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A novel mechanism of memory loss in Alzheimer’s disease mic
RV-eGFP virus were used for retrograde monosynaptic tracing to determine direct synaptic connections, ChR2-eGFP virus were used for optogenetic manipulation to determine the functional properties.
The viruses used in this article are in the table below
RV  ΔG-rabies-eGFP
Tracing Helper  Rosa-CAG-Flag-TVA/G-WPRE
Optogenetic  Rosa-CAG-Flag-ChR2-eGFP-WPRE
CRE Recombinase  rAAV1/2-D28K-Cre
Pub Date: 2016-09-27, DOI: 10.1038/mp.2016.151  Email: [email protected]
X Yang, C Yao, T Tian, X Li, H Yan, J Wu, H Li, L Pei, D Liu, Q Tian, L-Q Zhu and Y Lu
The entorhinal cortex (EC) is one of the most vulnerable brain regions that is attacked during the early stage of Alzheimer’s disease(AD). Here, we report that the synaptic terminals of pyramidal neurons in the EC layer II (ECIIPN) directly innervate CA1 parvalbumin(PV) neurons (CA1PV) and are selectively degenerated in AD mice, which exhibit amyloid-β plaques similar to those observed in AD patients. A loss of ECIIPN–CA1PV synapses disables the excitatory and inhibitory balance in the CA1 circuit and impairs spatial learning and memory. Optogenetic activation of ECIIPN using a theta burst paradigm rescues ECIIPN–CA1PV synaptic defects and intercepts the decline in spatial learning and memory. These data reveal a novel mechanism of memory loss in AD mice via the selective degeneration of the ECIIPN–CA1PV pathway.

Fig.1 ECIIPN functionally targets CA1PV via a direct pathway.
To determine direct synaptic connections from ECIIPN to CA1PV,RV virus were used in a retrograde fashion across monosynaptic connections. To determine the functional properties of the ECIIPN–CA1PV pathway, ChR2-eGFP virus were used for optogenetic manipulation. The results demonstrated that CA1PV receive synaptic inputs directly from ECIIPN.
 
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