J 2016

Influence of caffeine on 3,4-methylenedioxymethamphetamine-induced dopaminergic neuron degeneration and neuroinflammation is age-dependent

FRAU, Lucia; Giulia COSTA; Pier Francesca PORCEDDU; Amit Suresh KHAIRNAR; Maria Paola CASTELLI et. al.

Basic information

Original name

Influence of caffeine on 3,4-methylenedioxymethamphetamine-induced dopaminergic neuron degeneration and neuroinflammation is age-dependent

Authors

FRAU, Lucia (380 Italy); Giulia COSTA (380 Italy); Pier Francesca PORCEDDU (380 Italy); Amit Suresh KHAIRNAR (356 India, guarantor, belonging to the institution); Maria Paola CASTELLI (380 Italy); Maria Grazia ENNAS (380 Italy); Camilla MADEDDU (380 Italy); Jadwiga WARDAS (616 Poland) and Micaela MORELLI (380 Italy)

Edition

Journal of Neurochemistry, HOBOKEN, Wiley-Blackwell, 2016, 0022-3042

Other information

Language

English

Type of outcome

Article in a journal

Field of Study

30000 3. Medical and Health Sciences

Country of publisher

United States of America

Confidentiality degree

is not subject to a state or trade secret

References:

Impact factor

Impact factor: 4.083

RIV identification code

RIV/00216224:14740/16:00092338

Organization unit

Central European Institute of Technology

UT WoS

000367192700012

EID Scopus

2-s2.0-84951907675

Keywords in English

adolescence; caudate-putamen; cytokines; nitric oxide; substantia nigra; tyrosine hydroxylase

Tags

Changed: 15/12/2016 10:46, Mgr. Eva Špillingová

Abstract

In the original language

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 (4x20mg/kg), alone or with caffeine (10mg/kg). Interleukin (IL)-1, tumor necrosis factor (TNF)-, 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-1, and TNF- 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.