, Ameneh, Hadizadeh, Farzin, Attaranzadeh, Armin, Alavi, Mohaddeseh Sadat, Etemad, Leila. (1397). 'Cinnamaldehyde improves methamphetamine-induced spatial learning and memory deficits and restores ERK signaling in the rat prefrontal cortex', , 21(12), pp. 1316-1321. doi: 10.22038/ijbms.2018.35368.8427
Saeed, Mohammad, Ghadiri, Ameneh, Hadizadeh, Farzin, Attaranzadeh, Armin, Alavi, Mohaddeseh Sadat, Etemad, Leila. Cinnamaldehyde improves methamphetamine-induced spatial learning and memory deficits and restores ERK signaling in the rat prefrontal cortex. , 1397; 21(12): 1316-1321. doi: 10.22038/ijbms.2018.35368.8427

Cinnamaldehyde improves methamphetamine-induced spatial learning and memory deficits and restores ERK signaling in the rat prefrontal cortex

Iranian Journal of Basic Medical Sciences
مقاله 17، دوره 21، شماره 12، اسفند 2018، صفحه 1316-1321    اصل مقاله (633.47 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2018.35368.8427
نویسندگان
Mohammad Saeed1؛ Ameneh Ghadiri2؛ Farzin Hadizadeh3، 4؛ Armin Attaranzadeh5؛ Mohaddeseh Sadat Alavi6؛ Leila Etemad* 7
1School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
2Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Rome, Italy
3Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
4Department of Medicinal Chemistry, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
5Milad Infertility Center, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
6Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
7Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
چکیده
Objective(s): Methamphetamine is a stimulant compound that penetrates readily into the central nervous system. Repeated exposure to methamphetamine leads to damage in the dopaminergic and serotonergic axons of selected brain regions. Previous studies showed that cinnamaldehyde improved memory impairment in animals. In the present study, we aimed to elucidate the effects of cinnamaldehyde on methamphetamine-induced memory impairment in rats.
Materials and Methods: Male Wistar rats received methamphetamine (10 mg/kg, intraperitoneally) for 7 days. Thirty minutes before each injection, animals were given cinnamaldehyde (20, 40, or 80 mg/kg) or rivastigmine (1 mg/kg). The spatial learning and memory were examined using the Morris water maze test. The expression of extracellular signal-regulated kinase (ERK) phosphorylation in the frontal cortex and hippocampus was also detected by immunohistochemical method.
Results: Administration of methamphetamine increased the latency to find the platform in the learning phase, while administration of cinnamaldehyde (40 mg/kg) or rivastigmine before methamphetamine reversed the increased latency. Administration of cinnamaldehyde, at the dose of 40 mg/kg with methamphetamine, increased the time and distance traveled in the target quadrant in comparison with the amphetamine group. Moreover, the methamphetamine and cinnamaldehyde-treated group had higher expression of phosphorylated ERK1/2 in the prefrontal cortex in comparison with the methamphetamine-treated animals.
Conclusion: The present data demonstrated that repeated METH administration impaired cognitive performance through the ERK pathway and decreased the phosphorylation of ERK1/2 in the prefrontal cortex while administration of cinnamaldehyde restored both effects. Accordingly, cinnamaldehyde may be a valuable therapeutic tool for the treatment of cognitive deficits associated with methamphetamine consumption.
کلیدواژه‌ها
Cinnamaldehyde؛ ERK1/2؛ Learning deficit؛ Memory deficit؛ Methamphetamine
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