Titolo:  Influence of caffeine on 3,4-methylenedioxymethamphetamine-induced dopaminergic neuron degeneration and neuroinflammation is age-dependent
Data di pubblicazione:  2016
Data di prima pubblicazione on-line:  2015
Autori: 
Autori:  Frau, Lucia; Costa, Giulia; Porceddu, Pier Francesca; Khairnar, Amit; Castelli, Maria Paola; Ennas, Maria Grazia; Madeddu, Camilla; Wardas, Jadwiga; Morelli, Micaela
Numero degli autori:  9
Lingua:  Inglese
Presenza coautori internazionali: 
Rivista:  JOURNAL OF NEUROCHEMISTRY
Volume:  136
Fascicolo:  1
Pagina iniziale:  148
Pagina finale:  162
Numero di pagine:  15
Digital Object Identifier (DOI):  http://dx.doi.org/10.1111/jnc.13377
Codice identificativo Pubmed:  26442661
Codice identificativo Scopus:  2-s2.0-84951907675
Codice identificativo ISI:  WOS:000367192700012
Abstract:  Previous studies have demonstrated that caffeine administration to adult mice potentiates glial activation induced by 3,4-methylenedioxymethamphetamine (MDMA). As neuroinflammatory response seems to correlate with neurodegeneration, and the young brain is particularly vulnerable to neurotoxicity, we evaluated dopamine neuron degeneration and glial activation in the caudate-putamen (CPu) and substantia nigra pars compacta (SNc) of adolescent and adult mice. Mice were treated with MDMA (4 × 20 mg/kg), alone or with caffeine (10 mg/kg). Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, neuronal nitric oxide synthase (nNOS) were evaluated in CPu, whereas tyrosine hydroxylase (TH), glial fibrillary acidic protein, and CD11b were evaluated in CPu and SNc by immunohistochemistry. MDMA decreased TH in SNc of both adolescent and adult mice, whereas TH-positive fibers in CPu were only decreased in adults. In CPu of adolescent mice, caffeine potentiated MDMA-induced glial fibrillary acidic protein without altering CD11b, whereas in SNc caffeine did not influence MDMA-induced glial activation. nNOS, IL-1β, and TNF-α were increased by MDMA in CPu of adults, whereas in adolescents, levels were only elevated after combined MDMA plus caffeine. Caffeine alone modified only nNOS. Results suggest that the use of MDMA in association with caffeine during adolescence may exacerbate the neurotoxicity and neuroinflammation elicited by MDMA. Previous studies have demonstrated that caffeine potentiated glial activation induced by 3,4-methylenedioxymethamphetamine (MDMA) in adult mice. In this study, caffeine was shown to potentiate MDMA-induced dopamine neuron degeneration in substantia nigra pars compacta, astrogliosis, and TNF-α levels in caudate-putamen of adolescent mice. Results suggest that combined use of MDMA plus caffeine during adolescence may worsen the neurotoxicity and neuroinflammation elicited by MDMA. Previous studies have demonstrated that caffeine potentiated glial activation induced by 3,4-methylenedioxymethamphetamine (MDMA) in adult mice. In this study, caffeine was shown to potentiate MDMA-induced dopamine neuron degeneration in substantia nigra pars compacta, astrogliosis, and TNF-α levels in caudate-putamen of adolescent mice. Results suggest that combined use of MDMA plus caffeine during adolescence may worsen the neurotoxicity and neuroinflammation elicited by MDMA.
Parole chiave:  Adolescence; Caudate-putamen; Cytokines; Nitric oxide; Substantia nigra; Tyrosine hydroxylase; Age factors; Aging; Animals; Caffeine; Dopaminergic neurons; Drug synergism; Inflammation; Male; Mice; Mice, inbred C57BL; N-Methyl-3,4-methylenedioxyamphetamine; Nerve degeneration; Biochemistry; Cellular and molecular neuroscience
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