Impaired hippocampal place cell dynamics in a mouse model of the 22q11.2 deletion.

Autor: Zaremba JD; Department of Neuroscience, Columbia University, New York, New York, USA., Diamantopoulou A; Department of Psychiatry, Columbia University, New York, New York, USA.; Department of Physiology and Cellular Biophysics, Columbia University, New York, New York, USA., Danielson NB; Department of Neuroscience, Columbia University, New York, New York, USA., Grosmark AD; Department of Neuroscience, Columbia University, New York, New York, USA., Kaifosh PW; Department of Neuroscience, Columbia University, New York, New York, USA.; Center for Theoretical Neuroscience, Columbia University, New York, New York, USA., Bowler JC; Department of Neuroscience, Columbia University, New York, New York, USA., Liao Z; Department of Neuroscience, Columbia University, New York, New York, USA., Sparks FT; Department of Neuroscience, Columbia University, New York, New York, USA., Gogos JA; Department of Neuroscience, Columbia University, New York, New York, USA.; Department of Physiology and Cellular Biophysics, Columbia University, New York, New York, USA., Losonczy A; Department of Neuroscience, Columbia University, New York, New York, USA.; Kavli Institute for Brain Science, Columbia University, New York, New York, USA.
Jazyk: angličtina
Zdroj: Nature neuroscience [Nat Neurosci] 2017 Nov; Vol. 20 (11), pp. 1612-1623. Date of Electronic Publication: 2017 Sep 04.
DOI: 10.1038/nn.4634
Abstrakt: Hippocampal place cells represent the cellular substrate of episodic memory. Place cell ensembles reorganize to support learning but must also maintain stable representations to facilitate memory recall. Despite extensive research, the learning-related role of place cell dynamics in health and disease remains elusive. Using chronic two-photon Ca 2+ imaging in hippocampal area CA1 of wild-type and Df(16)A +/- mice, an animal model of 22q11.2 deletion syndrome, one of the most common genetic risk factors for cognitive dysfunction and schizophrenia, we found that goal-oriented learning in wild-type mice was supported by stable spatial maps and robust remapping of place fields toward the goal location. Df(16)A +/- mice showed a significant learning deficit accompanied by reduced spatial map stability and the absence of goal-directed place cell reorganization. These results expand our understanding of the hippocampal ensemble dynamics supporting cognitive flexibility and demonstrate their importance in a model of 22q11.2-associated cognitive dysfunction.
Databáze: MEDLINE
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