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Andres Morales Calderon

Name: Morales Calderon, AndresDr. Andres Morales Calderon
Citizenship: Spanish
Institution: Universidad de Alicante
Center: Dpto. de Fisiologia, Genetica y Microbiologia
Address: Div. de Fisiologia. Dpto. de Fisiologia, Genetica y Microbiologia
Universidad de Alicante. Apartado de Correos 99.
E03080 Alicante. Spain
Phone: + 34 96-590 3949
Fax: + 34 96 590 9569


Our group is mainly engaged in the study of the modulation of nAChRs and others LGICs by different intrinsic and extrinsic factors, including membrane lipids (J Mol Neurosci 30: 5-6, 2006; J Mol Neurosci 30: 121-124, 2006) and molecules with quaternary ammonium groups (Br J Pharmacol. 144: 88-9, 2005; Br J Pharmacol. 151: 1280-1292, 2007).

For detailed biophysical, physiological and pharmacological studies concerning modulation of LGICs, our group uses the methodology of transplantation of fully processed proteins to the Xenopus oocyte (Proc Natl Acad Sci USA. 92:8468-8472, 1995; J. Membr. Biol. 185, 2:117-127, 2002) to avoid the complexity of the neuronal tissue and the number and heterogeneity of receptors present in a single neurone. This technique offers many advantages over the classical expression of membrane proteins, in which mRNA or cDNA are injected into the oocyte, because it avoids both post-translational modification of the protein coded by the exogenous mRNA and differences in the stequiometry of the oligomeric receptor/channel complexes.

So far, we have studied the allosteric modulation of nAChR from the electroplax of Torpedo marmorata, (similar to synaptic muscular nAChRs) and neuronal nAChR, GABAAR, and GluR, functionally transplanted to oocytes. A deep knowledge of the function and regulation of LGIC, which can be acquired by synergic work with other groups of this Consortium, will contribute to a better understanding of the physiopathology of neurodegenerative diseases, in which LGIC are involved, and to the design of specific drugs for their treatment.

In addition, we are also interested in the mechanisms underlying the modulation of GPCRs by membrane potential, recently observed in a variety of cell types, including oocytes (J Biol Chem. 280: 1490-1498, 2005; Acta Physiol, 190: 50, 2007). Modulation of metabotropic receptor signaling by membrane potential may have important consequences for Ca2+ regulation both in excitable and non-excitable tissues and could be a new target for therapeutic action.

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