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Long-term social isolation inhibits autophagy activation, induces postsynaptic dysfunctions and impairs spatial
Bin Wang1, Qiong Wu1, Lei Lei2
1Liaoning Provincial Key Laboratory of Cerebral Diseases, Department of Physiology, Dalian Medical University, Dalian, Liaoning, China.
Experimental Neurology
|September 17, 2018
Summary
Long-term social isolation in adolescence impairs spatial memory and hippocampal function by disrupting synaptic plasticity and inhibiting autophagy. Rapamycin treatment rescued these cognitive deficits, highlighting autophagy
Area of Science:
- Neuroscience
- Molecular Biology
- Behavioral Science
Background:
- Adolescent social isolation causes lasting deficits in hippocampal-dependent tasks, but effects on learning, memory, and synaptic proteins are inconsistent.
- The role of autophagy in cognitive changes associated with social isolation remains unclear.
Purpose of the Study:
- To establish a stable long-term post-weaning social isolation (L-PWSI) mouse model.
- To investigate the effects of L-PWSI on spatial learning, memory, and synaptic function.
- To explore the role of autophagy activation in cognitive changes using the mTOR inhibitor rapamycin.
Main Methods:
- Established a six-month L-PWSI mouse model.
- Assessed spatial learning and memory using behavioral tasks.
- Measured hippocampal long-term potentiation (LTP), paired-pulse facilitation (PPF), and input/output (I/O) curves.
- Quantified protein expression of synaptic markers (PSD-95, GluA1, NR1, NR2B, synaptophysin, etc.) and autophagy-related proteins (p-AKT, p-mTOR, p62, LC3B, Beclin1).
- Administered rapamycin to L-PWSI mice and evaluated its effects on synaptic function and cognitive proteins.
Main Results:
- L-PWSI induced significant deficits in spatial learning and memory and inhibited CA1 LTP.
- L-PWSI decreased hippocampal expression of postsynaptic proteins (PSD-95, GluA1, NR1, NR2B) but did not affect glutamate release or presynaptic proteins.
- L-PWSI inhibited autophagy, evidenced by increased p-AKT, p-mTOR, p62, and decreased LC3B and Beclin1.
- Rapamycin administration significantly improved synaptic function (fEPSP slope) and cognition-related protein expression in L-PWSI mice.
Conclusions:
- Long-term social isolation in adolescence impairs spatial memory and hippocampal synaptic plasticity.
- L-PWSI induces postsynaptic dysfunction by disrupting AMPAR, NMDAR, and PSD-95 interactions and inhibits autophagy.
- Activating autophagy via rapamycin can ameliorate cognitive deficits induced by L-PWSI, suggesting therapeutic potential.
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