This study investigates how Kv7 potassium channel dysfunction and modulation of Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) channels influence excitatory synaptic integration in ventrobasal (VB) thalamic neurons of leptin-deficient obese (ob/ob) mice versus wild-type (WT). HCN channels mediate the hyperpolarization-activated Ih current, which stabilizes resting membrane potential and input resistance. Electrophysiological recordings from brain slices of WT and ob/ob mice were used to characterize AMPA receptor kinetics (τ1 ≈ 1.19 ms, τ2 ≈ 1.22 ms) as well as Kv7 and HCN levels, which were then incorporated into a realistic multicompartmental NEURON model. AMPA receptors were placed at the dendritic level and activated using a stochastic event generator. WT and ob/ob models were tested under varying Kv7 and HCN conductances. WT responses remained stable, whereas ob/ob neurons—due to Kv7 dysfunction—exhibited heightened sensitivity, with spike output strongly modulated by HCN alterations. In ob/ob neurons, impaired Kv7 function reduces subthreshold stabilization, making excitability highly dependent on HCN activity. This interaction amplifies synaptic variability and responsiveness, suggesting disrupted sensory processing in obesity-related pathophysiology. These findings highlight the critical Kv7-HCN interplay in maintaining excitability stability and implicate their dysfunction as a potential mechanism underlying thalamocortical alterations in obesity.