In line with the present data, in hippocampus a weak tetanic stimulation, which ordinarily leads to an early potentiation lasting less than 3 hours, CHIR-99021 252917-06-9 results in an LTP lasting for at least 8 hours, when a repeated tetanization has already been applied at another heterosynaptic input to the same population of neurons. In vivo, such an early potentiation is transformed into a LTP by appetitive and aversive stimuli and this reinforcement is blocked in BLA-lesioned animals. Accordingly, BLA stimulation facilitates the electrical induction of LTP in hippocampus, thalamocortical system, and striatum, while the inactivation of BLA decreases LTP in hippocampus when performed during, but not 20 min after, the application of the tetanus. On this ground, our results provide the first evidence that the synaptic strengthening occurring during memory trace formation is heterosynaptic in nature and requires BLA activity. To date, there is no evidence of a direct anatomic pathway connecting BLA to the cerebellum. Thus, BLA may influence cerebellar plasticity via two mechanisms: first, this site may regulate cerebellar level of monoamine, like noradrenalin, serotonin and dopamine. It is known that BLA modulates the influences of adrenal stress hormones on memory consolidation. Indeed, monoamine signals are involved in cerebellar learning. The other possibility relies on the fact that BLA sends direct projections to brain sites that in turn act on cerebellum. For instance, during eye blink conditioning, it has been proposed that BLA exerts an excitatory influence on cerebellum via the lateral tegmental field. In addition, BLA is anatomically connected with the hypothalamus, a region that is bidirectionally connected with the cerebellar vermis. Several findings support the involvement of the cerebellum in learned fear. In humans, the cerebellum is strongly activated during mental recall of personal fear-related events and by associating sensory stimuli with a painful stimulation. Changes in heart rate induced by repeated pairing of CS and US are hampered in patients with medial cerebellar lesion and in animals with vermal lesions. In all studies, these effects are due to an interference with associative processes, because baseline responses to CS and US are not affected. In addition, the reversible inactivation of cerebellar cortex during memory consolidation impairs fear memory retention. This result has been obtained by blocking this site after training and by performing the retention trial when the reversible blockade was over, i.e. with no interference with sensory or motor response. However, the role played by the vermis in fear conditioning remains to be clearly defined. Given its well known role in associative motor learning, it has been suggested that the cerebellum coordinates the adequate motor response. However, by way of the fastigial nucleus, vermis is connected also to the hypothalamus, to periaqueductal gray area.