期刊
BRAIN STRUCTURE & FUNCTION
卷 224, 期 4, 页码 1659-1676出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00429-019-01865-1
关键词
Anterior cingulate cortex; c-Fos imaging; Dendritic spines; Golgistaining; Hippocampus; Medial prefrontal cortex; Rat; Spatial memory; Systems-level consolidation
资金
- Agence Nationale de la Recherche (ANR) [14-CE13-0029-01]
- University of Strasbourg
- CNRS
- INSERM
- Region Alsace
- ANR [14-CE13-0029-01]
- French government
The ventral midline thalamus contributes to hippocampo-cortical interactions supporting systems-level consolidation of memories. Recent hippocampus-dependent memories rely on hippocampal connectivity remodeling. Remote memories are underpinned by neocortical connectivity remodeling. After a ventral midline thalamus lesion, recent spatial memories are formed normally but do not last. Why these memories do not endure after the lesion is unknown. We hypothesized that a lesion could interfere with hippocampal and/or neocortical connectivity remodeling. To test this hypothesis, in a first experiment male rats were subjected to lesion of the reuniens and rhomboid (ReRh) nuclei, trained in a water maze, and tested in a probe trial 5 or 25days post-acquisition. Dendritic spines were counted in the dorsal hippocampus and medial prefrontal cortex. Spatial learning resulted in a significant increase of mushroom spines in region CA1. This modification persisted between 5 and 25days post-acquisition in Sham rats, not in rats with ReRh lesion. Furthermore, 25days after acquisition, the number of mushroom spines in the anterior cingulate cortex (ACC) had undergone a dramatic increase in Sham rats; ReRh lesion prevented this gain. In a second experiment, the increase of c-Fos expression in CA1 accompanying memory retrieval was not affected by the lesion, be it for recent or remote memory. However, in the ACC, the lesion had reduced the retrieval-triggered c-Fos expression observed 25days post-acquisition. These observations suggest that a ReRh lesion might disrupt spatial remote memory formation by preventing persistence of early remodeled hippocampal connectivity, and spinogenesis in the ACC.
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