{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T14:07:43Z","timestamp":1791036463151,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2001,6,1]],"date-time":"2001-06-01T00:00:00Z","timestamp":991353600000},"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":[[2001,6]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item>\n<jats:p>The role of Ca<jats:sup>2+<\/jats:sup>\u2010calmodulin (CaM) signalling cascades in modulating glutamatergic synaptic transmission on CA1 non\u2010pyramidal fast\u2010spiking neurons was investigated using whole\u2010cell recording and perfusion in rat hippocampal slices.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>Paired stimuli (PS), consisting of postsynaptic depolarization to 0 mV and presynaptic stimulation at 1 Hz for 30 s, enhanced excitatory postsynaptic currents (EPSCs) on non\u2010pyramidal neurons in the stratum pyramidale (SP). The potentiation was reduced by the extracellular application of <jats:sc>d<\/jats:sc>\u2010amino\u20105\u2010phosphonovaleric acid (DAP\u20105, 40 \u03bc<jats:sc>m<\/jats:sc>), and blocked by the postsynaptic perfusion of 1,2\u2010bis(2\u2010aminophenoxy)\u2010ethane\u2010<jats:italic>N,N,N\u2032,N\u2032<\/jats:italic>\u2010tetraacetic acid (BAPTA, 10 m<jats:sc>m<\/jats:sc>), a CaM\u2010binding peptide (100 \u03bc<jats:sc>m<\/jats:sc>) or CaMKII (281\u2013301) (an autoinhibitory peptide of CaM\u2010dependent protein kinases, 100 \u03bc<jats:sc>m<\/jats:sc>).<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>The application of adenophostin, an agonist of inositol trisphosphate receptors (IP<jats:sub>3<\/jats:sub>Rs) that evokes Ca<jats:sup>2+<\/jats:sup> release, into SP non\u2010pyramidal neurons via the patch pipette (1 \u03bc<jats:sc>m<\/jats:sc>) enhanced EPSCs and occluded PS\u2010induced synaptic potentiation. The co\u2010application of BAPTA (10 m<jats:sc>m<\/jats:sc>) with adenophostin blocked synaptic potentiation. In addition, Ca<jats:sup>2+<\/jats:sup>\u2010CaM (40:10 \u03bc<jats:sc>m<\/jats:sc>) induced synaptic potentiation, which occluded PS\u2010induced potentiation and was attenuated by introducing CaMKII (281\u2013301) (100 \u03bc<jats:sc>m<\/jats:sc>). EPSCs were sensitive to an antagonist of \u03b1\u2010amino\u20103\u2010hydroxy\u20105\u2010methyl\u20104\u2010isoxazole propionic acid receptor (AMPAR).<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>Application of Ca<jats:sup>2+<\/jats:sup>\u2010CaM into SP non\u2010pyramidal neurons induced the emergence of AMPAR\u2010mediated EPSCs that were not evoked by low stimulus intensity before perfusion. Ca<jats:sup>2+<\/jats:sup>\u2010CaM also increased the amplitude and frequency of spontaneous EPSCs. A scavenger of nitric oxide, carboxy\u2010PTIO (30 \u03bc<jats:sc>m<\/jats:sc> in slice\u2010perfusion solution), did not affect these increases in sEPSCs.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>The magnitude of PS\u2010, adenophostin\u2010 or Ca<jats:sup>2+<\/jats:sup>\u2010CaM\u2010induced synaptic potentiation in SP non\u2010pyramidal neurons increased during postnatal development.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>These results indicate that Ca<jats:sup>2+<\/jats:sup>\u2010CaM signalling pathways in CA1 SP non\u2010pyramidal neurons up\u2010regulate glutamatergic synaptic transmission probably through the conversion of inactive\u2010to\u2010active synapses.<\/jats:p>\n<\/jats:list-item>\n<\/jats:list>\n<\/jats:p>","DOI":"10.1111\/j.1469-7793.2001.0407a.x","type":"journal-article","created":{"date-parts":[[2004,8,5]],"date-time":"2004-08-05T10:08:46Z","timestamp":1091700526000},"page":"407-422","source":"Crossref","is-referenced-by-count":101,"title":["Calcium\u2010calmodulin signalling pathway up\u2010regulates glutamatergic synaptic function in non\u2010pyramidal, fast spiking rat hippocampal CA1 neurons"],"prefix":"10.1113","volume":"533","author":[{"given":"Jin\u2010Hui","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Kelly","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2001,6]]},"reference":[{"key":"e_1_2_5_1_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1991.tb25929.x"},{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1980.sp013256"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.276.5321.2042"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)80510-3"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1982.48.3.597"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.1997.tb01520.x"},{"key":"e_1_2_5_7_1","first-page":"145","volume-title":"Calmodulin","author":"Cohen P.","year":"1988"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.15.9956"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/381071a0"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/0959-4388(95)80042-5"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-2236(99)01492-7"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1987.sp016865"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1063(1996)6:4<347::AID-HIPO1>3.0.CO;2-I"},{"key":"e_1_2_5_14_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.57.030195.003423"},{"key":"e_1_2_5_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(94)90306-9"},{"key":"e_1_2_5_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)41915-1"},{"key":"e_1_2_5_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(89)90091-X"},{"key":"e_1_2_5_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(95)90046-2"},{"key":"e_1_2_5_19_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.10-06-01830.1990"},{"key":"e_1_2_5_20_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF02935544"},{"key":"e_1_2_5_21_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.3.945"},{"key":"e_1_2_5_22_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.14.5326"},{"key":"e_1_2_5_23_1","first-page":"225","volume-title":"Calmodulin","author":"Klee C. 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