The role of T‐type calcium channels in the subiculum: to burst or not to burst?
Key points Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T‐channels switched burst firing with lo...
Saved in:
| Published in | The Journal of physiology Vol. 595; no. 19; pp. 6327 - 6348 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Wiley Subscription Services, Inc
01.10.2017
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3751 1469-7793 1469-7793 |
| DOI | 10.1113/JP274565 |
Cover
| Abstract | Key points
Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum.
Pharmacological inhibition of T‐channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization‐induced burst firing.
Our molecular studies showed that CaV3.1 is the most abundantly expressed isoform of T‐channels in the rat subiculum.
Consistent with this finding, both regular‐spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV3.1 isoform of T‐channels.
Selective inhibition of T‐channels and global deletion of CaV3.1 channels completely suppressed development of long‐term potentiation (LTP) in the CA1–subiculum, but not in the CA3–CA1 pathway.
Several studies suggest that voltage‐gated calcium currents are involved in generating high frequency burst firing in the subiculum, but the exact nature of these currents remains unknown. Here, we used selective pharmacology, molecular and genetic approaches to implicate Cav3.1‐containing T‐channels in subicular burst firing, in contrast to several previous reports discounting T‐channels as major contributors to subicular neuron physiology. Furthermore, pharmacological antagonism of T‐channels, as well as global deletion of CaV3.1 isoform, completely suppressed development of long‐term potentiation (LTP) in the CA1–subiculum, but not in the CA3–CA1 pathway. Our results indicate that excitability and synaptic plasticity of subicular neurons relies heavily on T‐channels. Hence, T‐channels may be a promising new drug target for different cognitive deficits.
Key points
Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum.
Pharmacological inhibition of T‐channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization‐induced burst firing.
Our molecular studies showed that CaV3.1 is the most abundantly expressed isoform of T‐channels in the rat subiculum.
Consistent with this finding, both regular‐spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV3.1 isoform of T‐channels.
Selective inhibition of T‐channels and global deletion of CaV3.1 channels completely suppressed development of long‐term potentiation (LTP) in the CA1–subiculum, but not in the CA3–CA1 pathway. |
|---|---|
| AbstractList | Pharmacological, molecular and genetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T-channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization-induced burst firing. Our molecular studies showed that Ca
3.1 is the most abundantly expressed isoform of T-channels in the rat subiculum. Consistent with this finding, both regular-spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of Ca
3.1 isoform of T-channels. Selective inhibition of T-channels and global deletion of Ca
3.1 channels completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway.
Several studies suggest that voltage-gated calcium currents are involved in generating high frequency burst firing in the subiculum, but the exact nature of these currents remains unknown. Here, we used selective pharmacology, molecular and genetic approaches to implicate Cav3.1-containing T-channels in subicular burst firing, in contrast to several previous reports discounting T-channels as major contributors to subicular neuron physiology. Furthermore, pharmacological antagonism of T-channels, as well as global deletion of CaV3.1 isoform, completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway. Our results indicate that excitability and synaptic plasticity of subicular neurons relies heavily on T-channels. Hence, T-channels may be a promising new drug target for different cognitive deficits. Key points Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T‐channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization‐induced burst firing. Our molecular studies showed that CaV3.1 is the most abundantly expressed isoform of T‐channels in the rat subiculum. Consistent with this finding, both regular‐spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV3.1 isoform of T‐channels. Selective inhibition of T‐channels and global deletion of CaV3.1 channels completely suppressed development of long‐term potentiation (LTP) in the CA1–subiculum, but not in the CA3–CA1 pathway. Several studies suggest that voltage‐gated calcium currents are involved in generating high frequency burst firing in the subiculum, but the exact nature of these currents remains unknown. Here, we used selective pharmacology, molecular and genetic approaches to implicate Cav3.1‐containing T‐channels in subicular burst firing, in contrast to several previous reports discounting T‐channels as major contributors to subicular neuron physiology. Furthermore, pharmacological antagonism of T‐channels, as well as global deletion of CaV3.1 isoform, completely suppressed development of long‐term potentiation (LTP) in the CA1–subiculum, but not in the CA3–CA1 pathway. Our results indicate that excitability and synaptic plasticity of subicular neurons relies heavily on T‐channels. Hence, T‐channels may be a promising new drug target for different cognitive deficits. Key points Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T‐channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization‐induced burst firing. Our molecular studies showed that CaV3.1 is the most abundantly expressed isoform of T‐channels in the rat subiculum. Consistent with this finding, both regular‐spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV3.1 isoform of T‐channels. Selective inhibition of T‐channels and global deletion of CaV3.1 channels completely suppressed development of long‐term potentiation (LTP) in the CA1–subiculum, but not in the CA3–CA1 pathway. Key points Pharmacological, molecular and genetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T-channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization-induced burst firing. Our molecular studies showed that CaV3.1 is the most abundantly expressed isoform of T-channels in the rat subiculum. Consistent with this finding, both regular-spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV3.1 isoform of T-channels. Selective inhibition of T-channels and global deletion of CaV3.1 channels completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway. Several studies suggest that voltage-gated calcium currents are involved in generating high frequency burst firing in the subiculum, but the exact nature of these currents remains unknown. Here, we used selective pharmacology, molecular and genetic approaches to implicate Cav3.1-containing T-channels in subicular burst firing, in contrast to several previous reports discounting T-channels as major contributors to subicular neuron physiology. Furthermore, pharmacological antagonism of T-channels, as well as global deletion of CaV3.1 isoform, completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway. Our results indicate that excitability and synaptic plasticity of subicular neurons relies heavily on T-channels. Hence, T-channels may be a promising new drug target for different cognitive deficits. Key points Pharmacological, molecular and genetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T-channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization-induced burst firing. Our molecular studies showed that CaV3.1 is the most abundantly expressed isoform of T-channels in the rat subiculum. Consistent with this finding, both regular-spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV3.1 isoform of T-channels. Selective inhibition of T-channels and global deletion of CaV3.1 channels completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway. Pharmacological, molecular and genetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T-channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization-induced burst firing. Our molecular studies showed that CaV 3.1 is the most abundantly expressed isoform of T-channels in the rat subiculum. Consistent with this finding, both regular-spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV 3.1 isoform of T-channels. Selective inhibition of T-channels and global deletion of CaV 3.1 channels completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway.KEY POINTSPharmacological, molecular and genetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T-channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization-induced burst firing. Our molecular studies showed that CaV 3.1 is the most abundantly expressed isoform of T-channels in the rat subiculum. Consistent with this finding, both regular-spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of CaV 3.1 isoform of T-channels. Selective inhibition of T-channels and global deletion of CaV 3.1 channels completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway.Several studies suggest that voltage-gated calcium currents are involved in generating high frequency burst firing in the subiculum, but the exact nature of these currents remains unknown. Here, we used selective pharmacology, molecular and genetic approaches to implicate Cav3.1-containing T-channels in subicular burst firing, in contrast to several previous reports discounting T-channels as major contributors to subicular neuron physiology. Furthermore, pharmacological antagonism of T-channels, as well as global deletion of CaV3.1 isoform, completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway. Our results indicate that excitability and synaptic plasticity of subicular neurons relies heavily on T-channels. Hence, T-channels may be a promising new drug target for different cognitive deficits.ABSTRACTSeveral studies suggest that voltage-gated calcium currents are involved in generating high frequency burst firing in the subiculum, but the exact nature of these currents remains unknown. Here, we used selective pharmacology, molecular and genetic approaches to implicate Cav3.1-containing T-channels in subicular burst firing, in contrast to several previous reports discounting T-channels as major contributors to subicular neuron physiology. Furthermore, pharmacological antagonism of T-channels, as well as global deletion of CaV3.1 isoform, completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathway. Our results indicate that excitability and synaptic plasticity of subicular neurons relies heavily on T-channels. Hence, T-channels may be a promising new drug target for different cognitive deficits. Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing activity of both pyramidal and inhibitory interneurons in the subiculum. Pharmacological inhibition of T‐channels switched burst firing with lower depolarizing stimuli to regular spiking, and fully abolished hyperpolarization‐induced burst firing. Our molecular studies showed that Ca V 3.1 is the most abundantly expressed isoform of T‐channels in the rat subiculum. Consistent with this finding, both regular‐spiking and burst firing patterns were profoundly depressed in the mouse with global deletion of Ca V 3.1 isoform of T‐channels. Selective inhibition of T‐channels and global deletion of Ca V 3.1 channels completely suppressed development of long‐term potentiation (LTP) in the CA1–subiculum, but not in the CA3–CA1 pathway. |
| Author | Eggan, Pierce Herson, Paco S. Joksimovic, Sonja Lj Jevtovic‐Todorovic, Vesna Todorovic, Slobodan M. DiGruccio, Michael R. Tesic, Vesna Izumi, Yukitoshi Orfila, James E. Joksimovic, Srdjan M. Zorumski, Charles F. Dietz, Robert M. |
| AuthorAffiliation | 2 Department of Psychiatry & Taylor Family Institute for Innovative Psychiatric Research Washington University School of Medicine St Louis MO 63110 USA 1 Department of Anesthesiology University of Colorado, School of Medicine Aurora CO 80045 USA 3 Department of Neurobiology, Physiology and Behavior, College of Biological Sciences University of California Davis CA 95616 USA |
| AuthorAffiliation_xml | – name: 3 Department of Neurobiology, Physiology and Behavior, College of Biological Sciences University of California Davis CA 95616 USA – name: 2 Department of Psychiatry & Taylor Family Institute for Innovative Psychiatric Research Washington University School of Medicine St Louis MO 63110 USA – name: 1 Department of Anesthesiology University of Colorado, School of Medicine Aurora CO 80045 USA |
| Author_xml | – sequence: 1 givenname: Srdjan M. surname: Joksimovic fullname: Joksimovic, Srdjan M. organization: University of Colorado, School of Medicine – sequence: 2 givenname: Pierce surname: Eggan fullname: Eggan, Pierce organization: University of Colorado, School of Medicine – sequence: 3 givenname: Yukitoshi orcidid: 0000-0002-5596-1031 surname: Izumi fullname: Izumi, Yukitoshi organization: Washington University School of Medicine – sequence: 4 givenname: Sonja Lj surname: Joksimovic fullname: Joksimovic, Sonja Lj organization: University of Colorado, School of Medicine – sequence: 5 givenname: Vesna orcidid: 0000-0002-7247-1034 surname: Tesic fullname: Tesic, Vesna organization: University of Colorado, School of Medicine – sequence: 6 givenname: Robert M. surname: Dietz fullname: Dietz, Robert M. organization: University of Colorado, School of Medicine – sequence: 7 givenname: James E. surname: Orfila fullname: Orfila, James E. organization: University of Colorado, School of Medicine – sequence: 8 givenname: Michael R. surname: DiGruccio fullname: DiGruccio, Michael R. organization: University of California – sequence: 9 givenname: Paco S. surname: Herson fullname: Herson, Paco S. organization: University of Colorado, School of Medicine – sequence: 10 givenname: Vesna surname: Jevtovic‐Todorovic fullname: Jevtovic‐Todorovic, Vesna organization: University of Colorado, School of Medicine – sequence: 11 givenname: Charles F. surname: Zorumski fullname: Zorumski, Charles F. organization: Washington University School of Medicine – sequence: 12 givenname: Slobodan M. orcidid: 0000-0003-2613-0391 surname: Todorovic fullname: Todorovic, Slobodan M. email: slobodan.todorovic@ucdenver.edu organization: University of Colorado, School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28744923$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1kdFqFDEUhoNU7LYKPoEEvPFmak6SSSZeKFK0WgpWWK9DJpNxUzLJmswoe-cj-Iw-Sad0d1tFr8Ih3_n4zzlH6CCm6BB6CuQEANjL80sqeS3qB2gBXKhKSsUO0IIQSismazhER6VcEQKMKPUIHdJGcq4oW6DPy5XDOQWHU4-Xv3_-Gjdrh60J1k8DtisTowsF-4jHGSxT6-0UpuEVHhNup1xGnDKOadzXbx6jh70JxT3Zvsfoy_t3y9MP1cWns4-nby8qy5lqqhpoK5SDHhwoY1lnQInW0k7UBBSlxDbQOmY5mEYBSGlZy0hnu75vpTCCHaPXt9711A6usy6O2QS9zn4weaOT8frPn-hX-mv6rmtBgSs2C15sBTl9m1wZ9eCLdSGY6NJU9JyCzVslpJnR53-hV2nKcR5vpjinEoSEmXp2P9E-ym7bM3ByC9icSsmu19aPZvTpJqAPGoi-OafenfMu4r5h5_wHunX_8MFt_svp5fkl0Jo27BoeLKxr |
| CitedBy_id | crossref_primary_10_3389_fnins_2024_1483708 crossref_primary_10_1113_JP274981 crossref_primary_10_3389_fncel_2021_670998 crossref_primary_10_1007_s00213_018_5040_3 crossref_primary_10_1016_j_pnpbp_2023_110913 crossref_primary_10_1523_ENEURO_0201_20_2020 crossref_primary_10_1016_j_pneurobio_2021_102029 crossref_primary_10_1016_j_bbrc_2018_12_073 crossref_primary_10_3390_cells10092277 crossref_primary_10_1016_j_neuropharm_2018_03_028 crossref_primary_10_1523_ENEURO_0016_18_2018 crossref_primary_10_1152_jn_00564_2020 crossref_primary_10_1523_ENEURO_0083_20_2020 crossref_primary_10_1515_revneuro_2020_0091 crossref_primary_10_1016_j_neuropharm_2021_108565 crossref_primary_10_1016_j_heliyon_2021_e08612 crossref_primary_10_3389_fncel_2021_741292 crossref_primary_10_1007_s00424_020_02429_7 crossref_primary_10_1523_JNEUROSCI_1656_18_2019 crossref_primary_10_1016_j_bja_2017_12_039 crossref_primary_10_1016_j_bja_2019_01_029 crossref_primary_10_1096_fj_202002754R crossref_primary_10_1186_s13041_022_00923_w crossref_primary_10_1016_j_neuropharm_2025_110424 crossref_primary_10_1038_s41467_022_32742_x |
| Cites_doi | 10.1113/jphysiol.1991.sp018577 10.1016/S0166-2236(03)00034-1 10.1113/jphysiol.2010.203836 10.1523/JNEUROSCI.0624-05.2005 10.1152/physrev.00018.2002 10.1152/jn.1999.82.4.1895 10.1152/jn.1998.80.1.162 10.1111/j.1535-7511.2005.00049.x 10.1523/JNEUROSCI.19-06-01895.1999 10.1016/S0959-4388(00)00076-3 10.1523/JNEUROSCI.4101-10.2010 10.1093/cercor/bhm056 10.1016/j.neuroscience.2006.07.019 10.1016/0006-8993(96)00149-7 10.1097/00001756-199812210-00019 10.1371/journal.pbio.0030175 10.1152/jn.1993.70.1.232 10.1523/JNEUROSCI.23-29-09650.2003 10.1152/jn.00536.2001 10.1038/sj.bjp.0706020 10.1126/science.1089268 10.1016/S0306-4522(99)00521-7 10.1016/0304-3940(94)11127-5 10.1111/j.1460-9568.2008.06384.x 10.1097/01.anes.0000267601.09764.e6 10.1523/JNEUROSCI.18-19-07613.1998 10.1046/j.1460-9568.2002.02086.x 10.1371/journal.pone.0123636 10.1523/JNEUROSCI.0362-10.2010 10.1124/mol.111.073205 10.1124/jpet.110.171058 10.1007/s002329900059 10.1523/JNEUROSCI.4883-13.2015 10.1038/sj.emboj.7600515 10.1523/JNEUROSCI.4866-06.2007 10.1152/jn.1991.65.1.148 10.1152/jn.00166.2006 10.1016/S0166-2236(96)10070-9 10.1002/hipo.10123 10.1016/j.neuroscience.2016.03.052 10.1038/nrn2402 10.1113/jphysiol.2005.084590 10.1152/jn.2000.84.5.2398 10.1523/JNEUROSCI.21-10-03312.2001 10.1111/ejn.12683 10.1111/j.1469-7580.2005.00446.x 10.1097/j.pain.0000000000000263 10.1523/JNEUROSCI.4305-09.2010 10.1152/jn.1998.79.1.240 10.1016/j.neuropharm.2010.03.016 10.1021/bi981255g 10.1523/JNEUROSCI.18-18-07118.1998 10.1002/hup.2289 10.1111/j.1469-7793.1999.0571p.x 10.1111/j.1460-9568.2006.05136.x 10.1523/JNEUROSCI.1362-12.2012 10.1152/jn.1993.70.1.223 10.1152/jn.1995.73.6.2553 10.1002/hipo.20931 10.1016/S0006-3495(99)77134-1 10.1016/j.celrep.2017.01.011 10.1371/journal.pone.0029384 10.1021/jm800419w 10.1073/pnas.1311686110 10.1007/BF00227110 |
| ContentType | Journal Article |
| Copyright | 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society. Journal compilation © 2017 The Physiological Society |
| Copyright_xml | – notice: 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society – notice: 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society. – notice: Journal compilation © 2017 The Physiological Society |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7QP 7QR 7TK 7TS 8FD FR3 P64 7X8 5PM |
| DOI | 10.1113/JP274565 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Calcium & Calcified Tissue Abstracts Chemoreception Abstracts Neurosciences Abstracts Physical Education Index Technology Research Database Engineering Research Database Biotechnology and BioEngineering Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Technology Research Database Chemoreception Abstracts Engineering Research Database Calcium & Calcified Tissue Abstracts Neurosciences Abstracts Physical Education Index Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
| DatabaseTitleList | MEDLINE Technology Research Database MEDLINE - Academic CrossRef |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Anatomy & Physiology |
| DocumentTitleAlternate | S. M. Joksimovic and others |
| EISSN | 1469-7793 |
| EndPage | 6348 |
| ExternalDocumentID | PMC5621493 28744923 10_1113_JP274565 TJP12528 |
| Genre | article Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: University of Virginia – fundername: Department of Anesthesiology – fundername: National Institute of General Medical Sciences funderid: R01GM102525; R01GM118197 – fundername: Bantly Foundation – fundername: Department of Anesthesiology University of Colorado Anschutz Medical Camus – fundername: National Institute of Mental Health funderid: MH077791 – fundername: NIGMS NIH HHS grantid: R01 GM118197 – fundername: NIGMS NIH HHS grantid: R01 GM102525 – fundername: NICHD NIH HHS grantid: K12 HD068372 – fundername: NIMH NIH HHS grantid: R01 MH077791 – fundername: National Institute of General Medical Sciences grantid: R01GM102525; R01GM118197 – fundername: National Institute of Mental Health grantid: MH077791 |
| GroupedDBID | --- -DZ -~X .3N .GA 05W 0R~ 0YM 10A 123 18M 1OC 29L 2WC 33P 36B 3SF 4.4 50Y 50Z 51W 51X 52M 52N 52O 52P 52R 52S 52T 52U 52V 52W 52X 53G 5GY 5HH 5LA 5RE 5VS 66C 702 7PT 8-0 8-1 8-3 8-4 8-5 8UM 930 A01 A03 AAESR AAEVG AAFWJ AAHQN AAIPD AAMNL AANLZ AAONW AASGY AAXRX AAYCA AAZKR ABCQN ABCUV ABEML ABITZ ABIVO ABJNI ABOCM ABPPZ ABPVW ABQWH ABXGK ACAHQ ACCZN ACFBH ACGFO ACGFS ACGOF ACIWK ACMXC ACNCT ACPOU ACPRK ACSCC ACXBN ACXQS ADBBV ADBTR ADEOM ADIZJ ADKYN ADMGS ADOZA ADXAS ADZMN AEGXH AEIGN AEIMD AEUYR AEYWJ AFBPY AFEBI AFFPM AFGKR AFWVQ AFZJQ AGHNM AGYGG AHBTC AI. AIACR AIAGR AITYG AIURR ALAGY ALMA_UNASSIGNED_HOLDINGS ALUQN ALVPJ AMBMR AMYDB AOIJS ATUGU AZBYB AZVAB BAFTC BAWUL BFHJK BHBCM BMXJE BROTX BRXPI BY8 C45 CS3 D-6 D-7 D-E D-F DCZOG DIK DPXWK DR2 DRFUL DRMAN DRSTM E3Z EBS EJD EMOBN EX3 F00 F01 F04 F5P FIJ FUBAC G-S G.N GODZA GX1 H.X HGLYW HZI HZ~ IHE IX1 J0M K48 KBYEO LATKE LC2 LC3 LEEKS LH4 LITHE LOXES LP6 LP7 LUTES LW6 LYRES MEWTI MK4 MRFUL MRMAN MRSTM MSFUL MSMAN MSSTM MXFUL MXMAN MXSTM N04 N05 N9A NF~ O66 O9- OIG OK1 OVD P2P P2W P2X P2Z P4B P4D Q.N Q11 QB0 R.K ROL RPM RX1 SUPJJ TEORI TLM TN5 TR2 UB1 UPT V8K VH1 W8F W8V W99 WBKPD WH7 WIH WIJ WIK WIN WNSPC WOHZO WOQ WOW WQJ WXI WXSBR WYISQ XG1 YBU YHG YKV YQT YSK YZZ ZZTAW ~IA ~WT .55 .GJ .Y3 31~ 3EH 3O- AAHHS AAYJJ AAYXX ACCFJ ADXHL AEEZP AEQDE AFFNX AIWBW AJBDE C1A CAG CHEAL CITATION COF FA8 H13 HF~ H~9 MVM NEJ OHT RIG UKR WHG X7M XOL YXB YYP ZGI ZXP 1OB 24P AEUQT AFPWT CGR CUY CVF ECM EIF NPM WRC 7QP 7QR 7TK 7TS 8FD FR3 P64 7X8 5PM |
| ID | FETCH-LOGICAL-c4398-512b69e1f1e19ac3da196bc2d65019220c81be3c41a891177c3b30dcdffb76a63 |
| IEDL.DBID | DR2 |
| ISSN | 0022-3751 1469-7793 |
| IngestDate | Thu Aug 21 14:34:54 EDT 2025 Fri Jul 11 03:53:47 EDT 2025 Fri Jul 25 12:13:45 EDT 2025 Wed Feb 19 02:23:58 EST 2025 Thu Apr 24 22:57:53 EDT 2025 Tue Jul 01 04:29:19 EDT 2025 Sun Sep 21 06:18:21 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 19 |
| Keywords | hippocampus low-threshold-activated calcium |
| Language | English |
| License | http://onlinelibrary.wiley.com/termsAndConditions#vor 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c4398-512b69e1f1e19ac3da196bc2d65019220c81be3c41a891177c3b30dcdffb76a63 |
| Notes | https://doi.org/10.1113/JP274981 Linked articles This article is highlighted by a Perspective by Turner. To read this Perspective, visit . ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Linked articles This article is highlighted by a Perspective by Turner. To read this Perspective, visit https://doi.org/10.1113/JP274981. |
| ORCID | 0000-0003-2613-0391 0000-0002-5596-1031 0000-0002-7247-1034 |
| OpenAccessLink | https://physoc.onlinelibrary.wiley.com/doi/pdfdirect/10.1113/JP274565 |
| PMID | 28744923 |
| PQID | 1944271671 |
| PQPubID | 1086388 |
| PageCount | 22 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_5621493 proquest_miscellaneous_1923745008 proquest_journals_1944271671 pubmed_primary_28744923 crossref_citationtrail_10_1113_JP274565 crossref_primary_10_1113_JP274565 wiley_primary_10_1113_JP274565_TJP12528 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 1 October 2017 |
| PublicationDateYYYYMMDD | 2017-10-01 |
| PublicationDate_xml | – month: 10 year: 2017 text: 1 October 2017 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | England |
| PublicationPlace_xml | – name: England – name: London – name: Hoboken |
| PublicationTitle | The Journal of physiology |
| PublicationTitleAlternate | J Physiol |
| PublicationYear | 2017 |
| Publisher | Wiley Subscription Services, Inc John Wiley and Sons Inc |
| Publisher_xml | – name: Wiley Subscription Services, Inc – name: John Wiley and Sons Inc |
| References | 2015; 35 2002; 16 1995; 73 2010; 59 2013; 28 2007; 106 2003; 13 2008; 9 2000; 95 1998; 80 1999; 82 1991; 436 2005; 24 2005; 25 1998; 18 2005; 144 2006; 24 1999; 19 1993; 70 2000; 10 2002; 87 2008; 28 2013; 110 2003; 83 2012; 22 2010; 30 2007; 27 2006; 95 2011; 80 1997; 20 2008; 18 2015; 10 1995 2016; 325 2014; 40 2008; 51 2012; 32 1996; 721 2001; 21 2011; 589 1998; 37 1991; 65 2010; 335 2015; 156 2005; 567 1993; 96 2005; 5 1996; 151 2005; 207 2000; 84 2003; 26 1999; 77 2006; 143 2017; 18 2005; 3 2003; 302 2012; 7 1995; 183 1999; 518 1998; 9 2003; 23 1998; 79 e_1_2_6_51_1 e_1_2_6_53_1 e_1_2_6_32_1 e_1_2_6_30_1 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_59_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_17_1 e_1_2_6_55_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_57_1 e_1_2_6_62_1 e_1_2_6_64_1 e_1_2_6_43_1 e_1_2_6_20_1 e_1_2_6_41_1 e_1_2_6_60_1 e_1_2_6_9_1 e_1_2_6_5_1 e_1_2_6_7_1 e_1_2_6_24_1 e_1_2_6_49_1 e_1_2_6_3_1 e_1_2_6_22_1 e_1_2_6_66_1 e_1_2_6_28_1 e_1_2_6_45_1 e_1_2_6_26_1 e_1_2_6_47_1 e_1_2_6_52_1 e_1_2_6_54_1 e_1_2_6_10_1 e_1_2_6_31_1 e_1_2_6_50_1 Amaral DG (e_1_2_6_2_1) 1995 e_1_2_6_14_1 e_1_2_6_35_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_18_1 e_1_2_6_39_1 e_1_2_6_56_1 e_1_2_6_16_1 e_1_2_6_37_1 e_1_2_6_58_1 e_1_2_6_63_1 e_1_2_6_42_1 e_1_2_6_65_1 e_1_2_6_21_1 e_1_2_6_40_1 e_1_2_6_61_1 e_1_2_6_8_1 e_1_2_6_4_1 e_1_2_6_6_1 e_1_2_6_25_1 e_1_2_6_48_1 e_1_2_6_23_1 e_1_2_6_29_1 e_1_2_6_44_1 e_1_2_6_67_1 e_1_2_6_27_1 e_1_2_6_46_1 28786112 - J Physiol. 2017 Oct 1;595(19):6223 |
| References_xml | – volume: 79 start-page: 240 year: 1998 end-page: 252 article-title: Pharmacological properties of T‐type Ca current in adult rat sensory neurons: effects of anticonvulsant and anesthetic agents publication-title: J Neurophysiol – volume: 302 start-page: 1416 year: 2003 end-page: 1418 article-title: Abnormal coronary function in mice deficient in α1H T‐type Ca channels publication-title: Science – volume: 32 start-page: 12228 year: 2012 end-page: 12236 article-title: T‐type calcium channels consolidate tonic action potential output of thalamic neurons to neocortex publication-title: J Neurosci – volume: 24 start-page: 2581 year: 2006 end-page: 2594 article-title: Ca 3 T‐type calcium channel isoforms differentially distribute to somatic and dendritic compartments in rat central neurons publication-title: Eur J Neurosci – volume: 207 start-page: 271 year: 2005 end-page: 282 article-title: The subiculum: what it does, what it might do, and what neuroanatomy has yet to tell us publication-title: J Anat – volume: 83 start-page: 117 year: 2003 end-page: 161 article-title: Molecular physiology of low‐voltage‐activated T‐type calcium channels publication-title: Physiol Rev – volume: 65 start-page: 148 year: 1991 end-page: 155 article-title: Kinetic properties of T‐type Ca currents in isolated rat hippocampal CA1 pyramidal neurons publication-title: J Neurophysiol – volume: 59 start-page: 58 year: 2010 end-page: 69 article-title: Mechanisms of inhibition of CaV3.1 T‐type calcium current by aliphatic alcohols publication-title: Neuropharmacology – volume: 95 start-page: 3297 year: 2006 end-page: 3308 article-title: Bursting of thalamic neurons and states of vigilance publication-title: J Neurophysiol – volume: 18 start-page: 7118 year: 1998 end-page: 7126 article-title: Postsynaptic complex spike bursting enables the induction of LTP by theta frequency synaptic stimulation publication-title: J Neurosci – volume: 589 start-page: 1707 year: 2011 end-page: 1724 article-title: Minimal alterations in T‐type calcium channel gating markedly modify physiological firing dynamics publication-title: J Physiol – volume: 335 start-page: 409 year: 2010 end-page: 417 article-title: In vitro characterization of T‐type calcium channel antagonist TTA‐A2 and in vivo effects on arousal in mice publication-title: J Pharmacol Exp Ther – volume: 567 start-page: 79 year: 2005 end-page: 93 article-title: A transitional period of Ca ‐dependent spike afterdepolarization and bursting in developing rat CA1 pyramidal cells publication-title: J Physiol – volume: 9 start-page: 557 year: 2008 end-page: 568 article-title: Petilla terminology: nomenclature of features of GABAergic interneurons of the cerebral cortex publication-title: Nat Rev Neurosci – volume: 51 start-page: 3692 year: 2008 end-page: 3695 article-title: Design, synthesis, and evaluation of a novel 4‐aminomethyl‐4‐fluoropiperidine as a T‐type Ca channel antagonist publication-title: J Med Chem – volume: 35 start-page: 1481 year: 2015 end-page: 1492 article-title: Hyperexcitability of rat thalamocortical networks after exposure to general anesthesia during brain development publication-title: J Neurosci – volume: 80 start-page: 162 year: 1998 end-page: 171 article-title: Limbic gamma rhythms. II. Synaptic and intrinsic mechanisms underlying spike doublets in oscillating subicular neurons publication-title: J Neurophysiol – volume: 721 start-page: 59 year: 1996 end-page: 65 article-title: Activation of 5‐HT1B receptors suppresses low but not high frequency synaptic transmission in the rat subicular cortex in vitro publication-title: Brain Res – volume: 18 start-page: 1109 year: 2017 end-page: 1117 article-title: Autonomous CaMKII Activity as a drug target for histological and functional neuroprotection after resuscitation from cardiac arrest publication-title: Cell Rep – volume: 70 start-page: 223 year: 1993 end-page: 231 article-title: Contribution of the low‐threshold T‐type calcium current in generating the post‐spike depolarizing afterpotential in dentate granule neurons of immature rats publication-title: J Neurophysiol – volume: 30 start-page: 99 year: 2010 end-page: 109 article-title: Selective T‐type calcium channel block in thalamic neurons reveals channel redundancy and physiological impact of publication-title: J Neurosci – volume: 95 start-page: 965 year: 2000 end-page: 972 article-title: Subthreshold inward membrane currents in guinea‐pig frontal cortex neurons publication-title: Neuroscience – volume: 18 start-page: 7613 year: 1998 end-page: 7624 article-title: Dendritic hyperpolarization‐activated currents modify the integrative properties of hippocampal CA1 pyramidal neurons publication-title: J Neurosci – volume: 106 start-page: 1177 year: 2007 end-page: 1185 article-title: Mutation of α1GT‐type calcium channels in mice does not change anesthetic requirements for loss of the righting reflex and minimum alveolar concentration but delays the onset of anesthetic induction publication-title: Anesthesiology – volume: 9 start-page: 4109 year: 1998 end-page: 4113 article-title: Interaction between paired‐pulse facilitation and long‐term potentiation in the projection from hippocampal area CA1 to the subiculum publication-title: Neuroreport – volume: 87 start-page: 1169 year: 2002 end-page: 1174 article-title: Distance‐dependent Ni ‐sensitivity of synaptic plasticity in apical dendrites of hippocampal CA1 pyramidal cells publication-title: J Neurophysiol – volume: 70 start-page: 232 year: 1993 end-page: 245 article-title: Intrinsic properties and evoked responses of guinea pig subicular neurons in vitro publication-title: J Neurophysiol – volume: 73 start-page: 2553 year: 1995 end-page: 2557 article-title: Different Ca channels in soma and dendrites of hippocampal pyramidal neurons mediate spike‐induced Ca influx publication-title: J Neurophysiol – volume: 28 start-page: 124 year: 2013 end-page: 133 article-title: Randomized controlled study of the T‐type calcium channel antagonist MK‐8998 for the treatment of acute psychosis in patients with schizophrenia publication-title: Hum Psychopharmacol – volume: 151 start-page: 77 year: 1996 end-page: 90 article-title: Nickel block of a family of neuronal calcium channels: subtype‐ and subunit‐dependent action at multiple sites publication-title: J Membr Biol – volume: 37 start-page: 15353 year: 1998 end-page: 15362 article-title: Selective peptide antagonist of the class E calcium channel from the venom of the tarantula publication-title: Biochemistry – volume: 22 start-page: 693 year: 2012 end-page: 706 article-title: Target‐specific output patterns are predicted by the distribution of regular‐spiking and bursting pyramidal neurons in the subiculum publication-title: Hippocampus – volume: 77 start-page: 3034 year: 1999 end-page: 3042 article-title: Nickel block of three cloned T‐type calcium channels: low concentrations selectively block alpha1H publication-title: Biophys J – volume: 82 start-page: 1895 year: 1999 end-page: 901 article-title: Dendritic voltage‐gated ion channels regulate the action potential firing mode of hippocampal CA1 pyramidal neurons publication-title: J Neurophysiol – volume: 19 start-page: 1895 year: 1999 end-page: 1911 article-title: Differential distribution of three members of a gene family encoding low voltage‐activated (T‐type) calcium channels publication-title: J Neurosci – volume: 325 start-page: 132 year: 2016 end-page: 141 article-title: Therapeutic hypothermia protects against ischemia‐induced impairment of synaptic plasticity following juvenile cardiac arrest in sex‐dependent manner publication-title: Neuroscience – volume: 16 start-page: 259 year: 2002 end-page: 266 article-title: Long‐lasting modification of intrinsic discharge properties in subicular neurons following status epilepticus publication-title: Eur J Neurosci – volume: 80 start-page: 900 year: 2011 end-page: 910 article-title: TTA‐P2 is a potent and selective blocker of T‐type calcium channels in rat sensory neurons and a novel antinociceptive agent publication-title: Mol Pharmacol – volume: 436 start-page: 739 year: 1991 end-page: 767 article-title: Single calcium channels in rat and guinea‐pig hippocampal neurons publication-title: J Physiol – volume: 26 start-page: 161 year: 2003 end-page: 167 article-title: Bursts as a unit of neural information: selective communication via resonance publication-title: Trends Neurosci – volume: 110 start-page: 20302 year: 2013 end-page: 20307 article-title: T‐type channel blockade impairs long‐term potentiation at the parallel fiber–Purkinje cell synapse and cerebellar learning publication-title: Proc Natl Acad Sci USA – volume: 40 start-page: 3179 year: 2014 end-page: 3188 article-title: Increasing small conductance Ca ‐activated potassium channel activity reverses ischemia‐induced impairment of long‐term potentiation publication-title: Eur J Neurosci – volume: 518 start-page: 571 year: 1999 end-page: 576 article-title: Postsynaptic bursting is essential for ‘Hebbian’ induction of associative longterm potentiation at excitatory synapses in rat hippocampus publication-title: J Physiol – volume: 156 start-page: 2013 year: 2015 end-page: 2020 article-title: A randomized double‐blind, placebo‐, and active‐controlled study of T‐type calcium channel blocker ABT‐639 in patients with diabetic peripheral neuropathic pain publication-title: Pain – start-page: 247 year: 1995 end-page: 291 – volume: 10 start-page: 172 year: 2000 end-page: 179 article-title: Natural patterns of activity and long‐term synaptic plasticity publication-title: Curr Opin Neurobiol – volume: 84 start-page: 2398 year: 2000 end-page: 2408 article-title: Resting and active properties of pyramidal neurons in subiculum and CA1 of rat hippocampus publication-title: J Neurophysiol – volume: 144 start-page: 59 year: 2005 end-page: 70 article-title: Contrasting anesthetic sensitivities of T‐type Ca channels of reticular thalamic neurons and recombinant Ca 3.3 channels publication-title: Br J Pharmacol – volume: 13 start-page: 728 year: 2003 end-page: 744 article-title: Electrophysiological and morphological diversity of neurons from the rat subicular complex in vitro publication-title: Hippocampus – volume: 143 start-page: 189 year: 2006 end-page: 212 article-title: Expression pattern of voltage‐dependent calcium channel subunits in hippocampal inhibitory neurons in mice publication-title: Neuroscience – volume: 21 start-page: 3312 year: 2001 end-page: 3321 article-title: Action potential bursting in subicular pyramidal neurons is driven by a calcium tail current publication-title: J Neurosci – volume: 25 start-page: 5763 year: 2005 end-page: 5773 article-title: R‐type calcium channels contribute to afterdepolarization and bursting in hippocampal CA1 pyramidal neurons publication-title: J Neurosci – volume: 96 start-page: 304 year: 1993 end-page: 318 article-title: Electrophysiological properties of neurons in the rat subiculum in vitro publication-title: Exp Brain Res – volume: 20 start-page: 38 year: 1997 end-page: 43 article-title: Bursts as a unit of neural information: making unreliable synapses reliable publication-title: Trends Neurosci – volume: 28 start-page: 730 year: 2008 end-page: 743 article-title: Involvement of T‐type Ca channels in the potentiation of synaptic and visual responses during the critical period in rat visual cortex publication-title: Eur J Neurosci – volume: 7 start-page: e29384 year: 2012 article-title: Retrieval of context‐associated memory is dependent on the Cav3.2 T‐s publication-title: PLoS One – volume: 183 start-page: 112 year: 1995 end-page: 115 article-title: Voltage‐gated Ca channel blockers, omega‐AgaIVA and Ni , suppress the induction of theta‐burst induced long‐term potentiation in guinea‐pig hippocampal CA1 neurons publication-title: Neurosci Lett – volume: 3 start-page: e175 year: 2005 article-title: Output‐mode transitions are controlled by prolonged inactivation of sodium channels in pyramidal neurons of subiculum publication-title: PLoS Biology – volume: 27 start-page: 3305 year: 2007 end-page: 3316 article-title: Cell‐specific alterations of T‐type calcium current in painful diabetic neuropathy enhance excitability of sensory neurons publication-title: J Neurosci – volume: 10 start-page: e0123636 year: 2015 article-title: Cell type‐specific separation of subicular principal neurons during network activities publication-title: PLoS One – volume: 18 start-page: 315 year: 2008 end-page: 330 article-title: Quantitative chemical composition of cortical GABAergic neurons revealed in transgenic Venus‐expressing rats publication-title: Cereb Cortex – volume: 24 start-page: 315 year: 2005 end-page: 324 article-title: Silencing of the Cav3.2 T‐type calcium channel gene in sensory neurons demonstrates its major role in nociception publication-title: EMBO J – volume: 30 start-page: 10601 year: 2010 end-page: 10608 article-title: A study of clustered data and approaches to its analysis publication-title: J Neurosci – volume: 30 start-page: 16788 year: 2010 end-page: 16795 article-title: Midazolam inhibits hippocampal long‐term potentiation and learning through dual central and peripheral benzodiazepine receptor activation and neurosteroidogenesis publication-title: J Neurosci – volume: 5 start-page: 121 year: 2005 end-page: 129 article-title: The role of the subiculum in epilepsy and epileptogenesis publication-title: Epilepsy Curr – volume: 23 start-page: 9650 year: 2003 end-page: 9663 article-title: Ionic mechanisms of burst firing in dissociated Purkinje neurons publication-title: J Neurosci – ident: e_1_2_6_40_1 doi: 10.1113/jphysiol.1991.sp018577 – ident: e_1_2_6_24_1 doi: 10.1016/S0166-2236(03)00034-1 – ident: e_1_2_6_60_1 doi: 10.1113/jphysiol.2010.203836 – ident: e_1_2_6_38_1 doi: 10.1523/JNEUROSCI.0624-05.2005 – ident: e_1_2_6_44_1 doi: 10.1152/physrev.00018.2002 – ident: e_1_2_6_36_1 doi: 10.1152/jn.1999.82.4.1895 – ident: e_1_2_6_51_1 doi: 10.1152/jn.1998.80.1.162 – ident: e_1_2_6_50_1 doi: 10.1111/j.1535-7511.2005.00049.x – ident: e_1_2_6_55_1 doi: 10.1523/JNEUROSCI.19-06-01895.1999 – ident: e_1_2_6_43_1 doi: 10.1016/S0959-4388(00)00076-3 – ident: e_1_2_6_59_1 doi: 10.1523/JNEUROSCI.4101-10.2010 – ident: e_1_2_6_61_1 doi: 10.1093/cercor/bhm056 – ident: e_1_2_6_62_1 doi: 10.1016/j.neuroscience.2006.07.019 – ident: e_1_2_6_3_1 doi: 10.1016/0006-8993(96)00149-7 – ident: e_1_2_6_5_1 doi: 10.1097/00001756-199812210-00019 – ident: e_1_2_6_11_1 doi: 10.1371/journal.pbio.0030175 – ident: e_1_2_6_52_1 doi: 10.1152/jn.1993.70.1.232 – ident: e_1_2_6_53_1 doi: 10.1523/JNEUROSCI.23-29-09650.2003 – ident: e_1_2_6_22_1 doi: 10.1152/jn.00536.2001 – ident: e_1_2_6_26_1 doi: 10.1038/sj.bjp.0706020 – ident: e_1_2_6_6_1 doi: 10.1126/science.1089268 – ident: e_1_2_6_21_1 doi: 10.1016/S0306-4522(99)00521-7 – ident: e_1_2_6_23_1 doi: 10.1016/0304-3940(94)11127-5 – ident: e_1_2_6_64_1 doi: 10.1111/j.1460-9568.2008.06384.x – ident: e_1_2_6_46_1 doi: 10.1097/01.anes.0000267601.09764.e6 – ident: e_1_2_6_35_1 doi: 10.1523/JNEUROSCI.18-19-07613.1998 – ident: e_1_2_6_63_1 doi: 10.1046/j.1460-9568.2002.02086.x – ident: e_1_2_6_19_1 doi: 10.1371/journal.pone.0123636 – ident: e_1_2_6_20_1 doi: 10.1523/JNEUROSCI.0362-10.2010 – ident: e_1_2_6_9_1 doi: 10.1124/mol.111.073205 – ident: e_1_2_6_29_1 doi: 10.1124/jpet.110.171058 – ident: e_1_2_6_65_1 doi: 10.1007/s002329900059 – ident: e_1_2_6_15_1 doi: 10.1523/JNEUROSCI.4883-13.2015 – ident: e_1_2_6_4_1 doi: 10.1038/sj.emboj.7600515 – ident: e_1_2_6_25_1 doi: 10.1523/JNEUROSCI.4866-06.2007 – ident: e_1_2_6_54_1 doi: 10.1152/jn.1991.65.1.148 – ident: e_1_2_6_32_1 doi: 10.1152/jn.00166.2006 – ident: e_1_2_6_31_1 doi: 10.1016/S0166-2236(96)10070-9 – ident: e_1_2_6_37_1 doi: 10.1002/hipo.10123 – ident: e_1_2_6_13_1 doi: 10.1016/j.neuroscience.2016.03.052 – ident: e_1_2_6_45_1 doi: 10.1038/nrn2402 – ident: e_1_2_6_8_1 doi: 10.1113/jphysiol.2005.084590 – ident: e_1_2_6_49_1 doi: 10.1152/jn.2000.84.5.2398 – ident: e_1_2_6_27_1 doi: 10.1523/JNEUROSCI.21-10-03312.2001 – ident: e_1_2_6_42_1 doi: 10.1111/ejn.12683 – ident: e_1_2_6_41_1 doi: 10.1111/j.1469-7580.2005.00446.x – ident: e_1_2_6_67_1 doi: 10.1097/j.pain.0000000000000263 – ident: e_1_2_6_16_1 doi: 10.1523/JNEUROSCI.4305-09.2010 – ident: e_1_2_6_58_1 doi: 10.1152/jn.1998.79.1.240 – ident: e_1_2_6_17_1 doi: 10.1016/j.neuropharm.2010.03.016 – ident: e_1_2_6_39_1 doi: 10.1021/bi981255g – ident: e_1_2_6_57_1 doi: 10.1523/JNEUROSCI.18-18-07118.1998 – ident: e_1_2_6_18_1 doi: 10.1002/hup.2289 – ident: e_1_2_6_47_1 doi: 10.1111/j.1469-7793.1999.0571p.x – ident: e_1_2_6_34_1 doi: 10.1111/j.1460-9568.2006.05136.x – ident: e_1_2_6_12_1 doi: 10.1523/JNEUROSCI.1362-12.2012 – ident: e_1_2_6_66_1 doi: 10.1152/jn.1993.70.1.223 – ident: e_1_2_6_10_1 doi: 10.1152/jn.1995.73.6.2553 – ident: e_1_2_6_28_1 doi: 10.1002/hipo.20931 – ident: e_1_2_6_30_1 doi: 10.1016/S0006-3495(99)77134-1 – ident: e_1_2_6_14_1 doi: 10.1016/j.celrep.2017.01.011 – ident: e_1_2_6_7_1 doi: 10.1371/journal.pone.0029384 – ident: e_1_2_6_48_1 doi: 10.1021/jm800419w – start-page: 247 volume-title: The Rat Nervous System year: 1995 ident: e_1_2_6_2_1 – ident: e_1_2_6_33_1 doi: 10.1073/pnas.1311686110 – ident: e_1_2_6_56_1 doi: 10.1007/BF00227110 – reference: 28786112 - J Physiol. 2017 Oct 1;595(19):6223 |
| SSID | ssj0013099 |
| Score | 2.3981209 |
| Snippet | Key points
Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing... Pharmacological, molecular and genetic data indicate a prominent role of low‐voltage‐activated T‐type calcium channels (T‐channels) in the firing activity of... Pharmacological, molecular and genetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activity of... Key points Pharmacological, molecular and genetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing... |
| SourceID | pubmedcentral proquest pubmed crossref wiley |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 6327 |
| SubjectTerms | Action Potentials Animals Antagonism calcium Calcium channels Calcium channels (T-type) Calcium channels (voltage-gated) Calcium Channels, T-Type - metabolism Cognitive ability Depolarization Excitability Female Firing pattern Firing rate Hippocampus Hippocampus - metabolism Hippocampus - physiology Hyperpolarization Interneurons Long-Term Potentiation low‐threshold‐activated Male Mice Mice, Inbred C57BL Neuroscience ‐ Cellular/Molecular Rats Rats, Sprague-Dawley Rats, Wistar Research Paper Rodents Subiculum Synaptic plasticity |
| Title | The role of T‐type calcium channels in the subiculum: to burst or not to burst? |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1113%2FJP274565 https://www.ncbi.nlm.nih.gov/pubmed/28744923 https://www.proquest.com/docview/1944271671 https://www.proquest.com/docview/1923745008 https://pubmed.ncbi.nlm.nih.gov/PMC5621493 |
| Volume | 595 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1LS8QwEA7iyYuv9bG-iCB6qm6aNt14EfHJgqKywoKHkqQpLmorbnvQkz_B3-gvcZI-dF0F8VIomTRpZyb5kky_QWhDuBHAYqUcYXiGPMa4w7VqO6wVKSp9L_Js_pSzc3Z67XV6fq-MqjT_whT8EPWGm_EMO14bBxeyzEJCDNlA5wIWVABHYPgllBna_MMr9_MAocV5TRQe-KTknYWqO1XF4ZloBF6ORkl-Ra92-jmeQjdVx4uok7vtPJPb6uUbp-P_3mwaTZaoFO8XZjSDxnQyixr7CazIH57xJrZxonYDvoEuwbKwCUrEaYy7769vZhcXg6pVP3_A5kdiaH-A-wkGbIkHuSx2GHdxlmLQ4CDD6RNO0qy-35tD18dH3YNTp0zM4CjAL20HQIJkXJOYaMKFopEAP5YK1O4bxOi2FIBhTZVHRJubU2FQOwXlR3EsAyYYnUfjSZroRYQBX0hJfUKFJp4bBFxFgYgj6sZBBMJxE21VSgpVyVpukmfch8XqhYbV12qi9VrysWDq-EFmpdJzWPrqICTcg5YJCwg8oi4GLzNHJyLRaW5kXApPAMDURAuFWdSN2AwCUN5EwZDB1AKGwXu4JOnfWiZvAJ-wQoWaW9Yefu132O1cABJ120t_llxGE65BIDbucAWNZ0-5XgX8lMk16ylwPemRD4EfFkk |
| linkProvider | Wiley-Blackwell |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1JT9wwFH5iOZRLy9oOZTESKqfAOM4yLgeEEGg6LKLVIHFAimzHUUdAgpjk0J74CfzG_hKenaUMi4Q4Rn5ekvde_Pn5-TPAunBjhMVKOcLwDHlBwB2uVccJ2rFi0vdiz96fcnwSdM-83rl_Pgbb9VmYkh-iCbgZz7D_a-PgJiBdeblhG-id4ooK8cg4TNrtOYOIfrn_txDanDdU4aFPK-ZZrLtV1xydi54BzOd5ko_xq52ADj7BRT30Mu_kcrPI5ab6-4TV8Z3vNg0fK2BKdktLmoExnc7C3G6Ki_LrP-QbsamiNgY_Bz_RuIjJSyRZQvr_7u5NIJegttWguCbmLDEOYEgGKUF4SYaFLIOM30meEVTiMCfZLUmzvHnemYezg_3-Xtep7mZwFEKYjoM4QQZc04RqyoVisUBXlgo17xvQ6LYV4mHNlEdFh5uNYdQ8Q_3HSSLDQARsASbSLNVfgCDEkJL5lAlNPTcMuYpDkcTMTcIYhZMWbNRailRFXG7uz7iKygUMi-qv1YK1RvKmJOt4QWapVnRUueswotzDnmkQUmyiKUZHM7snItVZYWRchi0gZmrB59Iumk7sJQJY3oJwxGIaAUPiPVqSDn5bMm_En7hIxZob1iBeHXfU750iGHU7i2-WXIUP3f7xUXT04-TwK0y5BpDYNMQlmMhvC72McCqXK9ZtHgBJGRl2 |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwEB7RIqFeKNACWwp1JURPaddx4qy5oApYlW2pFrSVKnGI_IpYtZtU3eQAJ34Cv5Ffwth50G2phDhGHj-SmYm_scefAV7K0CAs1jqQjmco4lwEwupBwPtGMxVHJvL3p3w85gcn0eg0Pm2yKt1ZmJofoltwc57h_9fOwS9M1ji5IxsYjTGgQjiyBHcjjrOkA0Sfwz87CH0hOqbwJKYN8SzW3WtrLk5FN_DlzTTJq_DVzz_DVfjSjrxOOznbrUq1q79fI3X8v1d7APcbWEr2azt6CHds_gjW9nMMyWffyCviE0X9CvwafELTIi4rkRQZmfz68dMt4xLUtZ5WM-JOEmP_czLNCYJLMq9UvcT4mpQFQRXOS1Jckrwou-c363AyfD95exA0NzMEGgHMIECUoLiwNKOWCqmZkejISqPeYwcZw75GNGyZjqgcCLctjHpnqH2TZSrhkrPHsJwXuX0KBAGGUiymTFoahUkitElkZliYJQaFsx7stEpKdUNb7m7POE_r8IWl7dfqwXYneVFTdfxFZrPVc9o46zylIsKeKU8oNtEVo5u5vROZ26JyMiHDFhAx9eBJbRZdJ_4KASzvQbJgMJ2Ao_BeLMmnXz2VN6JPDFGx5o63h1vHnU5GY4Si4WDjnyW34N743TA9-nB8-AxWQodGfA7iJiyXl5V9jliqVC-80_wG7JcYJQ |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=The+role+of+T%E2%80%90type+calcium+channels+in+the+subiculum%3A+to+burst+or+not+to+burst%3F&rft.jtitle=The+Journal+of+physiology&rft.au=Joksimovic%2C+Srdjan+M.&rft.au=Eggan%2C+Pierce&rft.au=Izumi%2C+Yukitoshi&rft.au=Joksimovic%2C+Sonja+Lj&rft.date=2017-10-01&rft.issn=0022-3751&rft.eissn=1469-7793&rft.volume=595&rft.issue=19&rft.spage=6327&rft.epage=6348&rft_id=info:doi/10.1113%2FJP274565&rft.externalDBID=n%2Fa&rft.externalDocID=10_1113_JP274565 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-3751&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-3751&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-3751&client=summon |