Abstract:
Learning to fear dangerous situations requires the participation of basolateral
amygdala (BLA). In the present study, we provide evidence that BLA is necessary
for the synaptic strengthening occurring during memory formation in the
cerebellum in rats. In the cerebellar vermis the parallel fibers (PF) to Purkinje
cell (PC) synapse is potentiated one day following fear learning. Pretraining BLA
inactivation impaired such a learning-induced long-term potentiation (LTP).
Similarly, cerebellar LTP is affected when BLA is blocked shortly, but not 6 h,
after training. The latter result shows that the effects of BLA inactivation on
cerebellar plasticity, when present, are specifically related to memory processes
and not due to an interference with sensory or motor functions. These data
indicate that fear memory induces cerebellar LTP provided that a heterosynaptic
input coming from BLA sets the proper local conditions. Therefore, in the
cerebellum, learning-induced plasticity is a heterosynaptic phenomenon that
requires inputs from other regions. Studies employing the electrically-induced
LTP in order to clarify the cellular mechanisms of memory should therefore take
into account the inputs arriving from other brain sites, considering them as
integrative units. Based on previous and the present findings, we proposed that
BLA enables learning-related plasticity to be formed in the cerebellum in order
to respond appropriately to new stimuli or situations.
