Finally, in two additional groups, we blocked BLA protein synthesis by administering anisomycin 5 min or 6 h after conditioning. Fig. 2B indicates the position of the needle track. Fig. 2C shows freezing response in all subjects. During CS presentation, one-way ANOVA revealed significant differences among groups =33.08; P,0.001). Newman-Keuls test showed differences among animals that received anisomycin shortly after the acquisition and all the other groups. Muscimol-treated subjects never differed from Fingolimod conditioned animals. These data indicate that muscimol does not affect fear memory consolidation. On the other hand, the blockade of protein synthesis into BLA caused amnesia when performed 5 min, but not 6 h, after learning, as previously reported. Our data are in line with previous findings showing that although pre-training functional inactivation of BLA with muscimol impaired Pavlovian fear conditioning, immediate post-training inactivation had no effect. In contrast, posttraining inactivation of BLA consistently impaired inhibitory avoidance learning. These results are consistent with those of previous studies in which intra-amygdala administration of AP-5 impaired Pavlovian fear conditioning if given before, but not immediately after, training. In contrast, post-training infusion of AP-5 has been shown to impair inhibitory avoidance learning. Collectively, the findings indicate that Pavlovian fear conditioning and inhibitory avoidance are differentially affected by post-training pharmacological manipulations of BLA and suggest that fundamental differences exist in the underlying neural mechanisms mediating memory consolidation in the two learning paradigms. Overall, it should be pointed out that muscimol increases GABAergic activity, while anisomycin blocks the synthesis of new proteins in both glutamatergic and GABAergic neurons, i.e. these two substances have a completely different impact on the global activity of the injected site. Such a difference may be responsible of the differential effects that the two substances had on the consolidation of fear conditioned memories. In the present study, we showed that during fear memorization BLA reversible blockade impairs learning-induced LTP in the cerebellum. Our findings reveal that BLA modulates cerebellar plasticity. Moreover, they suggest that the synaptic strengthening underlying learning is a heterosynaptic phenomenon that requires inputs from other neural structures. Previous studies showed that in cerebellum PF-PC LTP is strictly related to learning processes. It is i) present in subjects that received CS and US in a temporally paired way, but not in those receiving the same two stimuli separately, ii) long-lasting, iii) localized to the lobules and synapses engaged by fear learning. Mutant mice lacking PF-PC LTP were also impaired in fear memory retention.