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

<jats:p><jats:bold>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‐Chrna7<jats:sup>tm1Bay</jats:sup>/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 (<jats:italic>CHRNA7</jats:italic>) in schizophrenia and its endophenotypes.</jats:bold></jats:p>