Cellular and Molecular Basis of Sensory Disorders
This programme focuses on investigating genetic and acquired causes of sensory disorders to identify potential targets for treatment as well as for preservation of sensory functions during ageing. Animal models and first-line methodologies, such as super-resolution fluorescence microscopy, RNA-seq and proteomics, are used to identify the cellular and molecular mechanisms leading to sensory loss.
Principal Investigators
Alejandro Barrallo-Gimeno
Associate Professor
Jordi Llorens
Full Professor
Ana Mendez
Associate Professor
Technologies & Methods
- Generation of vestibular deficient rodents
- Assessment of vestibular dysfunction in rodents
- Morphological analysis of vestibular sensory epithelia
- Vestibular epithelia organotypic cultures
- Immunostaining
- Light and advanced confocal microscopy
- Scanning electron microscopy
- Transmission electron microscopy
- Life imaging of zebrafish organs
- CRISPR/Cas9 gene edition in zebrafish
- Gene expression analyses by qRT-PCR, RNA-scope and RNAseq
- Rodent models of retinal function by transient transgenesis in rods by in vivo DNA electroporation
- Protein biochemistry
- Protein-protein interactions
- Retinal morphological studies by light and electron microscopy
- Retinal proteomics and phosphoproteomics
- Visual function analysis by electroretinography (ERG)
- Isoelectrofocusing gels
Research Team
Mireia Borrajo
Early Stage Researcher
Aïda Palou
Early Stage Researcher
Xavier Vallvé
Lecturer
Emma Cerrato Valtuena
Early Stage Researcher
Víctor Giménez-Esbrí
Postdoctoral Researcher
Active Projects
Vestibular Loss and Spatial Orientation
Ministerio de Ciencia, Innovación y Universidades. PCI2020-120681-2. Jordi Llorens.
Adaptación de la retina a la luz e identificación de dianas terapéuticas para las cegueras hereditarias: IMPDH1 y metabolismo energético
Ministerio de Ciencia e Innovación (MICINN). PID2020-115431RB-I00. Ana Mendez.
A patient centered research: awareness of patients needs, clinical phenotyping and molecular parthenogenesis in Neurofibromatosis type 2
Fundació La Marató de TV3. 126/C/2020. Jordi Llorens.
Desarrollo de MP004 como tratamiento innovador para la retinosis pigmentaria y otras enfermedades retinianas: estudio de eficacia y toxicología, validación delmecanismo de acción y plan de desarrollo de actividades regulatorias preclínicas
Ministerio de Ciencia e Innovación (MICINN). CPP2022-009867. Ana Mendez.
Nuevos mecanismos moleculares en el daño vestibular crónico
Ministerio de Ciencia e Innovación (MICINN). PID2021-124678OB-I00. Jordi Llorens.
Nous medicaments basats en àcids nucleics per tractar les distròfies de retina associades a mutacions en PDE6A, PDE6B, PDE6G, AIPL1 i IMPDH1
Fundación de lucha contra la ceguera. Ana Mendez.
Bases Cel·lulars i Moleculars dels Trastorns Sensorials
Agència de Gestió d'Ajuts Universitaris i de Recerca (AGAUR). 2021 SGR 00368. Jordi Llorens.
Selected publications
Greguske, E. A., Maroto, A. F., Borrajo, M., Palou, A., Gut, M., Esteve-Codina, A., Barrallo-Gimeno, A., & Llorens, J. (2023). Decreased expression of synaptic genes in the vestibular ganglion of rodents following subchronic ototoxic stress. Neurobiology of Disease, 182, 106134. https://doi.org/10.1016/j.nbd.2023.106134
Maroto, A. F., Borrajo, M., Prades, S., Callejo, À., Amilibia, E., Pérez-Grau, M., Roca-Ribas, F., Castellanos, E., Barrallo-Gimeno, A., & Llorens, J. (2023). The vestibular calyceal junction is dismantled following subchronic streptomycin in rats and sensory epithelium stress in humans. Archives of Toxicology, 97(7), 1943–1961. https://doi.org/10.1007/s00204-023-03518-z
Schenberg, L., Palou, A., Simon, F., Bonnard, T., Barton, C.-E., Fricker, D., Tagliabue, M., Llorens, J., & Beraneck, M. (2023). Subchronic alteration of vestibular hair cells in mice: implications for multisensory gaze stabilization. https://doi.org/10.7554/elife.88819.2
Sirés, A., Pazo-González, M., López-Soriano, J., Méndez, A., de la Rosa, E. J., de la Villa, P., Comella, J. X., Hernández-Sánchez, C., & Solé, M. (2023). The Absence of FAIM Leads to a Delay in Dark Adaptation and Hampers Arrestin-1 Translocation upon Light Reception in the Retina. Cells, 12(3), 487. https://doi.org/10.3390/cells12030487