Dual depolarization responses generated within the same lateral septal neurons by TRPC4-containing channels
In the central nervous system, canonical transient receptor potential (TRPC) channels have been implicated in mediating neuronal excitation induced by stimulating metabotropic receptors, including group 1 metabotropic glutamate receptors (mGluRs). Lateral septal (LS) neurons express high levels of T...
Gespeichert in:
| Hauptverfasser: | , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2014
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| In: |
Pflügers Archiv
Year: 2013, Jahrgang: 466, Heft: 7, Pages: 1301-1316 |
| ISSN: | 1432-2013 |
| DOI: | 10.1007/s00424-013-1362-5 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s00424-013-1362-5
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| Verfasserangaben: | Jinbin Tian, Dhananjay P. Thakur, Yungang Lu, Yingmin Zhu, Marc Freichel, Veit Flockerzi, Michael X. Zhu |
MARC
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| 245 | 1 | 0 | |a Dual depolarization responses generated within the same lateral septal neurons by TRPC4-containing channels |c Jinbin Tian, Dhananjay P. Thakur, Yungang Lu, Yingmin Zhu, Marc Freichel, Veit Flockerzi, Michael X. Zhu |
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| 520 | |a In the central nervous system, canonical transient receptor potential (TRPC) channels have been implicated in mediating neuronal excitation induced by stimulating metabotropic receptors, including group 1 metabotropic glutamate receptors (mGluRs). Lateral septal (LS) neurons express high levels of TRPC4 and group I mGluRs. However, to what extent native TRPC4-containing channels (TRPC4-cc) are activated as well as the impact of different levels of TRPC4-cc activation on neuronal excitability remain elusive. Here, we report that stimulating LS neurons with group I mGluR agonist, (S)-3,5-DHPG, causes either an immediate increase in firing rate or an initial burst followed by a pause of firing, which can be correlated with below-threshold-depolarization (BTD) or above-threshold-plateau-depolarization (ATPD), respectively, in whole-cell recordings. The early phase of BTD and the entire ATPD are completely absent in neurons from TRPC4−/− mice. Moreover, in the same LS neurons, BTD can be converted to ATPD at more depolarized potentials or with a brief current injection, suggesting that BTD and ATPD may represent partial and full activations of TRPC4-cc, respectively. We show that coincident mGluR stimulation and depolarization is required to evoke strong TRPC4-cc current, and Na+ and Ca2+ influx, together with dynamic changes of intracellular Ca2+, are essential for ATPD induction. Our results suggest that TRPC4-cc integrates metabotropic receptor stimulation with intracellular Ca2+ signals to generate two interconvertible depolarization responses to affect excitability of LS neurons in distinct fashions. | ||
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