Opioid μ receptors mediate the stress-induced spatial reference memory impairment.
- Author:
Lan-Qin CAO
1
;
Jie WEN
1
;
Zhi-Qiang LIU
2
Author Information
1. College of Life Sciences, Shaanxi Normal University, Xi'an 710062, China.
2. Key Laboratory of Modern Teaching Technology, Shaanxi Normal University, Xi'an 710062, China. zqliu1969@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Enkephalin, Ala(2)-MePhe(4)-Gly(5)-;
pharmacology;
Maze Learning;
Memory Disorders;
Mice;
Receptors, Opioid, mu;
physiology;
Spatial Memory;
Stress, Physiological
- From:
Acta Physiologica Sinica
2015;67(2):173-180
- CountryChina
- Language:Chinese
-
Abstract:
Learning/memory impairment is one of the most serious problems induced by stress, and the underlying mechanisms remain unclear. Opiates and opioid receptors are implicated in multiple physiological functions including learning and memory. However, there is no clear evidence whether the endogenous opioid system is involved in the formation of the stress-induced spatial reference memory impairment. The aim of the present study was to evaluate the role of μ opioid receptor in the stress-induced spatial reference memory impairment by means of Morris water maze (MWM) test in a mouse elevated platform stress model. The mice were trained in the MWM for four trials a session for 4 consecutive days after receiving the elevated platform stress, and intracerebroventricular injection of μ opioid receptor agonist DAMGO, antagonist CTAP or saline. Retention of the spatial training was assessed 24 h after the last training session with a 60-s free-swim probe trial using a new starting position. The results showed that intracerebroventricular injection of μ opioid receptor agonist DAMGO but not antagonist CTAP before MWM training impaired the memory retrieval of mice. Elevated platform stress before MWM training also impaired memory retrieval, which could be reversed by pre-injection of CTAP, and aggravated by DAMGO. These results suggest that endogenous opioid system may play a crucial role in the formation of the stress-induced memory impairment.
