Developmental cortical malformations are a major cause of intractable seizures. Determining the location and timing of susceptibility for epileptiform activity is critical to identifying what mechanisms contribute to epileptogenesis in any model. Using the freeze lesion rat model of polymicrogyria, we have identified, in lesioned cortex, these two aspects of epileptogenesis. Previous studies have demonstrated that epileptiform activity cannot be evoked prior to postnatal day (P) 12, but the malformed cortex is more susceptible to seizures as early as P10. An increase in excitatory afferents to the epileptogenic zone occurs before the onset of network epileptiform activity. Whether or not these afferents are a major contributor to the hyperexcitability of the malformed cortex can be investigated by determining if they specifically create a susceptibility for epileptiform activity. We have examined that here by measuring whether that timing coincides with an increased susceptibility for evoked and spontaneous epileptiform activity. We report that the malformed cortex is more susceptible to evoked epileptiform activity than control cortex as earlier as P7 and as late as P36. Further, we also find that the form of spontaneous epileptiform activity in malformed cortex is altered as early as P7. The timing of these early disruptions of cortical function found here suggests additional epileptogenic mechanisms exist prior to the reported increase in excitatory afferents at P10. Determining the location of the seizure initiation is an essential part of epilepsy research. Some patients with developmental cortical malformations have seizures initiated within the malformation, while others have seizures generated by the surrounding cortex. Previous data in the freeze lesion model of microgyria suggests that the timing of freeze lesion (from P0 to P1) can shift the epileptogenic focus from the malformation to the paramicrogyrial region (PMR). We report that both the timing of the freeze lesion and the survival age of the animal can alter the epileptogenic circuitry of the malformation and surrounding tissue. These findings provide new insight to the timeline of hyperexcitability in malformed cortex and will possibly lead to greater surgical success for patients with intractable epilepsy.