Help Privacy Policy Disclaimer
  Advanced SearchBrowse




Journal Article

Hippocampal CA1 replay becomes less prominent but more rigid without inputs from medial entorhinal cortex


Chenani,  Alireza
Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available

Chenani, A., Sabariego, M., Schlesiger I, M., Leutgeb, J. K., Leutgeb, S., & Leibold, C. (2019). Hippocampal CA1 replay becomes less prominent but more rigid without inputs from medial entorhinal cortex. NATURE COMMUNICATIONS, 10: 1341. doi:10.1038/s41467-019-09280-0.

Cite as: https://hdl.handle.net/21.11116/0000-0009-6C42-4
The hippocampus is an essential brain area for learning and memory. However, the network mechanisms underlying memory storage, consolidation and retrieval remain incompletely understood. Place cell sequences during theta oscillations are thought to be replayed during non-theta states to support consolidation and route planning. In animals with medial entorhinal cortex (MEC) lesions, the temporal organization of theta-related hippocampal activity is disrupted, which allows us to test whether replay is also compromised. Two different analyses-comparison of co-activation patterns between running and rest epochs and analysis of the recurrence of place cell sequences-reveal that the enhancement of replay by behavior is reduced in MEC-lesioned versus control rats. In contrast, the degree of intrinsic network structure prior and subsequent to behavior remains unaffected by MEC lesions. The MEC-dependent temporal coordination during theta states therefore appears to facilitate behavior-related plasticity, but does not disrupt pre-existing functional connectivity.