In addition to changes in facilitative or inhibitory modulation of spinal circuits, loss of descending monoaminergic input may also change the intrinsic excitability of the spinal neurons themselves. Following complete spinal transection, studies of electrical properties of spinal neurons below the lesion reveal that initially, interneurons, especially in the dorsal horn, become hyperexcitable, whereas motoneuron excitability plummets. In the motoneuron, a key factor in this drastic decrease is a loss of persistent inward currents (PICs). Persistent currents are conductances that, once activated, do not turn off, or at least inactivate at an extremely slow rate. PICs have a profound effect on the excitability of spinal neurons, both amplifying and prolonging their input (Prescott and De Koninck 2005) and allowing them to produce long lasting outputs, plateau potentials and bistable behavior (Heckman et al. 2005; Hounsgaard et al. 1984; Lee and Heckman 1998). The loss of PICs has such a strong impact that motoneurons produce only brief and weak outputs to the hyperexcitable interneuron inputs (Baldissera et al. 1981; Heckman 1994; Kehne et al. 1985; Nygren and Olson 1976).