Effects of acute fear stress on spatial memory and neuronal plasticity in the medial prefrontal cortex in mice.
- Author:
Dong-Bo LIU
1
;
Yan SHI
2
;
Chuan-Hao CHEN
3
;
Heng TAO
3
;
Xing-Hao LU
3
;
Jin LU
3
Author Information
1. Department of Anatomy, Bengbu Medical College, Bengbu 233030, China. liudongbo@bbmc.edu.cn.
2. Department of Ultrasound Medicine, the First Affiliated Hospital, Bengbu Medical College, Bengbu 233004, China.
3. Department of Anatomy, Bengbu Medical College, Bengbu 233030, China.
- Publication Type:Randomized Controlled Trial, Veterinary
- MeSH:
Animals;
Male;
Mice;
Fear;
Mice, Inbred C57BL;
Neuronal Plasticity;
Prefrontal Cortex;
Spatial Memory
- From:
Acta Physiologica Sinica
2022;74(5):705-714
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to investigate the effects of acute fear stress on the spatial memory and neuronal plasticity of medial prefrontal cortex (mPFC) neurons in mice, and to elucidate the mechanisms underlying mPFC plasticity and post-stress memory regulation. Male C57BL/6 mice (6 weeks old) were randomly divided into control group and stress group. Foot shock stress was applied to establish an acute fear stress model. Changes in spatial memory were examined by the Morris water maze test, and the dynamic changes in the spike encoding of pyramidal neurons and GABAergic neurons in the prelimbic cortex (PrL) and infralimbic cortex (IL) of mPFC were detected by whole-cell recording. The results showed that acute fear stress significantly enhanced the percentage of freezing and the number of freezing, reduced the average speed, decreased the escape latency during acquisition phase, extended the probing time in the first quadrant and shortened the probing time in the third quadrant during probe trial, increased inter-spike interval, energy barrier and absolute refractory period of GABAergic neurons in the PrL and pyramidal neurons in the IL, while decreased inter-spike interval, energy barrier and absolute refractory period of pyramidal neurons in the PrL and GABAergic neurons in the IL. These results suggest that acute fear stress can enhance the spatial memory of mice, elevate the excitability and function of the PrL, while deteriorate the excitability and function of the IL, and the underlying mechanism may involve the role of mPFC microcircuitry plasticity in spatial memory after stress.
