The Cellular Prion Protein Prevents Copper-Induced Inhibition of P2X4Receptors

Author:

Lorca Ramón A.1,Varela-Nallar Lorena2,Inestrosa Nibaldo C.2,Huidobro-Toro J. Pablo1

Affiliation:

1. Departamento de Fisiología, Centro de Envejecimiento y Regeneración (CARE), Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago 8331150, Chile

2. Departamento de Biología Celular y Molecular, Centro de Envejecimiento y Regeneración (CARE), Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago 8331150, Chile

Abstract

Although the physiological function of the cellular prion protein (PrPC) remains unknown, several evidences support the notion of its role in copper homeostasis. PrPCbinds Cu2+through a domain composed by four to five repeats of eight amino acids. Previously, we have shown that the perfusion of this domain prevents and reverses the inhibition by Cu2+of the adenosine triphosphate (ATP)-evoked currents in the P2X4receptor subtype, highlighting a modulatory role for PrPCin synaptic transmission through regulation of Cu2+levels. Here, we study the effect of full-length PrPCin Cu2+inhibition of P2X4receptor when both are coexpressed. PrPCexpression does not significantly change the ATP concentration-response curve in oocytes expressing P2X4receptors. However, the presence of PrPCreduces the inhibition by Cu2+of the ATP-elicited currents in these oocytes, confirming our previous observations with the Cu2+binding domain. Thus, our observations suggest a role for PrPCin modulating synaptic activity through binding of extracellular Cu2+.

Funder

Comisión Nacional de Investigación Científica y Tecnológica

Publisher

Hindawi Limited

Subject

Behavioral Neuroscience,Cellular and Molecular Neuroscience,Cognitive Neuroscience,Neurology (clinical),Neurology,Aging,General Medicine

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1. SERS-based detection of biomolecules;Nanophotonics;2014-12-01

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