Functional double dissociation within the entorhinal cortex for visual scene-dependent choice behavior
Abstract
How visual scene memory is processed differentially by the upstream structures of the hippocampus is largely unknown. We sought to dissociate functionally the lateral and medial subdivisions of the entorhinal cortex (LEC and MEC, respectively) in visual scene-dependent tasks by temporarily inactivating the LEC and MEC in the same rat. When the rat made spatial choices in a T-maze using visual scenes displayed on LCD screens, the inactivation of the MEC but not the LEC produced severe deficits in performance. However, when the task required the animal to push a jar or to dig in the sand in the jar using the same scene stimuli, the LEC but not the MEC became important. Our findings suggest that the entorhinal cortex is critical for scene-dependent mnemonic behavior, and the response modality may interact with sensory modality to determine the involvement of the LEC and MEC in scene-based memory tasks.
Article and author information
Author details
Funding
National Research Foundation of Korea (2015M3C7A1031969)
- Inah Lee
National Research Foundation of Korea (2013R1A1A2062882)
- Inah Lee
National Research Foundation of Korea (2016R1A2B4008692)
- Inah Lee
National Research Foundation of Korea (2014051826)
- Inah Lee
National Research Foundation of Korea (BK21 plus program)
- Inah Lee
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Neil Burgess, University College London, United Kingdom
Ethics
Animal experimentation: This study was performed in strict accordance with the guidelines of the Institutional Animal Care and Use Committee of the Seoul National University. All protocols (SNU-120925-1-7) were in compliance with the Institutional Animal Care and Use Committee of the Seoul National University.
Version history
- Received: September 14, 2016
- Accepted: February 6, 2017
- Accepted Manuscript published: February 7, 2017 (version 1)
- Version of Record published: February 14, 2017 (version 2)
- Version of Record updated: April 24, 2017 (version 3)
- Version of Record updated: April 24, 2017 (version 4)
- Version of Record updated: May 11, 2017 (version 5)
Copyright
© 2017, Yoo & Lee
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 2,519
- views
-
- 457
- downloads
-
- 12
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
- Neuroscience
Cholecystokinin (CCK) is an essential modulator for neuroplasticity in sensory and emotional domains. Here, we investigated the role of CCK in motor learning using a single pellet reaching task in mice. Mice with a knockout of Cck gene (Cck−/−) or blockade of CCK-B receptor (CCKBR) showed defective motor learning ability; the success rate of retrieving reward remained at the baseline level compared to the wildtype mice with significantly increased success rate. We observed no long-term potentiation upon high-frequency stimulation in the motor cortex of Cck−/− mice, indicating a possible association between motor learning deficiency and neuroplasticity in the motor cortex. In vivo calcium imaging demonstrated that the deficiency of CCK signaling disrupted the refinement of population neuronal activity in the motor cortex during motor skill training. Anatomical tracing revealed direct projections from CCK-expressing neurons in the rhinal cortex to the motor cortex. Inactivation of the CCK neurons in the rhinal cortex that project to the motor cortex bilaterally using chemogenetic methods significantly suppressed motor learning, and intraperitoneal application of CCK4, a tetrapeptide CCK agonist, rescued the motor learning deficits of Cck−/− mice. In summary, our results suggest that CCK, which could be provided from the rhinal cortex, may surpport motor skill learning by modulating neuroplasticity in the motor cortex.