The cortico-basal ganglia-thalamocortical circuit with synaptic plasticity. I. Modification rules for excitatory and inhibitory synapses in the striatum

摘要

It is pointed out that Ca2+-dependent modification rules for NMDA-dependent (NMDA-independent) synaptic plasticity in the striatum are similar to those in the neocortex and hippocampus (cerebellum). A unitary postsynaptic mechanism of synaptic modification is proposed. It is based on the assumption that, in diverse central nervous system structures, long-term potentiation/depression (LTP/LTD) of excitatory transmission (depression/potentiation of inhibitory transmission, LTDi/LTPi) is the result of an increasing/decreasing the number of phosphorylated AMPA and NMDA (GABA(A)) receptors. According to the suggested mechanism, Ca2+/calmodulin-dependent protein kinase II and protein kinase C, whose activity is positively correlated with Ca2+ enlargement, together with cAMP-dependent protein kinase A (cCMP-dependent protein kinase G, whose activity is negatively correlated with Ca2+ rise) mainly phosphorylate ionotropic striatal receptors, if NMDA channels are opened (closed). Therefore, the positiveegative post-tetanic Ca2+ shift in relation to a previous Ca2+ rise must cause NMDA-dependent LTP + LTDi/ LTD + LTPi or NMDA-independent LTD + LTPi/LTP + LTDi. Dopamine D-1/D-2 or adenosine A(2A)/A(1) receptor activation must facilitate LTP + LTDi/LTD + LTPi due to an augmenting/lowering PKA activity. Activation of muscarinic M-1/M-4 receptors must enhance LTP + LTDi/LTD + LTPi as a consequence of an increase/decrease in the activity of protein kinase C/A. The proposed mechanism is in agreement with known experimental data. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved. [References: 51]