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The Role of the A2A Receptor in Cell Apoptosis Caused by MDMA
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نویسنده
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Soleimani Mansooreh ,Katebi Majid ,Alizadeh Akram ,Mohammadzadeh Farzaneh ,Mehdizadeh Mehdi
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منبع
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cell journal (yakhteh) - 2012 - دوره : 14 - شماره : 3 - صفحه:231 -236
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چکیده
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objective: ecstasy, also known as 3, 4-methylenedioxymethamphetamine (mdma), is a psychoactive recreational hallucinogenic substance and a major worldwide recreational drug. there are neurotoxic effects observed in laboratory animals and humans following mdma use. mdma causes apoptosis in neurons of the central nervous system (cns). withdrawal signs are attenuated by treatment with the adenosine receptor (a2a receptor). this study reports the effects of glutamyl cysteine synthetase (gcs), as an a2a receptor agonist, and succinylcholine (sch), as an a2a receptor antagonist, on sprague dawley rats, both in the presence and absence of mdma.materials and methods: in this experimental study, we used seven groups of sprague dawley rats (200-250 g each). each group was treated with daily intraperitoneal (ip) injectionsfor a period of one week, as follows:i. mdma(10 mg/kg); ii.gcs (0.3 mg/kg); iii. sch(0.3 mg/kg); iv.gcs + sch (0.3 mg/kg each); v.mdma(10 mg/kg) + gcs (0.3 mg/kg);vi.mdma(10mg/kg)+sch(0.3mg/kg);andvi. normalsaline(1cc/kg)astheshamgroup.bax (apoptotic protein) andbcl-2 (anti-apoptotic protein)expressionswereevaluatedby striatum using rt-pcrand westernblot analysis. results: there was a significant increase in bax protein expression in the mdma+sch group and a significant decrease in bcl-2 protein expression in the mdma+sch group (p < 0.05). conclusion: a2a receptors have a role in the apoptotic effects of mdma via the bax and bcl-2 pathways. an agonist of this receptor (gcs) decreases the cytotoxcity of mdma, while the antagonist of this receptor (sch) increases its cytotoxcity.
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کلیدواژه
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Ecstasy or MDMA ,Neurotoxicity ,Adenosine Receptor ,Agonist of A2A Receptor ,Antagonist of A2A Receptor
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آدرس
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tehran university of medical sciences tums, ایران, hormozgan university of medical sciences, ایران, tehran university of medical sciences tums, ایران, tehran university of medical sciences tums, ایران, tehran university of medical sciences tums, ایران
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Authors
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