Recent experimental and modeling results demonstrated that surviving mossy cells 
in the dentate gyrus play key roles in the generation of network 
hyperexcitability. Here we examined if mossy cells exhibit long-term plasticity 
in the posttraumatic, hyperexcitable dentate gyrus. Mossy cells 1 wk after fluid 
percussion head injury did not show alterations in their current-firing 
frequency (I-F) and current-membrane voltage (I-V) relationships. In spite of 
the unchanged I-F and I-V curves, mossy cells showed extensive modifications in 
Na(+), K(+) and h-currents, indicating the coordinated nature of these opposing 
modifications. Computational experiments in a realistic large-scale model of the 
dentate gyrus demonstrated that individually, these perturbations could 
significantly affect network activity. Synaptic inputs also displayed 
systematic, opposing modifications. Miniature excitatory postsynaptic current 
(EPSC) amplitudes were decreased, whereas miniature inhibitory postsynaptic 
current (IPSC) amplitudes were increased as expected from a homeostatic response 
to network hyperexcitability. In addition, opposing alterations in miniature and 
spontaneous synaptic event frequencies and amplitudes were observed for both 
EPSCs and IPSCs. Despite extensive changes in synaptic inputs, 
cannabinoid-mediated depolarization-induced suppression of inhibition was not 
altered in posttraumatic mossy cells. These data demonstrate that many intrinsic 
and synaptic properties of mossy cells undergo highly specific, long-term 
alterations after traumatic brain injury. The systematic nature of such 
extensive and opposing alterations suggests that single-cell properties are 
significantly influenced by homeostatic mechanisms in hyperexcitable circuits.