We employed whole-cell patch-clamp recordings to establish the effect of Zn²⁺ on the gating the brain specific, T-type channel isoform Ca_V3.3 expressed in HEK-293 cells. Zn²⁺ (300 µM) modified the gating kinetics of this channel without influencing its steady-state properties. When inward Ca²⁺ currents were elicited by step depolarizations at voltages above the threshold for channel opening, current inactivation was significantly slowed down while current activation was moderately affected. In addition, Zn²⁺ slowed down channel deactivation but channel recovery from inactivation was only modestly changed. Zn²⁺ also decreased whole cell Ca²⁺ permeability to 45% of control values. In the presence of Zn²⁺, Ca²⁺ currents evoked by mock action potentials were more persistent than in its absence. Furthermore, computer simulation of action potential generation in thalamic reticular cells performed to model the gating effect of Zn²⁺ on T-type channels (while leaving the kinetic parameters of voltage-gated Na⁺ and K⁺ unchanged) revealed that Zn²⁺ increased the frequency and the duration of burst firing, which is known to depend upon T-type channel activity. In line with this finding, we discovered that chelation of endogenous Zn²⁺ decreased the frequency of occurrence of ictal-like epileptiform discharges in rat thalamocortical slices perfused with medium containing the convulsant 4-aminopyridine (50 µM). These data demonstrate that Zn²⁺ modulates Ca_V3.3 channel gating thus leading to increased neuronal excitability. We also propose that endogenous Zn²⁺ may have a role in controlling thalamocortical oscillations.