Projection neurons of the substantia nigra reticulata (SNr) convey basal ganglia (BG) processing to thalamocortical and brainstem circuits responsible for movement. Two models try to explain pathological BG performance during Parkinson disease (PD): the rate model, which posits an overexcitation of SNr neurons due to hyperactivity in the indirect pathway and hypoactivity of the direct pathway, and the oscillatory model, which explains PD as the product of pathological pattern generators disclosed by dopamine reduction. These models are, apparently, incompatible. We tested the predictions of the rate model by increasing the excitatory drive and reducing the inhibition upon SNr neurons in vitro. This was done pharmacologically with bath application of glutamate agonist N-methyl-D-aspartate and GABA_Areceptor blockers, respectively. Both maneuvers induced bursting behavior in SNr neurons. Therefore, synaptic changes forecasted by the rate model induce the electrical behavior predicted by the oscillatory model. In addition, we found evidence that Ca_V3.2 Ca²⁺ channels are a critical step in generating the bursting firing pattern in SNr neurons. Other ion channels involved are: hyperpolarization activated cation channels, high voltage activated Ca²⁺ channels and Ca²⁺ activated K⁺ channels. However, although these channels shape the temporal structure of bursting, only Ca_V3.2 Ca²⁺ channels are indispensable for the initiation of the bursting pattern.