From Abnormal Hippocampal Synaptic Plasticity in Down Syndrome Mouse Models to Cognitive Disability in Down Syndrome
Figure 3
Potential impact of altered synaptic plasticity on hippocampal processing in Ts65Dn mouse model of Down syndrome. Schematic of two main pathways through hippocampus arriving from the entorhinal cortex: temporoammonic (TA)—direct to CA1 distal dendrites; trisynaptic pathway from DG through CA3 to proximal CA1 dendrites. LTP and LTD are proposed to minimize interference between the two pathways [50, 131]. (a) In euploid hippocampi, high-frequency inputs induce LTP in CA1 resulting in enhanced suppression of inputs from TA by feed-forward inhibition arising from interneurons in stratum oriens. (b) Low-frequency inputs depress the trisynaptic pathway releasing distal CA1 dendrites from feed-forward inhibition and allowing information to flow through the TA pathway. (c) In Ts65Dn hippocampi, aberrant LTP in CA1 results in diminished feed-forward inhibition during high-frequency activity allowing TA inputs to become superimposed on those flowing through the trisynaptic pathway. (d) Enhanced LTD would be expected to facilitate flow of low-frequency information through the direct TA pathway in Ts65Dn mice.
