A similar LTP has been reported following motor learning in lobule HVI. Indeed, fear memory was impaired in mutant mice with a selective dysfunction of PF-PC synapses. Finally, PC-specific knockout of the protein phosphatase PP2B selectively impairs PF-PC LTP and cerebellar motor learning. The basolateral amygdala plays a crucial role in emotional memory. It has been proposed that BLA is the site of the associative changes related to memory formation. Furthermore, BLA may enable learning-induced plasticity to be formed in other brain sites. BLA and cerebellum may interact during memory processes. Therefore, in the present study, we investigate the impact of BLA inactivation on cerebellar plasticity occurring during memory formation. To block BLA without affecting the passing fibers, we used the GABAergic agonist muscimol . Fig. 1B shows the position of the needle track into BLA. At the selected coordinates, the injected volume primarily inactivates BLA. To inactivate BLA during fear memory acquisition, we injected muscimol one hour before training. To ensure that this procedure does not alter the spontaneous activity of the subjects, before conditioning we recorded several types of behavior that rats normally display in a new environment, namely freezing, rearing, grooming and exploring. Fig. 1C shows the mean percentage activities recorded during the 2 minutes GDC-0941 preceding the conditioning trial. Student’s t-test indicates no difference between rats infused with muscimol and the control subjects for all spontaneous activities, in line with previous findings. Long-term memory retention was tested one day after conditioning. At this time interval, we measured freezing response in three different groups: i) conditioned animals, which the day before received a series of pairings of tone and footshock, ii) naı ¨ve animals, which received no training; and iii) conditioned subjects that received muscimol before CS-US presentation. In these groups, freezing was measured during the presentation of the CS and also during the two min that precede this administration. Freezing before CS presentation did not differ among the three groups =0.21; NS), suggesting that all the employed procedures produce a very low generalized fear response. During CS presentation, one-way ANOVA showed a significant difference among naı ¨ve, conditioned and muscimol-injected subjects =251.65; P,0.001). Newman-Keuls test showed significant differences between conditioned animals and those that received muscimol, but not between muscimol-treated subjects and the naı ¨ve ones. Thus, BLA blockade performed during CS-US presentation prevents fear memory formation, as previously reported. We evaluated the role of BLA during fear memory consolidation by injecting muscimol shortly after the acquisition.