ROLE OF CA2+ IN STRIATAL LTD AND LTP

The corticostriatal projection has a major function in the control of movements. Alterations of the release of glutamate from corticostriata l terminals have been implicated in disorders of the basal ganglia suc h as Parkinsons's disease and Huntington's chorea. The long-term regul ation of corticostriatal transmission. might require the participation of different forms of striatal synaptic plasticity. In physiological condition (1.2mM external magnesium) the tetanic stimulation of cortic al afferents produces a LTD of excitatory synaptic potentials recorded in. the striatum. When the external magnesium is omitted, this tetanu s induces LTP. NMDA receptor antagonists prevent the induction of LTP, but not the generation of LTD. LTD is blocked either by BAPTA and EGT A or by thapsigargin suggesting that a rise of intracellular Ca2+ is r equired for this form of synaptic plasticity. Nifedipine is also able to prevent LTD indicating that high voltage-activated (HVA) Ca2+ chann els of the L-type are implicated in the formation of LTD. Moreover, LT D is blocked by inhibitors of Ca2+-dependent kinases suggesting that a rise in internal Ca2+ is a crucial step for the subsequent activation of a second messenger cascade. Although both striatal LTD and LTP see m to require an increase in intracellular Ca2+ concentration, this cha nge is probably arising from different sources.