Neuronal death does not appear to contribute to the learning deficits in rats with infant seizures. CA3 neurons in the tetanus toxin model of early onset epilepsy, however, show a reduction in the branching complexity of basal dendrites as well as a decrease in the spine density on both the apical dendrites and the basal dendrites. Similar data have been taken from epileptic human patients during surgical procedures. In neocortical and hippocampal foci, a decrease in length and branching complexity of dendritic arbors and a reduction in the branching complexity of the remaining dendrites were observed. The chronic alumina cream model of epilepsy in primates has produced similar data. Because dendrites and their spines are sites of excitatory synaptic input onto neurons, the results suggest that the glutaminergic synaptic transmission may be reduced. As these are sites active in long-term potentiation (LTP) and other alterations in synaptic transmission that underlie learning and memory, changes at these sites could explain learning and memory deficits associated with both early-onset and long-term epilepsy.