Publicacions en què col·labora amb JORDI CALDERO PARDO (22)

2023

  1. Persistent NRG1 Type III Overexpression in Spinal Motor Neurons Has No Therapeutic Effect on ALS-Related Pathology in SOD1G93A Mice

    Neurotherapeutics, Vol. 20, Núm. 6, pp. 1820-1834

2021

  1. Beneficial effects of dietary supplementation with green tea catechins and cocoa flavanols on aging-related regressive changes in the mouse neuromuscular system

    Aging, Vol. 13, Núm. 14, pp. 18051-18093

  2. Microglial recruitment and mechanisms involved in the disruption of afferent synaptic terminals on spinal cord motor neurons after acute peripheral nerve injury

    GLIA, Vol. 69, Núm. 5, pp. 1216-1240

2020

  1. Motoneuron deafferentation and gliosis occur in association with neuromuscular regressive changes during ageing in mice

    Journal of Cachexia, Sarcopenia and Muscle, Vol. 11, Núm. 6, pp. 1628-1660

  2. The Y172 Monoclonal Antibody Against p-c-Jun (Ser63) Is a Marker of the Postsynaptic Compartment of C-Type Cholinergic Afferent Synapses on Motoneurons

    Frontiers in Cellular Neuroscience, Vol. 13

2019

  1. Localization and dynamic changes of neuregulin-1 at C-type synaptic boutons in association with motor neuron injury and repair

    FASEB Journal, Vol. 33, Núm. 7, pp. 7833-7851

2018

  1. Accumulation of poly(A) RNA in nuclear granules enriched in Sam68 in motor neurons from the SMNΔ7 mouse model of SMA

    Scientific Reports, Vol. 8, Núm. 1

  2. Glial activation and central synapse loss, but not motoneuron degeneration, are prevented by the sigma-1 receptor agonist pre-084 in the SMN2B/ mouse model of spinal muscular atrophy

    Journal of Neuropathology and Experimental Neurology, Vol. 77, Núm. 7, pp. 577-597

2017

  1. Cellular bases of the RNA metabolism dysfunction in motor neurons of a murine model of spinal muscular atrophy: Role of Cajal bodies and the nucleolus

    Neurobiology of Disease, Vol. 108, pp. 83-99

  2. Neuregulin 1-ErbB module in C-bouton synapses on somatic motor neurons: Molecular compartmentation and response to peripheral nerve injury

    Scientific Reports, Vol. 7

2016

  1. Chronic Treatment with the AMPK Agonist AICAR Prevents Skeletal Muscle Pathology but Fails to Improve Clinical Outcome in a Mouse Model of Severe Spinal Muscular Atrophy

    Neurotherapeutics, Vol. 13, Núm. 1, pp. 198-216

2014

  1. Accumulation of misfolded SOD1 in dorsal root ganglion degenerating proprioceptive sensory neurons of transgenic mice with amyotrophic lateral sclerosis

    BioMed Research International, Vol. 2014

  2. Mechanisms involved in spinal cord central synapse loss in a mouse model of spinal muscular atrophy

    Journal of Neuropathology and Experimental Neurology, Vol. 73, Núm. 6, pp. 519-535

  3. Neuregulin-1 is concentrated in the postsynaptic subsurface cistern of C-bouton inputs to α-motoneurons and altered during motoneuron diseases

    FASEB Journal, Vol. 28, Núm. 8, pp. 3618-3632

2010

  1. Lithium prevents excitotoxic cell death of motoneurons in organotypic slice cultures of spinal cord

    Neuroscience, Vol. 165, Núm. 4, pp. 1353-1369

2009

  1. Excitotoxic motoneuron degeneration induced by glutamate receptor agonists and mitochondrial toxins in organotypic cultures of chick embryo spinal cord

    Journal of Comparative Neurology, Vol. 516, Núm. 4, pp. 277-290

2007

  1. Excitotoxic motoneuron disease in chick embryo evolves with autophagic neurodegeneration and deregulation of neuromuscular innervation

    Journal of Neuroscience Research

  2. Survival and death of mature avian motoneurons in organotypic slice culture: Trophic requirements for survival and different types of degeneration

    Journal of Comparative Neurology, Vol. 501, Núm. 5, pp. 669-690

2005

  1. Protein retention in the endoplasmic reticulum, blockade of programmed cell death and autophagy selectively occur in spinal cord motoneurons after glutamate receptor-mediated injury

    Molecular and Cellular Neuroscience, Vol. 29, Núm. 2, pp. 283-298

2001

  1. Long-lasting aberrant tubulovesicular membrane inclusions accumulate in developing motoneurons after a sublethal excitotoxic insult: A possible model for neuronal pathology in neurodegenerative disease

    Journal of Neuroscience, Vol. 21, Núm. 20, pp. 8072-8081