Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells.
Canonical transient receptor potential (TRPC) channels are widely expressed in the brain and play several roles in development and normal neuronal function. In the cerebellum, Purkinje cell TRPC3 channels underlie the slow excitatory postsynaptic potential observed after parallel fiber stimulation....
| Main Authors: | , |
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| Format: | Journal article |
| Language: | English |
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2012
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| _version_ | 1797072470017048576 |
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| author | Nelson, C Glitsch, M |
| author_facet | Nelson, C Glitsch, M |
| author_sort | Nelson, C |
| collection | OXFORD |
| description | Canonical transient receptor potential (TRPC) channels are widely expressed in the brain and play several roles in development and normal neuronal function. In the cerebellum, Purkinje cell TRPC3 channels underlie the slow excitatory postsynaptic potential observed after parallel fiber stimulation. In these cells TRPC3 channel opening requires stimulation of metabotropic glutamate receptor 1, activation of which can also lead to the induction of long term depression (LTD), which underlies cerebellar motor learning. LTD induction requires protein kinase C (PKC) and protein kinase G (PKG) activation, and although PKC phosphorylation targets are well established, virtually nothing is known about PKG targets in LTD. Because TRPC3 channels are inhibited after phosphorylation by PKC and PKG in expression systems, we examined whether native TRPC3 channels in Purkinje cells are a target for PKG or PKC, thereby contributing to cerebellar LTD. We find that in Purkinje cells, activation of TRPC3-dependent currents is not inhibited by conventional PKC or PKG to any significant extent and that inhibition of these kinases does not significantly impact on TRPC3-mediated currents either. Based on these and previous findings, we propose that TRPC3-dependent currents may differ significantly in their regulation from those overexpressed in expression systems. |
| first_indexed | 2024-03-06T23:08:08Z |
| format | Journal article |
| id | oxford-uuid:648ecc17-93f9-43c4-b4e0-e912eef4993d |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T23:08:08Z |
| publishDate | 2012 |
| record_format | dspace |
| spelling | oxford-uuid:648ecc17-93f9-43c4-b4e0-e912eef4993d2022-03-26T18:19:35ZLack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:648ecc17-93f9-43c4-b4e0-e912eef4993dEnglishSymplectic Elements at Oxford2012Nelson, CGlitsch, MCanonical transient receptor potential (TRPC) channels are widely expressed in the brain and play several roles in development and normal neuronal function. In the cerebellum, Purkinje cell TRPC3 channels underlie the slow excitatory postsynaptic potential observed after parallel fiber stimulation. In these cells TRPC3 channel opening requires stimulation of metabotropic glutamate receptor 1, activation of which can also lead to the induction of long term depression (LTD), which underlies cerebellar motor learning. LTD induction requires protein kinase C (PKC) and protein kinase G (PKG) activation, and although PKC phosphorylation targets are well established, virtually nothing is known about PKG targets in LTD. Because TRPC3 channels are inhibited after phosphorylation by PKC and PKG in expression systems, we examined whether native TRPC3 channels in Purkinje cells are a target for PKG or PKC, thereby contributing to cerebellar LTD. We find that in Purkinje cells, activation of TRPC3-dependent currents is not inhibited by conventional PKC or PKG to any significant extent and that inhibition of these kinases does not significantly impact on TRPC3-mediated currents either. Based on these and previous findings, we propose that TRPC3-dependent currents may differ significantly in their regulation from those overexpressed in expression systems. |
| spellingShingle | Nelson, C Glitsch, M Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells. |
| title | Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells. |
| title_full | Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells. |
| title_fullStr | Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells. |
| title_full_unstemmed | Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells. |
| title_short | Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells. |
| title_sort | lack of kinase regulation of canonical transient receptor potential 3 trpc3 channel dependent currents in cerebellar purkinje cells |
| work_keys_str_mv | AT nelsonc lackofkinaseregulationofcanonicaltransientreceptorpotential3trpc3channeldependentcurrentsincerebellarpurkinjecells AT glitschm lackofkinaseregulationofcanonicaltransientreceptorpotential3trpc3channeldependentcurrentsincerebellarpurkinjecells |