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Title: 3,4-Methylenedioxymethamphetamine enhances kainic acid convulsive susceptibility
Author: Abad, Sonia
Junyent Herena, Fèlix
Auladell i Costa, M. Carme
Pubill Sánchez, David
Pallàs i Llibería, Mercè, 1964-
Camarasa García, Jordi
Escubedo Rafa, Elena
Camins Espuny, Antoni
Keywords: Al·lucinògens
Compostos heterocíclics
Ratolins (Animals de laboratori)
Sistema nerviós central
Hallucinogenic drugs
Heterocyclic compounds
Mice (Laboratory animals)
Central nervous system
Issue Date: 28-Jun-2014
Publisher: Elsevier B.V.
Abstract: Abstract Kainic acid (KA) causes seizures and neuronal loss in the hippocampus. The present study investigated whether a recreational schedule of 3,4-methylenedioxymethamphetamine (MDMA) favours the development of a seizure state in a model of KA-induced epilepsy and potentiates the toxicity profile of KA (20 or 30 mg/kg). Adolescent male C57BL/6 mice received saline or MDMA t.i.d. (s.c. every 3 h), on 1 day a week, for 4 consecutive weeks. Twenty-four hours after the last MDMA exposure, the animals were injected with saline or KA (20 or 30 mg/kg). After this injection, we evaluated seizures, hippocampal neuronal cell death, microgliosis, astrogliosis, and calcium binding proteins. MDMA pretreatment, by itself, did not induce neuronal damage but increased seizure susceptibility in all KA treatments and potentiated the presence of Fluoro-Jade-positive cells in CA1. Furthermore, MDMA, like KA, significantly decreased parvalbumin levels in CA1 and dentate gyrus, where it potentiated the effects of KA. The amphetamine derivative also promoted a transient decrease in calbindin and calretinin levels, indicative of an abnormal neuronal discharge. In addition, treatment of cortical neurons with MDMA (10<br>50 μM) for 6 or 48 h significantly increased basal Ca2 +, reduced basal Na+ levels and potentiated kainate response. These results indicate that MDMA potentiates KA-induced neurodegeneration and also increases KA seizure susceptibility. The mechanism proposed includes changes in Calcium Binding Proteins expression, probably due to the disruption of intracellular ionic homeostasis, or/and an indirect effect through glutamate release.
Note: Versió postprint del document publicat a:
It is part of: Progress in Neuro-Psychopharmacology & Biological Psychiatry, 2014, vol. 54, p. 231-242
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ISSN: 0278-5846
Appears in Collections:Articles publicats en revistes (Institut de Biomedicina (IBUB))
Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica)
Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

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