Para acceder a los documentos con el texto completo, por favor, siga el siguiente enlace: http://hdl.handle.net/2445/43290

Título:	Neuronal nicotinic receptors as new targets foramphetamine-induced oxidative damage and neurotoxicity
Autor/a:	Pubill Sánchez, David; Garcia Ratés, Sara; Camarasa García, Jordi; Escubedo Rafa, Elena
Otros autores:	Universitat de Barcelona
Abstract:	Amphetamine derivatives such as methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) are drugs widely abused in a recreational context. This has led to concern because of the evidence that they are neurotoxic in animal models and cognitive impairments have been described in heavy abusers. The main targets of these drugs are plasmalemmal and vesicular monoamine transporters, leading to reverse transport and increased monoamine efflux to the synapse. As far as neurotoxicity is concerned, increased reactive oxygen species (ROS) production seems to be one of the main causes. Recent research has demonstrated that blockade of 7 nicotinic acetylcholine receptors (nAChR) inhibits METH- and MDMA-induced ROS production in striatal synaptosomes which is dependent on calcium and on NO-synthase activation. Moreover, 7 nAChR antagonists (methyllycaconitine and memantine) attenuated in vivo the neurotoxicity induced by METH and MDMA, and memantine prevented the cognitive impairment induced by these drugs. Radioligand binding experiments demonstrated that both drugs have affinity to 7 and heteromeric nAChR, with MDMA showing lower Ki values, while fluorescence calcium experiments indicated that MDMA behaves as a partial agonist on 7 and as an antagonist on heteromeric nAChR. Sustained Ca increase led to calpain and caspase-3 activation. In addition, modulatory effects of MDMA on 7 and heteromeric nAChR populations have been found.
Materia(s):	-Èxtasi (Droga) -Receptors nicotínics -Amfetamines -Neurotoxicologia -Ecstasy (Drug) -Nicotinic receptors -Amphetamines -Neurotoxicology
Derechos:	cc-by (c) Pubill Sánchez, David et al., 2011 http://creativecommons.org/licenses/by/3.0/es
Tipo de documento:	Artículo Artículo - Versión publicada
Editor:	MDPI Publishing
Compartir:

Mostrar el registro completo del ítem