Using temporal lobe epilepsy as an example, staging of long term plasticity in the hippocampus is considered. Major stages demonstrating opposite alterations in neuroplasticity are active epileptogenesis and the period of established temporal lobe epilepsy. During the epileptogenesis, multiple events resulting in forming of epileptic neuronal nets occur: changes in glutamatergic and GABAergic neurons, increase of aberrant neurogenesis, axonal sprouting and dendrite remodeling, particularly, supported by an excessive enhancement of the BDNF system in specific hippocampal regions. As epileptogenesis progresses, this stage of an aberrant superplasticity is changing for opposite events accompanying formation of the epileptogenic focus and limiting plasticity: axonal damage, neuronal cell death, hippocampal sclerosis, suppression of neurogenesis. At this neurodegenerative stage of temporal epilepsy, the inclusion of neuroprotectants with neurotrophic properties (e.g. drugs containing cerebral peptide hydrolizates) into the treatment protocol appears promising. Potential use of such neuroprotectants during the active epileptogenesis period is discussed.