Although the dysfunction of the pedunculopontine nucleus (PPN) has been related in the last decade to the pathophysiology of the Parkinson’s disease (PD), the changes in the extracellular concentration of aminoacid neurotransmitters in this structure have not been extensively studied. This study focuses on the changes in glutamate (Glu) and A-aminobutyric acid (GABA) of the PPN of hemiparkinsonian rats, and on the process of cellular death in this nucleus. Three groups of Wistar rats were examined: non-treated (n = 12), lesioned with 6-hydroxydopamine (6OHDA) (n=11), and sham-operated (n=10). In all groups, a microdialysis probe was implanted in the right PPN, ipsilateral to the injection of 6-OHDA. The dialyzates were analyzed using high performance liquid chromatography. The cellular death was studied by TUNEL inmunohistochemistry. There were statistically significant increases in the concentration of Glu and GABA in the PPN of hemiparkinsonian rats (p < 0.001) and the process of cell death was evidenced in the PPN ipsilateral to the susbtantia nigra compacta lesion. Higher Glu levels may be related to the excess of activity (hyperactivity) of the subthalamic nucleus-PPN pathway as well as the hyperactivity of the “indirect pathway” of the basal ganglia (BG). The increase in the glutamatergic tone may be the substratum for the cellular death events observed in the PPN. The increases in the GABA extracellular concentration in the PPN may be associated with the hyperactivity of the target nuclei in the BG. These results support the hypothesis concerning the involvement of the PPN in the pathophysiology of PD.