Molecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine.
Evidence of early changes in neural plasticity may aid the prediction of rapid-onset antidepressant drugs. Here we compared the dual α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, to the SNRI, venlafaxine, with regards to their effect on rat brain expression of a pa...
| Asıl Yazarlar: | , , |
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| Materyal Türü: | Journal article |
| Dil: | English |
| Baskı/Yayın Bilgisi: |
2012
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| _version_ | 1826298792188575744 |
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| author | Serres, F Millan, M Sharp, T |
| author_facet | Serres, F Millan, M Sharp, T |
| author_sort | Serres, F |
| collection | OXFORD |
| description | Evidence of early changes in neural plasticity may aid the prediction of rapid-onset antidepressant drugs. Here we compared the dual α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, to the SNRI, venlafaxine, with regards to their effect on rat brain expression of a panel of neural plasticity-related genes: Arc, BDNF, and VGLUT1, as well as Homer1a and Shank1B (not studied previously). Abundance of mRNA was determined by in-situ hybridization in cortical and hippocampal regions 2 h and 16 h following drug administration for 14, 7 and 1 d. After 14 d, both S35966 and venlafaxine increased mRNA of all genes, including Homer1a and Shank1B, and effects were similarly time- and region-dependent. After 7 d, S35966 elevated Arc, Shank1B and BDNF mRNA, whereas venlafaxine increased Shank1B mRNA only. Finally, after 1 d (acute administration), S35966 increased Arc and Homer1a mRNA whereas venlafaxine had no effect on any gene examined. In summary, a 14-d course of treatment with S35966 or venlafaxine induced similar region- and time-dependent increases in expression of neural plasticity-related genes including Shank1B and Homer1a. Some genes responded earlier to S35966, suggesting that drugs with combined α₂-adrenoceptor antagonist/SNRI properties may elicit more rapid changes in markers of neural plasticity than a SNRI alone. |
| first_indexed | 2024-03-07T04:52:13Z |
| format | Journal article |
| id | oxford-uuid:d55cd64f-a692-4acb-9695-9c52cf8e965c |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T04:52:13Z |
| publishDate | 2012 |
| record_format | dspace |
| spelling | oxford-uuid:d55cd64f-a692-4acb-9695-9c52cf8e965c2022-03-27T08:25:19ZMolecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:d55cd64f-a692-4acb-9695-9c52cf8e965cEnglishSymplectic Elements at Oxford2012Serres, FMillan, MSharp, TEvidence of early changes in neural plasticity may aid the prediction of rapid-onset antidepressant drugs. Here we compared the dual α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, to the SNRI, venlafaxine, with regards to their effect on rat brain expression of a panel of neural plasticity-related genes: Arc, BDNF, and VGLUT1, as well as Homer1a and Shank1B (not studied previously). Abundance of mRNA was determined by in-situ hybridization in cortical and hippocampal regions 2 h and 16 h following drug administration for 14, 7 and 1 d. After 14 d, both S35966 and venlafaxine increased mRNA of all genes, including Homer1a and Shank1B, and effects were similarly time- and region-dependent. After 7 d, S35966 elevated Arc, Shank1B and BDNF mRNA, whereas venlafaxine increased Shank1B mRNA only. Finally, after 1 d (acute administration), S35966 increased Arc and Homer1a mRNA whereas venlafaxine had no effect on any gene examined. In summary, a 14-d course of treatment with S35966 or venlafaxine induced similar region- and time-dependent increases in expression of neural plasticity-related genes including Shank1B and Homer1a. Some genes responded earlier to S35966, suggesting that drugs with combined α₂-adrenoceptor antagonist/SNRI properties may elicit more rapid changes in markers of neural plasticity than a SNRI alone. |
| spellingShingle | Serres, F Millan, M Sharp, T Molecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine. |
| title | Molecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine. |
| title_full | Molecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine. |
| title_fullStr | Molecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine. |
| title_full_unstemmed | Molecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine. |
| title_short | Molecular adaptation to chronic antidepressant treatment: evidence for a more rapid response to the novel α₂-adrenoceptor antagonist/5-HT-noradrenaline reuptake inhibitor (SNRI), S35966, compared to the SNRI, venlafaxine. |
| title_sort | molecular adaptation to chronic antidepressant treatment evidence for a more rapid response to the novel α₂ adrenoceptor antagonist 5 ht noradrenaline reuptake inhibitor snri s35966 compared to the snri venlafaxine |
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