The reticular thalamic nucleus (RTn) coordinates the overall traffic information to the cerebral cortex through modulates axons from cortico-thalamic (CT) and thalamic-cortical (TC) fibers. There are two spiking modalities of RTn neurons: electrical burst activity (synchronized mode) and electrical tonic activity (desynchronized mode) that occurs during awake state and REM sleep. Furthermore, burst activity synchronizes rhythmic oscillations into CT-TC fibers and its lost has been associated with pathological states such absence epilepsy and schizophrenia. The electrical activity of RTn depends on its afferent fibers and the membrane properties of reticular neurons. According with this, a GABAergic pathway was described from the globus pallidus externus (GP) an important nucleus that integrates and controls the information of basal ganglia. This afferent suggests important participation of GP in functional activity of RTn by influence of spiking activity. We studied the spontaneous electrical activity of RTn neurons by extracellular unit recording in vivo on male Wistar rats (300-350 g). To determine if the pallidoreticular pathway could modify the spontaneous RTn neurons discharge activity, we either activated it or blocked it by ipsilateral intrapallidal infusion of different concentrations of glutamate or GABA respectively (values are mean ±, compared by Student t-test and one-way ANOVA). Burst activity is reported in burst index (a minimum of two spikes and maximum interspike interval of 10 ms/ total events >10 ms) Rats were anesthetized with chloral hydrate (400 mg/kg i.p) and were placed in stereotaxic frame. Supplementary doses of anesthetic (50-70 mg/kg) were used as needed according to the presence of corneal reflex. We found that activation of pallidal neurons modify the spontaneous firing rate of RTn neurons. In a dose-dependent manner, glutamate decreases the spontaneous spiking rate of RTn neurons relative to basal values (30 PMol decreased the spiking rate by 35.13 ± 5.86%,n=11; 300 pMol by 45.82 ± 6.07%, n=10 and 3 nMol by 56.2 ± 6.81, n=13), without significance change in either the bursting index. Additionally, intrapallidal GABA application increases RTn neurons spiking rate in eight neurons tested per concentration (30 pMol increased the spiking rate by 25.96 ± 6.08%, 300 pMol by 64.3 ± 19.57%, 3 nMol by 77.16 ± 19.89%). Burst index remained without changes. Our results suggests that the GP exerts tight control over RTn activity.