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Type 3 adenylyl cyclase in the MOE is involved in learning and memory in mice
Xinxia Liu1, Yanfen Zhou2, Dong Yang2
1College of Life Science, Hebei University, Baoding, 071002, China; Medical College, Hebei University, 071000, Baoding, China.
Abstract:
Although olfactory dysfunction is related to learning and memory impairment, the causal relationship between main olfactory epithelium (MOE) disruption and learning and memory is still unknown. The present study aimed to establish whether MOE disruption causes learning and memory impairment and whether the expression of type 3 adenylyl cyclas (AC3) in the MOE is related to learning and memory. First, the buried food test was carried out to confirm that MOE function was disrupted in mice treated with nasal instillation of zinc sulfate (ZnSO4 mice), and mice with specific knockdown of AC3 in the MOE by CRISPR/Cas9 technology (AC3KD/MOE mice). Then, behavioural tasks associated with learning and memory were administered. ZnSO4 mice and AC3KD/MOE mice showed impairments in learning and memory tests, including the novel object recognition test, the step-down passive avoidance test, the Morris water maze test, and the Y-maze test. Our data demonstrate that MOE disruption caused by nasal exposure to ZnSO4 or specific knockdown of AC3 in the MOE resulted in learning and memory impairment, and they further demonstrate that the expression of AC3 in the MOE plays a major role in learning and memory.
Insights
Disrupting the main olfactory epithelium (MOE) in mice impairs learning and memory. This impairment is linked to the expression of type 3 adenylyl cyclase (AC3) in the MOE, highlighting its role in cognitive function.
Area of Science:
- Neuroscience
- Olfactory System Research
- Cognitive Function Studies
Background:
- Olfactory dysfunction is associated with cognitive deficits, but a direct causal link between main olfactory epithelium (MOE) disruption and learning/memory impairment remains unclear.
- Type 3 adenylyl cyclase (AC3) is crucial for olfactory sensory transduction, but its specific role in higher cognitive functions like learning and memory is not well-established.
Purpose of the Study:
- To investigate the causal relationship between main olfactory epithelium (MOE) disruption and impairments in learning and memory.
- To determine the role of type 3 adenylyl cyclase (AC3) expression in the MOE concerning learning and memory.
Main Methods:
- MOE function was disrupted in mice using nasal zinc sulfate (ZnSO4) instillation and CRISPR/Cas9-mediated AC3 knockdown in the MOE (AC3KD/MOE).
- Cognitive performance was assessed using a battery of behavioral tests, including the novel object recognition, step-down passive avoidance, Morris water maze, and Y-maze tests.
Main Results:
- Both ZnSO4-treated mice and AC3KD/MOE mice exhibited significant impairments across multiple learning and memory tasks.
- These deficits were consistently observed in tests evaluating recognition, spatial, and contextual memory.
Conclusions:
- Main olfactory epithelium (MOE) disruption, whether induced by chemical means or genetic knockdown of AC3, directly causes learning and memory impairment in mice.
- The expression of type 3 adenylyl cyclase (AC3) within the MOE is a critical factor influencing learning and memory capabilities.
