At parallel fiber (PF) to Purkinje cells (PCs) synapses, depolarization-induced suppression of excitation (DSE) and suppression of PF-EPSCs by activation of post-synaptic mGluR1 glutamate (Glu) receptors involve retrograde release of endocannabinoids. However, Levenes et al. (2001) suggested instead that Glu was the retrograde messenger in this latter case. Since the study by Levenes et al. was performed in nearly mature rats whereas most others were performed in juvenile animals, DSE was re-investigated in juvenile versus nearly mature rats and mice. Indeed, DSE was preferred here to agonist-induced suppression of PF-EPSCs, to avoid possible indirect effects in this latter case. In 10 to 12 day-old rats, DSE of PF-EPSCs was entirely mediated through retrograde release of endocannabinoids. In 18 to 22 day-old-rats, DSE was partly resistant to CB1 cannabinoid receptor antagonists. The remaining component was potentiated the Glu uptake inhibitor DL-TBOA and blocked by the desensitizing kainate (KA) receptor agonist SYM 2081. This SYM 2081-sensitive component of DSE was accompanied by a PPF increase that was also potentiated by DL-TBOA and blocked SYM 2081. In nearly mature wild type and GluR6 -/- mice, results fully confirmed the presence of an endocannabinoid-independent component of DSE that involves retrograde release of Glu and activation of pre-synaptic KA receptors including GluR6 receptor subunits. Therefore, retrograde release of Glu by PCs participates to DSE at PF-PC synapses in nearly mature rodents but not in juvenile ones, and Glu probably operates through activation of pre-synaptic KA receptors that include GluR6 receptor subunits.