Figure 1.

Schematic of the connectivity of hilar mossy cells and toxin-induced mossy cell degeneration. (A) Mossy fiber axon collaterals of dentate granule cells are the main input to the mossy cells at their proximal dendrites, called “thorny excrescences.” Mossy cells also receive strong excitatory inputs from semilunar granule cells at the relatively distal dendritic segments of mossy cells. A fraction of CA3 pyramidal cells “backproject” to mossy cells which also receive scarce input directly from the entorhinal cortex. Mossy cells also receive GABAergic inputs from hilar interneurons. Other inputs such as cholinergic and noradrenergic projections are known to modulate mossy cell activity. Mossy cell axons project to the dentate inner molecular layer (IML) along the septo-temporal axis and further contra-lateral hippocampus, where over 90% of asymmetric synaptic contacts are formed on granule cell proximal dendrites as well as semilunar granule cells. Mossy cells also send axon collaterals to dentate GABAergic interneurons in the different lamellae or in the contra-lateral hippocampus. Mutual connections between mossy cells are rare. For simplicity, not all the connections are shown. Ach, acetylcholine; EC, entorhinal cortex; GC, granule cell; GCL, granule cell layer; IN, interneuron; MC, mossy cell; NA, noradrenaline; PC, pyramidal cell; SGC, semilunar granule cell; 5-HT, serotonin. (B) Representative photographs of Nissl staining showing histological alterations in the hilar region in CA3c/mossy cell-cre/floxed-diphtheria toxin receptor mutant mouse (right) 4 weeks after diphtheria toxin (DT) administration. Compared to DT-treated control (left), mutant mouse showed the decreased cell number in the dentate hilus. Scale bar, 100 μm.