PKC and polyamine modulation of GluR2-deficient AMPA receptors in immature neocortical pyramidal neurons of the rat.

摘要: AMPA receptors (AMPARs) mediate the bulk of fast synaptic excitation in CNS. We have recently shown that AMPAR-dependent transmission immature neocortical pyramidal neurons is mediated by GluR2-deficient can be modulated intra- or extracellular polyamines (PAs). Phosphorylation AMPARs, e.g. PKC, lead to enhanced excitation, and PAs are known modulate PKC activity. Therefore, might interact influence AMPAR function. To test this hypothesis, we made whole cell recordings from (P12–14) layer V assayed two measures PA on function – inward rectification use-dependent unblock (UDU), with latter differences between a pair EPSCs evoked at short (50 ms) latencies. previously displayed rectification, which was intracellular spermine, as UDU. Staurosporin (ST), inhibitor, reversed effect UDU, suggesting modulates postsynaptic activation AMPARs. Similarly, polyamine-dependent spontaneous treatment ST GFX109203X, specific inhibitor. Chelating Ca2+ BAPTA reproduced effects ST. In addition, immunoreactivity reduced inhibition indicating activity influences metabolism. Taken together, these data support involvement both UDU rat cortex, suggest an important mechanism excitatory dynamically changes either [Ca2+]i [PA]i.