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Adiponectin Knockout Mice Display Cognitive and Synaptic Deficits
Jenna Bloemer1,2, Priyanka D Pinky1,2, Warren D Smith1,2
1Department of Drug Discovery and Development, Harrison School of Pharmacy, Auburn University, Auburn, AL, United States.
Frontiers in Endocrinology
|December 12, 2019
Summary
Adiponectin deficiency impairs cognitive function and hippocampal synaptic plasticity in mice. Restoring adiponectin receptor signaling improved long-term potentiation, highlighting adiponectin
Area of Science:
- Neuroscience
- Metabolic Research
- Molecular Biology
Background:
- Adiponectin, an adipokine, is explored for neuroprotective roles in brain disorders.
- Adiponectin receptors (AdipoR1, AdipoR2) are present in the hippocampus, but their synaptic and cognitive roles are unclear.
Purpose of the Study:
- To investigate the impact of adiponectin absence on cognitive and hippocampal synaptic function.
- To elucidate the role of adiponectin in regulating synaptic plasticity and neurotransmission.
Main Methods:
- Utilized 12-month-old adiponectin knockout (APN-KO) mice and age-matched controls.
- Assessed cognitive function using novel object recognition (NOR) and Y-maze tests.
- Evaluated hippocampal synaptic function, including long-term potentiation (LTP) and basal synaptic transmission.
Main Results:
- APN-KO mice exhibited significant cognitive deficits and impaired hippocampal LTP.
- Reduced basal synaptic transmission and increased presynaptic release probability were observed in APN-KO mice.
- Treatment with an adiponectin receptor agonist (AdipoRon) rescued LTP deficits.
Conclusions:
- Adiponectin is a critical regulator of hippocampal synaptic function and cognitive performance.
- Adiponectin receptor signaling directly influences synaptic plasticity and neurotransmission.
- Further research is warranted to explore the specific roles of AdipoR1 and AdipoR2 in synaptic processes.
