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Increased neurotransmitter release at the neuromuscular junction in a mouse model of polyglutamine disease

Opened Access Increased neurotransmitter release at the neuromuscular junction in a mouse model of polyglutamine disease
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Autor: Rozas Espadas, José Luis
Gómez-Sánchez, Leonardo
Tomás-Zapico, Cristina
Lucas Lozano, José J.
Fernández-Chacón, Rafael
Departamento: Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica
Fecha: 2011
Publicado en: The Journal of Neuroscience, January 19, 2011 • 31(3):1106 –1113
Tipo de documento: Artículo
Resumen: In Huntington’s disease (HD), the expansion of polyglutamine (polyQ) repeats at the N terminus of the ubiquitous protein huntingtin (htt) leads to neurodegeneration in specific brain areas. Neurons degenerating in HD develop synaptic dysfunctions. However, it is unknown whether mutant htt impacts synaptic function in general. To investigate that, we have focused on the nerve terminals of motor neurons that typically do not degenerate in HD. Here, we have studied synaptic transmission at the neuromuscular junction of transgenic mice expressing a mutant form of htt (R6/1 mice).Wehave found that the size and frequency of miniature endplate potentials are similar in R6/1 and control mice. In contrast, the amplitude of evoked endplate potentials in R6/1 mice is increased compared to controls. Consistent with a presynaptic increase of release probability, synaptic depression under high-frequency stimulation is higher in R6/1 mice. In addition, no changes were detected in the size and dynami...
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URI: http://hdl.handle.net/11441/17815

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