Ventral hippocampal projections to the medial prefrontal cortex regulate social memory
Mary L Phillips1, Holly Anne Robinson1, Lucas Pozzo-Miller1
1Department of Neurobiology, The University of Alabama at Birmingham, Birmingham, United States.
Elife
|May 22, 2019
Summary
Hyperactivity in the ventral hippocampus (vHIP) to medial prefrontal cortex (mPFC) pathways impairs social memory in Rett syndrome models. Inhibiting this pathway rescued deficits, highlighting its role in social recall.
Area of Science:
- Neuroscience
- Neurobiology
- Autism Spectrum Disorder Research
Background:
- Ventral hippocampus (vHIP) to medial prefrontal cortex (mPFC) projections are crucial for cognitive functions.
- Dysregulation of these pathways is linked to neuropsychiatric disorders.
- Rett syndrome, an autism spectrum disorder, involves social memory deficits.
Purpose of the Study:
- Investigate the role of vHIP-mPFC projections in social memory deficits observed in Rett syndrome.
- Determine if modulating vHIP-mPFC activity can rescue social memory impairments.
Main Methods:
- Utilized the Mecp2 knockout mouse model for Rett syndrome.
- Employed long-term excitation and inhibition techniques on vHIP neurons projecting to the mPFC.
- Performed in vitro slice electrophysiology to assess synaptic strength.
- Analyzed social memory recall behavior.
Main Results:
- vHIP-mPFC projection hyperactivity was observed in Rett syndrome model mice.
- Long-term excitation of vHIP-mPFC neurons impaired social memory in wild-type mice.
- Long-term inhibition of vHIP-mPFC neurons rescued social memory deficits in Rett mice.
- Aberrant vHIP innervation patterns and increased synaptic strength in layer five pyramidal neurons contributed to signaling abnormalities.
Conclusions:
- Proper vHIP-mPFC signaling is essential for social memory recall.
- Modulating vHIP-mPFC pathway activity presents a potential therapeutic target for social memory deficits in Rett syndrome and related disorders.
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