期刊
MOLECULAR NEUROBIOLOGY
卷 58, 期 2, 页码 617-630出版社
SPRINGER
DOI: 10.1007/s12035-020-02135-6
关键词
Short-term memory; Long-term memory; PKC-gamma; Memory acquisition; c-Fos expression
资金
- Ministerio de Economia, Innovacion y Competitividad (MINECO) [BFU2015-68568-P, SAF2017-84060-R]
- Instituto de Salud Carlos III [RD16/0017/0020]
- Ministerio de Ciencia, Innovacion y Universidades [RTI2018-099282-B-I00]
- Generalitat de Catalunya [2017SGR-669]
- ICREA (Institucio Catalana de Recerca i Estudis Avancats) Academia
- Grant Unidad de ExcelenciaMaria deMaeztu
- MINECO [MDM-2014-0370]
- PLAN E (Plan Espanol para el Estimulo de la Economia y el Empleo)
- FEDER
The study revealed that PKC-gamma knockout mice exhibit severe impairment in hippocampal-dependent short-term memory performance while long-term memory tasks remain unaffected. This indicates that PKC-gamma plays a crucial role in memory processes, particularly in the formation of short-term memory and the differential involvement in short-term and long-term memory processes.
The brain encodes, stores, and retrieves relevant information in the form of memories that are classified as short-term (STM) and long-term memories (LTM) depending on the interval between acquisition and retrieval. It is classically accepted that STM undergo a consolidation process to form LTM, but the molecular determinants involved are not well understood. Among the molecular components relevant for memory formation, we focused our attention on the protein kinase C (PKC) family of enzymes since they control key aspects of the synaptic plasticity and memory. Within the different PKC isoforms, PKC-gamma has been specifically associated with learning and memory since mice lacking this isoform (PKC-gamma KO mice) showed mild cognitive impairment and deficits in hippocampal synaptic plasticity. We now reveal that PKC-gamma KO mice present a severe impairment in hippocampal-dependent STM using different memory tests including the novel object-recognition and novel place-recognition, context fear conditioning and trace fear conditioning. In contrast, no differences between genotypes were observed in an amygdala-dependent test, the delay fear conditioning. Strikingly, all LTM tasks that could be assessed 24 h after acquisition were not perturbed in the KO mice. The analysis of c-Fos expression in several brain areas after trace fear conditioning acquisition showed a blunted response in the dentate gyrus of PKC-gamma KO mice compared with WT mice, but such differences between genotypes were absent when the amygdala or the prefrontal cortex were examined. In the hippocampus, PKC-gamma was found to translocate to the membrane after auditory trace, but not after delay fear conditioning. Together, these results indicate that PKC-gamma dysfunction affects specifically hippocampal-dependent STM performance and disclose PKC-gamma as a molecular player differentially involved in STM and LTM processes.
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