{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:21:02Z","timestamp":1791300062930,"version":"4.1.0"},"reference-count":50,"publisher":"Society for Neuroscience","issue":"7","license":[{"start":{"date-parts":[[2010,8,17]],"date-time":"2010-08-17T00:00:00Z","timestamp":1282003200000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2010,2,17]]},"abstract":"<jats:p>\n                    Homeostatic control of synaptic efficacy is often mediated by dynamic regulation of excitatory synaptic receptors. Here, we report a novel form of homeostatic synaptic plasticity based on regulation of shunt currents that control dendritosomatic information transfer. In cortical pyramidal neurons from wild-type mice, HCN1 channels underlie a dendritic hyperpolarization-activated cationic current (\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>h<\/jats:sub>\n                    ) that serves to limit temporal summation of synaptic inputs. In HCN1 knock-out mice, as expected,\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>h<\/jats:sub>\n                    is reduced in pyramidal neurons and its effects on synaptic summation are strongly diminished. Unexpectedly, we found a markedly enhanced bicuculline- and L-655,708-sensitive background GABA\n                    <jats:sub>A<\/jats:sub>\n                    current in these cells that could be attributed to selective upregulation of GABA\n                    <jats:sub>A<\/jats:sub>\n                    \u03b15 subunit expression in the cortex of HCN1 knock-out mice. Strikingly, despite diminished\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>h<\/jats:sub>\n                    , baseline sublinear summation of evoked EPSPs was unchanged in pyramidal neurons from HCN1 knock-out mice; however, blocking tonic GABA\n                    <jats:sub>A<\/jats:sub>\n                    currents with bicuculline enhanced synaptic summation more strongly in pyramidal cells from HCN1 knock-out mice than in those cells from wild-type mice. Increasing tonic GABA\n                    <jats:sub>A<\/jats:sub>\n                    receptor conductance in the context of reduced\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>h<\/jats:sub>\n                    , using computational or pharmacological approaches, restored normal baseline synaptic summation, as observed in neurons from HCN1 knock-out mice. These data indicate that upregulation of \u03b15 subunit-mediated GABA\n                    <jats:sub>A<\/jats:sub>\n                    receptor tonic current compensates quantitatively for loss of dendritic\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>h<\/jats:sub>\n                    in cortical pyramidal neurons from HCN1 knock-out mice to maintain normal synaptic summation; they further imply that dendritosomatic synaptic efficacy is a controlled variable for homeostatic regulation of cortical neuron excitability\n                    <jats:italic>in vivo<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1523\/jneurosci.3771-09.2010","type":"journal-article","created":{"date-parts":[[2010,2,17]],"date-time":"2010-02-17T13:19:56Z","timestamp":1266412796000},"page":"2611-2622","source":"Crossref","is-referenced-by-count":56,"title":["Homeostatic Regulation of Synaptic Excitability: Tonic GABA\n                    <sub>A<\/sub>\n                    Receptor Currents Replace\n                    <i>I<\/i>\n                    <sub>h<\/sub>\n                    in Cortical Pyramidal Neurons of HCN1 Knock-Out Mice"],"prefix":"10.1523","volume":"30","author":[{"given":"Xiangdong","family":"Chen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaofang","family":"Shu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren C.","family":"Schwartz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chengsan","family":"Sun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaideep","family":"Kapur","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas A.","family":"Bayliss","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"393","published-online":{"date-parts":[[2010,2,17]]},"reference":[{"key":"2023041303423590000_30.7.2611.1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.154336"},{"key":"2023041303423590000_30.7.2611.2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0551-07.2007"},{"key":"2023041303423590000_30.7.2611.3","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00029.2008"},{"key":"2023041303423590000_30.7.2611.4","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00482.2007"},{"key":"2023041303423590000_30.7.2611.5","doi-asserted-by":"publisher","DOI":"10.1038\/35051086"},{"key":"2023041303423590000_30.7.2611.6","doi-asserted-by":"publisher","DOI":"10.1002\/cne.10102"},{"key":"2023041303423590000_30.7.2611.7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0307231101"},{"key":"2023041303423590000_30.7.2611.8","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3481-08.2009"},{"key":"2023041303423590000_30.7.2611.9","doi-asserted-by":"publisher","DOI":"10.1152\/jn.01352.2007"},{"key":"2023041303423590000_30.7.2611.10","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.2650-05.2005"},{"key":"2023041303423590000_30.7.2611.11","doi-asserted-by":"publisher","DOI":"10.1038\/nature03011"},{"key":"2023041303423590000_30.7.2611.12","doi-asserted-by":"publisher","DOI":"10.1038\/nrn1198"},{"key":"2023041303423590000_30.7.2611.13","first-page":"25","article-title":"Double trouble: Potential for hyperexcitability following both channelopathic up- and downregulation of Ih in epilepsy","volume":"3","author":"Dyhrfjeld-Johnsen","year":"2009","journal-title":"Front Cell Neurosci"},{"key":"2023041303423590000_30.7.2611.14","doi-asserted-by":"publisher","DOI":"10.1038\/nrn1625"},{"key":"2023041303423590000_30.7.2611.15","doi-asserted-by":"publisher","DOI":"10.1038\/nn.2307"},{"key":"2023041303423590000_30.7.2611.16","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2007.11.002"},{"key":"2023041303423590000_30.7.2611.17","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4751-07.2008"},{"key":"2023041303423590000_30.7.2611.18","doi-asserted-by":"publisher","DOI":"10.1162\/neco.1997.9.6.1179"},{"key":"2023041303423590000_30.7.2611.19","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1531-09.2009"},{"key":"2023041303423590000_30.7.2611.20","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2370"},{"key":"2023041303423590000_30.7.2611.21","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3605-07.2007"},{"key":"2023041303423590000_30.7.2611.22","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.122028"},{"key":"2023041303423590000_30.7.2611.23","doi-asserted-by":"crossref","first-page":"4151","DOI":"10.1523\/JNEUROSCI.12-11-04151.1992","article-title":"The distribution of thirteen GABAA receptor subunit mRNAs in the rat brain. 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