Temporal lobe epilepsy is the most common form of epilepsy and is associated with hippocampal sclerosis and spontaneous recurrent seizures. These pathologies generally develop after a latent period from a precipitating brain injury, which often results in status epilepticus (SE). Sex and hormones have been reported to influence SE and mortality in both clinical and experimental settings. Temporal lobe epilepsy is also associated with an increase in reproductive disorders, which are often the result of altered pulsatile release of luteinizing hormone (LH). Gonadotropin-releasing hormone (GnRH) controls LH release; therefore, reproductive abnormalities associated with epilepsy could hypothetically involve hypothalamic disturbances, particularly to the GnRH network, resulting in altered secretion of GnRH. The aim of this dissertation was to (1) to examine the effects of SE and/or temporal lobe epilepsy on the GnRH neuronal network and (2) utilize recordings of electroencephalogram (EEG) activity to systematically quantify sex and hormone influences on SE and the subsequent recurrent seizures. I report that pilocarpine-induced SE resulted in reproductive alterations in two rodent models of temporal lobe epilepsy, which were not due to a detectable reduction in GnRH-positive neurons. There were no significant differences between the EEG parameters of SE or recurrent seizures between groups. Sex and the stage of the estrous cycle may influence pyramidal cell loss in the hippocampus at 24 h but the stage of the estrous cycle and/or sex do not seem to be predictors of long-term hippocampal damage. In summary, these data do not support the hypothesis that SE and/or temporal lobe epilepsy results in a reduction in the number of GnRH neurons or the hypothesis that sex/cycle stage influences SE, or the progression to temporal lobe epilepsy. However, these models of SE/temporal lobe epilepsy will be useful to further study temporal lobe epilepsy-associated reproductive alterations.