Temporal lobe epilepsy (TLE) is the most common focal epilepsy in adults, and people with TLE exhibit higher rates of reproductive endocrine dysfunction. Hypothalamic gonadotropin-releasing hormone (GnRH) neurons regulate reproductive function in mammals by regulating gonadotropin secretion from the anterior pituitary. Previous research demonstrated GnRH neuron hyperexcitability in both sexes in the intrahippocampal kainic acid (IHKA) mouse model of TLE. Fast-inactivating A-type (IA) and delayed rectifier K-type (IK) K+ currents play critical roles in modulating neuronal excitability, including in GnRH neurons. Here, we tested the hypothesis that GnRH neuron hyperexcitability is associated with reduced IA and IK conductances. At two months after IHKA or control saline injection, when IHKA mice exhibit chronic epilepsy, we recorded GnRH neuron excitability, IA, and IK using whole-cell patch-clamp electrophysiology. GnRH neurons from both IHKA male and diestrous female GnRH-GFP mice exhibited hyperexcitability compared to controls. In IHKA males, although maximum IA current density was increased, IK recovery from inactivation was significantly slower, consistent with a hyperexcitability phenotype. In IHKA females, however, both IA and IK were unchanged. Sex differences were not observed in IA or IK properties in controls, but IHKA mice exhibited sex effects in IA properties. These results indicate that although the emergent phenotype of increased GnRH neuron excitability is similar in IHKA males and diestrous females, the underlying mechanisms are distinct. This study thus highlights sex-specific changes in voltage-gated K+ currents in GnRH neurons in a mouse model of TLE and suggesting potential sex differences in GnRH neuron ion channel properties.Significance Statement Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy, and people with TLE are at a higher risk of developing reproductive endocrine issues compared to the general population. Previous research found increased excitability of gonadotropin-releasing hormone (GnRH) neurons, which control fertility, in a mouse model of TLE. We investigated whether voltage-gated potassium channels in these neurons play a role in driving this altered excitability by recording the ionic currents from these channels. Although some epilepsy-dependent and sex-specific modifications of potassium conductances were found, the findings overall suggest that epilepsy-associated GnRH neuron hyperexcitability is largely independent of changes in voltage-gated potassium conductances, indicating that other mechanisms are primarily responsible.