Performance deficit of α7 nicotinic receptor knockout mice in a delayed matching-to-place task suggests a mild impairment of working/episodic-like memory

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Patients with schizophrenia exhibit deficits in a range of cognitive functions, particularly working and episodic memory, which are thought to be core features of the disorder. Memory dysfunction in schizophrenia is familial and thus a promising endophenotype for genetic studies. Both human and animal studies suggest a role for the neural nicotinic acid receptor family in cognition and specifically the α7-receptor subunit in schizophrenia and its endophenotypes. Consequently, we tested mice lacking the α7 subunit of the neural nicotinic receptor (B6.129S7-Chrna7tm1Bay/J) in the delayed matching-to-place (DMP) task of the Morris water maze, a measure of working/episodic memory akin to human episodic memory. We report that a minor impairment in α7 knockout mice was observed in the DMP task, with knockout mice taking longer to find the hidden platform than their wildtype controls. This suggests a role for the α7 subunit in working/episodic memory and a potential role for the α7 neural nicotinic receptor gene (CHRNA7) in schizophrenia and its endophenotypes.

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