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Front Mol Neurosci. 2018 Apr 10;11:114. doi: 10.3389/fnmol.2018.00114. eCollection 2018.

Lack of Pannexin 1 Alters Synaptic GluN2 Subunit Composition and Spatial Reversal Learning in Mice.

Author information

1
Departamento de Patología y Fisiología, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
2
Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Valparaíso, Chile.
3
Escuela de Tecnología Médica, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
4
Centro de Investigaciones Biomédicas, Escuela de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
5
Institute for Physiology I, University of Freiburg, Freiburg, Germany.
6
Programa de Farmacología Molecular y Clínica, Instituto de Ciencias Biomédicas (ICBM), Facultad de Medicina, Universidad de Chile, Santiago, Chile.
7
Center for Applied Neurological Sciences, Faculty of Medicine, Universidad de Valparaíso, Valparaíso, Chile.
8
Centro Interdisciplinario de Estudios en Salud, Facultad de Medicina, Universidad de Valparaíso, Viña del Mar, Chile.

Abstract

Long-term potentiation (LTP) and long-term depression (LTD) are two forms of synaptic plasticity that have been considered as the cellular substrate of memory formation. Although LTP has received considerable more attention, recent evidences indicate that LTD plays also important roles in the acquisition and storage of novel information in the brain. Pannexin 1 (Panx1) is a membrane protein that forms non-selective channels which have been shown to modulate the induction of hippocampal synaptic plasticity. Animals lacking Panx1 or blockade of Pannexin 1 channels precludes the induction of LTD and facilitates LTP. To evaluate if the absence of Panx1 also affects the acquisition of rapidly changing information we trained Panx1 knockout (KO) mice and wild type (WT) littermates in a visual and hidden version of the Morris water maze (MWM). We found that KO mice find the hidden platform similarly although slightly quicker than WT animals, nonetheless, when the hidden platform was located in the opposite quadrant (OQ) to the previous learned location, KO mice spent significantly more time in the previous quadrant than in the new location indicating that the absence of Panx1 affects the reversion of a previously acquired spatial memory. Consistently, we observed changes in the content of synaptic proteins critical to LTD, such as GluN2 subunits of N-methyl-D-aspartate receptors (NMDARs), which changed their contribution to synaptic plasticity in conditions of Panx1 ablation. Our findings give further support to the role of Panx1 channels on the modulation of synaptic plasticity induction, learning and memory processes.

KEYWORDS:

GluN2 subunits; Pannexin 1; behavioral flexibility; long-term depression; synaptic plasticity

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