{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,14]],"date-time":"2024-07-14T01:38:23Z","timestamp":1720921103413},"reference-count":73,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,5,23]],"date-time":"2007-05-23T00:00:00Z","timestamp":1179878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p>AMPA receptors (AMPARs) mediate the bulk of fast synaptic excitation in the CNS. We have recently shown that AMPAR\u2010dependent synaptic transmission in immature neocortical pyramidal neurons is mediated by GluR2\u2010deficient receptors that can be modulated by intra\u2010 or extracellular polyamines (PAs). Phosphorylation of AMPARs, e.g. by PKC, can lead to enhanced excitation, and PAs are known to modulate PKC activity. Therefore, PAs and PKC might interact to influence AMPAR function. To test this hypothesis, we made whole cell recordings from immature (P12\u201314) layer V pyramidal neurons and assayed two measures of PA influence on synaptic AMPAR function \u2013 inward rectification and use\u2010dependent unblock (UDU), with the latter assayed by differences in rectification between a pair of EPSCs evoked at short (50 ms) latencies. We have previously shown that EPSCs in immature pyramidal neurons displayed inward rectification, which was enhanced by intracellular spermine, as was UDU. Staurosporin (ST), a PKC inhibitor, reversed the effect of PA on rectification and UDU, suggesting that PKC modulates postsynaptic activation of AMPARs. Similarly, polyamine\u2010dependent rectification of spontaneous EPSCs was reversed by treatment with ST or GFX109203X, a specific PKC inhibitor. Chelating intracellular Ca<jats:sup>2+<\/jats:sup> with BAPTA reproduced the effects of ST. In addition, PA immunoreactivity in layer V pyramidal neurons was reduced by PKC inhibition indicating that PKC activity influences PA metabolism. Taken together, these data support the involvement of postsynaptic PKC activation in both the inward rectification and UDU of EPSCs in immature rat cortex, and suggest an important mechanism by which excitatory synaptic transmission can be dynamically modulated by changes in either [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> or [PA]<jats:sub>i<\/jats:sub>.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.130963","type":"journal-article","created":{"date-parts":[[2007,3,23]],"date-time":"2007-03-23T00:08:22Z","timestamp":1174608502000},"page":"679-691","source":"Crossref","is-referenced-by-count":18,"title":["PKC and polyamine modulation of GluR2\u2010deficient AMPA receptors in immature neocortical pyramidal neurons of the 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