Role of Ca2+in striatal LTD and LTP

Abstract

The corticostriatal projection has a major function in the control of movements. Alterations of the release of glutamate from corticostriatal terminals have been implicated in disorders of the basal ganglia such as Parkinson's disease and Huntington's chorea. The long-term regulation of corticostriatal transmission might require the participation of different forms of striatal synaptic plasticity. In physiological condition (1·2 mM external magnesium) the tetanic stimulation of cortical afferents produces a LTD of excitatory synaptic potentials recorded in the striatum. When the external magnesium is omitted, this tetanus induces LTP. NMDA receptor antagonists prevent the induction of LTP, but not the generation of LTD. LTD is blocked either by BAPTA and EGTA or by thapsigargin suggesting that a rise of intracellular Ca²⁺is required for this form of synaptic plasticity. Nifedipine is also able to prevent LTD indicating that high voltage-activated (HVA) Ca²⁺channels of the L-type are implicated in the formation of LTD. Moreover, LTD 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 seem to require an increase in intracellular Ca²⁺concentration, this change is probably arising from different sources.