Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant.
In mice, disseminated coagulation, inflammation and ischemia induce neurological damages that can lead to the death. These symptoms result from circulating bubbles generated by a pathogenic decompression. An acute fluoxetine treatment or the presence of the TREK-1 potassium channel increased the sur...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2016-02-01
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| Series: | Frontiers in Physiology |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fphys.2016.00042/full |
| _version_ | 1818366715249033216 |
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| author | Nicolas eVallée Kate eLambrechts Kate eLambrechts Sébastien eDe Maistre Perrine eRoyal Jean eMazella Marc eBorsotto Catherine eHeurteaux Jacques eAbraini Jacques eAbraini Jacques eAbraini Jean-Jacques eRisso Jean-Eric eBlatteau |
| author_facet | Nicolas eVallée Kate eLambrechts Kate eLambrechts Sébastien eDe Maistre Perrine eRoyal Jean eMazella Marc eBorsotto Catherine eHeurteaux Jacques eAbraini Jacques eAbraini Jacques eAbraini Jean-Jacques eRisso Jean-Eric eBlatteau |
| author_sort | Nicolas eVallée |
| collection | DOAJ |
| description | In mice, disseminated coagulation, inflammation and ischemia induce neurological damages that can lead to the death. These symptoms result from circulating bubbles generated by a pathogenic decompression. An acute fluoxetine treatment or the presence of the TREK-1 potassium channel increased the survival rate when mice are subjected to an experimental dive/decompression protocol. This is a paradox because fluoxetine is a blocker of TREK-1 channels. First, we studied the effects of an acute dose of fluoxetine (50mg/kg) in wild-type (WT) and TREK-1 deficient mice (Knockout homozygous KO and heterozygous HET). Then, we combined the same fluoxetine treatment with a five-day treatment by spadin, in order to specifically block TREK-1 activity (KO-like mice). KO and KO-like mice could be regarded as antidepressed models.167 mice (45 WTcont 46 WTflux 30 HETflux and 46 KOflux) constituting the flux-pool and 113 supplementary mice (27 KO-like 24 WTflux2 24 KO-likeflux 21 WTcont2 17 WTno dive) constituting the spad-pool were included in this study. Only 7% of KO-TREK-1 treated with fluoxetine (KOflux) and 4% of mice treated with both spadin and fluoxetine (KO-likeflux) died from decompression sickness (DCS) symptoms. These values are much lower than those of WT control (62%) or KO-like mice (41%). After the decompression protocol, mice showed a significant consumption of their circulating platelets and leukocytes.Spadin antidepressed mice were more likely to declare DCS. Nevertheless, which had both blocked TREK-1 channel and were treated with fluoxetine were better protected against DCS. We conclude that the protective effect of such an acute dose of fluoxetine is enhanced when TREK-1 is inhibited. We confirmed that antidepressed models may have worse DCS outcomes, but a concomitant fluoxetine treatment not only decreases DCS severity but increases the survival rate. |
| first_indexed | 2024-12-13T22:40:34Z |
| format | Article |
| id | doaj.art-0cc5efede64546bc80fa01fd558c7c4a |
| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-12-13T22:40:34Z |
| publishDate | 2016-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Physiology |
| spelling | doaj.art-0cc5efede64546bc80fa01fd558c7c4a2022-12-21T23:28:51ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2016-02-01710.3389/fphys.2016.00042166571Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant.Nicolas eVallée0Kate eLambrechts1Kate eLambrechts2Sébastien eDe Maistre3Perrine eRoyal4Jean eMazella5Marc eBorsotto6Catherine eHeurteaux7Jacques eAbraini8Jacques eAbraini9Jacques eAbraini10Jean-Jacques eRisso11Jean-Eric eBlatteau12Institut de Recherche Biomédicale des ArméesInstitut de Recherche Biomédicale des ArméesUniversité du Sud Toulon VarHôpital d’Instruction des ArméesInstitut de Recherche Biomédicale des ArméesCentre National de la Recherche Scientifique and Université de Nice Sophia AntipolisCentre National de la Recherche Scientifique and Université de Nice Sophia AntipolisCentre National de la Recherche Scientifique and Université de Nice Sophia AntipolisInstitut de Recherche Biomédicale des ArméesUniversité LavalUniversité de Caen NormandieInstitut de Recherche Biomédicale des ArméesInstitut de Recherche Biomédicale des ArméesIn mice, disseminated coagulation, inflammation and ischemia induce neurological damages that can lead to the death. These symptoms result from circulating bubbles generated by a pathogenic decompression. An acute fluoxetine treatment or the presence of the TREK-1 potassium channel increased the survival rate when mice are subjected to an experimental dive/decompression protocol. This is a paradox because fluoxetine is a blocker of TREK-1 channels. First, we studied the effects of an acute dose of fluoxetine (50mg/kg) in wild-type (WT) and TREK-1 deficient mice (Knockout homozygous KO and heterozygous HET). Then, we combined the same fluoxetine treatment with a five-day treatment by spadin, in order to specifically block TREK-1 activity (KO-like mice). KO and KO-like mice could be regarded as antidepressed models.167 mice (45 WTcont 46 WTflux 30 HETflux and 46 KOflux) constituting the flux-pool and 113 supplementary mice (27 KO-like 24 WTflux2 24 KO-likeflux 21 WTcont2 17 WTno dive) constituting the spad-pool were included in this study. Only 7% of KO-TREK-1 treated with fluoxetine (KOflux) and 4% of mice treated with both spadin and fluoxetine (KO-likeflux) died from decompression sickness (DCS) symptoms. These values are much lower than those of WT control (62%) or KO-like mice (41%). After the decompression protocol, mice showed a significant consumption of their circulating platelets and leukocytes.Spadin antidepressed mice were more likely to declare DCS. Nevertheless, which had both blocked TREK-1 channel and were treated with fluoxetine were better protected against DCS. We conclude that the protective effect of such an acute dose of fluoxetine is enhanced when TREK-1 is inhibited. We confirmed that antidepressed models may have worse DCS outcomes, but a concomitant fluoxetine treatment not only decreases DCS severity but increases the survival rate.http://journal.frontiersin.org/Journal/10.3389/fphys.2016.00042/fullDecompression SicknessDepressionDivingFluoxetineInflammationIschemia |
| spellingShingle | Nicolas eVallée Kate eLambrechts Kate eLambrechts Sébastien eDe Maistre Perrine eRoyal Jean eMazella Marc eBorsotto Catherine eHeurteaux Jacques eAbraini Jacques eAbraini Jacques eAbraini Jean-Jacques eRisso Jean-Eric eBlatteau Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant. Frontiers in Physiology Decompression Sickness Depression Diving Fluoxetine Inflammation Ischemia |
| title | Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant. |
| title_full | Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant. |
| title_fullStr | Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant. |
| title_full_unstemmed | Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant. |
| title_short | Fluoxetine protection in decompression sickness in mice is enhanced by blocking TREK-1 potassium channel with the spadin antidepressant. |
| title_sort | fluoxetine protection in decompression sickness in mice is enhanced by blocking trek 1 potassium channel with the spadin antidepressant |
| topic | Decompression Sickness Depression Diving Fluoxetine Inflammation Ischemia |
| url | http://journal.frontiersin.org/Journal/10.3389/fphys.2016.00042/full |
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