Full professor, Biochemistry and Microbiology Institute, Faculty of Sciences, Universidad Austral de Chile.
Visiting Scientist, Janelia Research Campus HHMI, VA, USA.
Director, International Affairs Office, Universidad Austral de Chile.
PhD in Cellular and Molecular Biology, Universidad Austral de Chile.
Biochemist, Universidad de Concepción.
Pasaje Harrington 287 Playa Ancha. Valparaíso, Chile.
The brain makes up 2% of a person’s weight. Despite this, even at rest, the brain consumes 25% of the body’s energy. Most of the energy consumed in the brain is attributable to restoration of the membrane gradient following neuronal depolarization. Neurotransmitter recycling, intracellular signaling and dendritic and axonal transport also require energy. Even though neurons are responsible for massive energy consumption, the brain is made up of many cells, including neurons, glial and ependymal cells. Every brain cell has a specific function and thus every brain cell has different metabolic needs. Many of these specific functions are concerned with maintenance of neuronal transmission. There have been several reports of metabolic impairment in a variety of neurodegenerative disorders such as Alzheimer’s disease, Huntington’s disease and Parkinson’s disease, among others. Moreover, deregulation of energy metabolism could be implicated in an increased production of oxidative species. During the last 16 years I have been making steady progress in the mechanisms of communication between neurons and glial cells and the way they regulate their metabolism. My interest has been to study metabolic neuron-glia interactions in aging and neurodegenerative diseases. I would like to understand whether glial cells contribute to neuronal energy metabolism in a healthy brain during aging with the idea to unveil new therapeutic targets for neurodegeneration. Our laboratory combines the use of electrophysiology and imaging (confocal, TIRF and 2-photon microscopy), biochemical and cellular molecular techniques on acute slices, primary cell cultures and in vivo experiments using transgenic model mice.
- Rosas-Arellano, A., Tejeda-Guzmán, C., Lorca-Ponce, E., Palma-Tirado, L., Rojas, P., Missirlis, F., Castro, M.A. 2018. Huntington’s disease leads to decrease of GABA-A tonic subunits in D2 neostriatal pathway and their relocalization in to the synaptic cleft. Neurobiology of Disease, 110:142-153. doi: 10.1016/j.nbd.2017.11.010.
- Covarrubias-Pinto A., Acuña A.I., Boncompain G., Pápic E., Burgos P.V., Perez F. and Castro M.A. 2018. Ascorbic acid increases SVCT2 localization at the plasma membrane by accelerating its trafficking from early secretory compartments and through the endocytic-recycling pathway. Free Radic Biol Med, 120:181-191. doi: 10.1016/j.freeradbiomed.2018.03.013.
- Covarrubias-Pinto, A., Moll, P., Solís, M., Acuña, A.I., Riveros, A., Miró, M.P., Papic, E., Cepeda, C., Concha, I.I., Brauchi, S., Castro, M.A. 2015. Beyond the redox imbalance: oxidative stress contributes to an impaired GLUT3 modulation in Huntington’s disease. Free Radic Biol Med, 89:1085-96. doi: 10.1016/j.freeradbiomed.2015.09.024.
- Acuña A.I., Esparza M., Kramm C., Beltrán F.A., Parra A., Cepeda C., Toro C., Vidal R., Hetz C., Concha I.I., Brauchi S., Levine M.S. and Castro M.A. 2013. Failure on energy metabolism and antioxidant uptake precede the onset of Huntington’s disease. Nature Comm, 4:2917. doi: 10.1038/ncomms3917.
- Beltrán, F.A., Acuña, A.I., Miró, M.P., Angulo, C., Concha, I.I., Castro, M.A. 2011. Ascorbic acid-dependent GLUT3 inhibition is a critical step for switching neuronal metabolism, Journal Cell Physiology, 226:3286-94. doi: 10.1002/jcp.22674.