Author:

Abstract:

Previous studies investigated the role of the metabotropic glutamate receptor subtype 7 (mGluR7) in working memory and extinction. In these studies, mGluR7-deficient mice show more errors in spatial working memory tasks compared to controls. At the same time, they exhibit a delayed extinction of both spatial preference and conditioned fear. These concomitant deficits have been assumed to reflect a common neurobiological mechanism underlying working memory and extinction, with mGluR7 playing a central role in that mechanism. According to this view, mGluR7 deficiency might compromise the common mechanism and therefore cause concurrent deficits in tasks relying on the mechanism. However, independent mechanisms underlying working memory and extinction are equally plausible. Since mGluR7 is present in many different brain areas, mGluR7 deficiency can cause concurrent deficits in each of these brain areas and corresponding functions without necessarily affecting any common mechanism. To differentiate between these two explanations, we used correlational analysis. If working memory and extinction are based on a shared neurobiological mechanism, we predict a specific pattern of correlations between working memory and extinction performance. These correlations should be absent in the case of multiple independent mechanisms. Performance of two groups of mGluR7 knock-out mice and wild-type controls were tested in a spatial working memory task in the Radial Arm Maze, a spatial extinction task in the Morris Water Maze and extinction of conditioned fear in a CER paradigm. Correlations between different performance measures suggest a common mechanism underlying spatial working memory and extinction of spatial preference and conditioned fear