Trends in Neurosciences
Cellular mechanisms of cerebellar LTD
Section snippets
Involvement of Ca2+ flow into PCs through VGCCs
Early in vivo experiments suggested that the flow of Ca2+ through VGCCs was involved in LTD induction because hyperpolarization evoked by the activation of stellate cells prevented the occurrence of LTD ([1]), probably by blocking Ca2+-dependent plateau potentials in PC dendrites following their activation by climbing fibers (CFs)[2]. In subsequent experiments in acute cerebellar slices maintained in vitro, it was also shown that LTD of synaptic transmission at PF–PC synapses can be induced by
Role of Ca2+ release from internal stores
Although Ca2+ has been shown to play a crucial role in cerebellar LTD, the physiological significance of Ca2+ release from internal stores is still a matter of debate. PC dendrites express two types of intracellular Ca2+ stores: ryanodine- and InsP3-sensitive stores21, 22, 23, 24, 25, and it was hypothesized that the cascade of events leading to LTD might involve Ca2+ release from these stores, in addition to Ca2+ entry through VGCCs (see above). In cultured PCs, depletion of ryanodine- and InsP
Concluding remarks
Before providing conclusions, it is worth mentioning other players recently discovered in the cellular mechanisms leading to LTD induction. In cultured PCs, it has been shown that the increase in the cytosolic Ca2+ concentration required for LTD induction probably involves activation of a Na+–Ca2+ exchanger[52]. In the same preparation, it has also been established that the full activation of PKC required for LTD induction involves activation of the Ca2+-dependent enzyme phospholipase A2 (PLA2
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