Abstract
Deletion of the GluA1 AMPA receptor subunit impairs short-term spatial recognition memory. It has been suggested that short-term recognition depends upon memory caused by the recent presentation of a stimulus that is independent of contextual–retrieval processes. The aim of the present set of experiments was to test whether the role of GluA1 extends to nonspatial recognition memory. Wild-type and GluA1 knockout mice were tested on the standard object recognition task and a context-independent recognition task that required recency-dependent memory. In a first set of experiments it was found that GluA1 deletion failed to impair performance on either of the object recognition or recency-dependent tasks. However, GluA1 knockout mice displayed increased levels of exploration of the objects in both the sample and test phases compared to controls. In contrast, when the time that GluA1 knockout mice spent exploring the objects was yoked to control mice during the sample phase, it was found that GluA1 deletion now impaired performance on both the object recognition and the recency-dependent tasks. GluA1 deletion failed to impair performance on a context-dependent recognition task regardless of whether object exposure in knockout mice was yoked to controls or not. These results demonstrate that GluA1 is necessary for nonspatial as well as spatial recognition memory and plays an important role in recency-dependent memory processes.
Highlights
The GluA1 subunit of the AMPA receptor is a key mediator of hippocampal synaptic plasticity (Zamanillo et al 1999)
In contrast to the impairment shown by GluA12/2 mice on short-term, spatial recognition memory (Sanderson et al 2007, 2009), a recent study has reported no effect of GluA1 deletion on object recognition (Wiedholz et al 2008)
Experiment 1—Object recognition In Experiment 1 female WT (N 1⁄4 12) and GluA12/2 (N 1⁄4 12) mice were tested on the standard object recognition task
Summary
The GluA1 subunit of the AMPA receptor is a key mediator of hippocampal synaptic plasticity (Zamanillo et al 1999). We have recently shown that GluA1 knockout (GluA12/2) mice display a deficit in hippocampus-dependent, short-term spatial recognition memory, but in contrast, show successful long-term spatial recognition memory (Sanderson et al 2009). GluA1 deletion impairs the expression of short-term visual recognition memory, but leaves long-term visual habituation intact (Sanderson et al 2011). In contrast to the impairment shown by GluA12/2 mice on short-term, spatial recognition memory (Sanderson et al 2007, 2009), a recent study has reported no effect of GluA1 deletion on object recognition (Wiedholz et al 2008). This could reflect a difference between spatial and nonspatial stimulus processing. The results provide further evidence for the hypothesis that GluA1 is necessary for recency-dependent recognition memory
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