Objectives – It was shown previously that low-Mg2+-induced epileptiform activity in rat entorhinal cortex slices changes with time from a pattern of serial seizure-like events (SLEs) to a state of continuously recurring epileptiform activity. Valproic acid blocked the early SLEs but not the late activity. It was proposed that the late activity is a model for pharmacoresistant status epilepticus since it was also refractory to phenytoin, carbamazepine, phenobarbital, and midazolam. In the present study, it is demonstrated that phenytoin (50 μM, n=6), phenobarbital (150 μM, n=7), and midazolam (50 μM, n=5) were able to block the early SLEs but not the late activity at the same concentrations. Carbamazepine (50 μM) reduced the duration of the SLEs from 21±5 s to 4±3 s (P<0.01), the interictal interval from 123±27 s to 27±19 s (P<0.01), the SLE-associated rise of [K+]0 from 7.7±0.5 mM to 5.7±0.8 mM (n=4, P<0.05), and the spread of the SLE between entorhinal cortex and neocortex from 4.0±0.6 s to 0.8±0.1 s (n=4, P<0.05). Lower concentrations of phenytoin (5 and 10 μM, n=5), carbamazepine (10 μM, n=6), and phenobarbital (50 μM, n=4) had no effect. In conclusion, the hypothesis is supported that low-Mg2+-induced epileptiform activity in rat entorhinal cortex is an in vitro model for the transition from pharmacosensitive to pharmacoresistant status epilepticus.