Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure
[Display omitted] Changes in endogenous cannabinoid homeostasis are associated with both ethanol-related neuroinflammation and memory decline. Extensive research is still required to unveil the role of endocannabinoid signaling activation on hippocampal microglial cells after ethanol exposure. Eithe...
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| Veröffentlicht in: | Biochemical pharmacology 2018-11, Vol.157, p.244-257 |
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| creator | Rivera, Patricia Fernández-Arjona, María del Mar Silva-Peña, Daniel Blanco, Eduardo Vargas, Antonio López-Ávalos, María Dolores Grondona, Jesús M. Serrano, Antonia Pavón, Francisco Javier Rodríguez de Fonseca, Fernando Suárez, Juan |
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Changes in endogenous cannabinoid homeostasis are associated with both ethanol-related neuroinflammation and memory decline. Extensive research is still required to unveil the role of endocannabinoid signaling activation on hippocampal microglial cells after ethanol exposure. Either microglial morphology, phenotype and recruitment may become notably altered after chronic alcohol-related neurodegeneration. Here, we evaluated the pharmacological effects of fatty-acid amide-hydrolase (FAAH) inhibitor URB597 (0.3 mg/kg), oleoylethanolamide (OEA, 10 mg/kg), arachidonoylethanolamide (AEA, 10 mg/kg), the CB1 receptor agonist ACEA (3 mg/kg) and the CB2 receptor agonist JWH133 (0.2 mg/kg) administered for 5 days in a rat model of subchronic (2 weeks) ethanol diet (11% v/v) exposure. URB597 turned to be the most effective treatment. URB597 increased microglial (IBA-1+) cell population, and changed morphometric features (cell area and perimeter, roughness, fractal dimension, lacunarity) associated with activated microglia in the hippocampus of ethanol-exposed rats. Regarding innate immune activity, URB597 specifically increased mRNA levels of toll-like receptor 4 (TLR4), glial fibrillary acidic protein (Gfap) and the chemokine stromal cell-derived factor 1 (SDF-1α/CXCL12), and elevated the cell population expressing the chemokine receptors CX3CR1, CCR2 and CCR4 in the ethanol-exposed rat hippocampus. Contrary to ethanol effect, URB597 reduced mRNA levels of Iba-1, Tnfα, IL-6 and the monocyte chemoattractant protein-1 (MCP-1/CCL2), as well as cell population expressing iNOS. URB597 effects on hippocampal immune system were accompanied by changes in short and long-term visual recognition memory. These results suggest that FAAH inhibition may modulates hippocampal microglial recruitment and activation that can be associated with improved hippocampal-dependent memory despite ethanol exposure. |
| doi_str_mv | 10.1016/j.bcp.2018.08.005 |
| format | Article |
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Changes in endogenous cannabinoid homeostasis are associated with both ethanol-related neuroinflammation and memory decline. Extensive research is still required to unveil the role of endocannabinoid signaling activation on hippocampal microglial cells after ethanol exposure. Either microglial morphology, phenotype and recruitment may become notably altered after chronic alcohol-related neurodegeneration. Here, we evaluated the pharmacological effects of fatty-acid amide-hydrolase (FAAH) inhibitor URB597 (0.3 mg/kg), oleoylethanolamide (OEA, 10 mg/kg), arachidonoylethanolamide (AEA, 10 mg/kg), the CB1 receptor agonist ACEA (3 mg/kg) and the CB2 receptor agonist JWH133 (0.2 mg/kg) administered for 5 days in a rat model of subchronic (2 weeks) ethanol diet (11% v/v) exposure. URB597 turned to be the most effective treatment. URB597 increased microglial (IBA-1+) cell population, and changed morphometric features (cell area and perimeter, roughness, fractal dimension, lacunarity) associated with activated microglia in the hippocampus of ethanol-exposed rats. Regarding innate immune activity, URB597 specifically increased mRNA levels of toll-like receptor 4 (TLR4), glial fibrillary acidic protein (Gfap) and the chemokine stromal cell-derived factor 1 (SDF-1α/CXCL12), and elevated the cell population expressing the chemokine receptors CX3CR1, CCR2 and CCR4 in the ethanol-exposed rat hippocampus. Contrary to ethanol effect, URB597 reduced mRNA levels of Iba-1, Tnfα, IL-6 and the monocyte chemoattractant protein-1 (MCP-1/CCL2), as well as cell population expressing iNOS. URB597 effects on hippocampal immune system were accompanied by changes in short and long-term visual recognition memory. These results suggest that FAAH inhibition may modulates hippocampal microglial recruitment and activation that can be associated with improved hippocampal-dependent memory despite ethanol exposure.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/j.bcp.2018.08.005</identifier><identifier>PMID: 30098312</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Alcohol ; Amidohydrolases - antagonists & inhibitors ; Animals ; Arachidonic Acids - pharmacology ; Benzamides - pharmacology ; Carbamates - pharmacology ; Chemokines - genetics ; Chemokines - metabolism ; Cytokines - genetics ; Cytokines - metabolism ; Dentate Gyrus - drug effects ; Endocannabinoids - pharmacology ; Enzyme Inhibitors - pharmacology ; Ethanol - toxicity ; FAAH ; Gene Expression - drug effects ; Glial Fibrillary Acidic Protein - analysis ; Hippocampus ; Hippocampus - cytology ; Hippocampus - drug effects ; Hippocampus - immunology ; Male ; Memory - drug effects ; Memory, Long-Term - drug effects ; Memory, microglia ; Memory, Short-Term - drug effects ; Microglia - cytology ; Microglia - drug effects ; Microglia - enzymology ; Nitric Oxide Synthase Type II - analysis ; Phenotype ; Polyunsaturated Alkamides - pharmacology ; Rats, Wistar ; Receptors, Chemokine - metabolism</subject><ispartof>Biochemical pharmacology, 2018-11, Vol.157, p.244-257</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-d0f86d202599624414f4c5bd50ee649c450cfaca8372672c4cc957b1099d8dc73</citedby><cites>FETCH-LOGICAL-c396t-d0f86d202599624414f4c5bd50ee649c450cfaca8372672c4cc957b1099d8dc73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006295218303253$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30098312$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rivera, Patricia</creatorcontrib><creatorcontrib>Fernández-Arjona, María del Mar</creatorcontrib><creatorcontrib>Silva-Peña, Daniel</creatorcontrib><creatorcontrib>Blanco, Eduardo</creatorcontrib><creatorcontrib>Vargas, Antonio</creatorcontrib><creatorcontrib>López-Ávalos, María Dolores</creatorcontrib><creatorcontrib>Grondona, Jesús M.</creatorcontrib><creatorcontrib>Serrano, Antonia</creatorcontrib><creatorcontrib>Pavón, Francisco Javier</creatorcontrib><creatorcontrib>Rodríguez de Fonseca, Fernando</creatorcontrib><creatorcontrib>Suárez, Juan</creatorcontrib><title>Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>[Display omitted]
Changes in endogenous cannabinoid homeostasis are associated with both ethanol-related neuroinflammation and memory decline. Extensive research is still required to unveil the role of endocannabinoid signaling activation on hippocampal microglial cells after ethanol exposure. Either microglial morphology, phenotype and recruitment may become notably altered after chronic alcohol-related neurodegeneration. Here, we evaluated the pharmacological effects of fatty-acid amide-hydrolase (FAAH) inhibitor URB597 (0.3 mg/kg), oleoylethanolamide (OEA, 10 mg/kg), arachidonoylethanolamide (AEA, 10 mg/kg), the CB1 receptor agonist ACEA (3 mg/kg) and the CB2 receptor agonist JWH133 (0.2 mg/kg) administered for 5 days in a rat model of subchronic (2 weeks) ethanol diet (11% v/v) exposure. URB597 turned to be the most effective treatment. URB597 increased microglial (IBA-1+) cell population, and changed morphometric features (cell area and perimeter, roughness, fractal dimension, lacunarity) associated with activated microglia in the hippocampus of ethanol-exposed rats. Regarding innate immune activity, URB597 specifically increased mRNA levels of toll-like receptor 4 (TLR4), glial fibrillary acidic protein (Gfap) and the chemokine stromal cell-derived factor 1 (SDF-1α/CXCL12), and elevated the cell population expressing the chemokine receptors CX3CR1, CCR2 and CCR4 in the ethanol-exposed rat hippocampus. Contrary to ethanol effect, URB597 reduced mRNA levels of Iba-1, Tnfα, IL-6 and the monocyte chemoattractant protein-1 (MCP-1/CCL2), as well as cell population expressing iNOS. URB597 effects on hippocampal immune system were accompanied by changes in short and long-term visual recognition memory. These results suggest that FAAH inhibition may modulates hippocampal microglial recruitment and activation that can be associated with improved hippocampal-dependent memory despite ethanol exposure.</description><subject>Alcohol</subject><subject>Amidohydrolases - antagonists & inhibitors</subject><subject>Animals</subject><subject>Arachidonic Acids - pharmacology</subject><subject>Benzamides - pharmacology</subject><subject>Carbamates - pharmacology</subject><subject>Chemokines - genetics</subject><subject>Chemokines - metabolism</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Dentate Gyrus - drug effects</subject><subject>Endocannabinoids - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Ethanol - toxicity</subject><subject>FAAH</subject><subject>Gene Expression - drug effects</subject><subject>Glial Fibrillary Acidic Protein - analysis</subject><subject>Hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - immunology</subject><subject>Male</subject><subject>Memory - drug effects</subject><subject>Memory, Long-Term - drug effects</subject><subject>Memory, microglia</subject><subject>Memory, Short-Term - drug effects</subject><subject>Microglia - cytology</subject><subject>Microglia - drug effects</subject><subject>Microglia - enzymology</subject><subject>Nitric Oxide Synthase Type II - analysis</subject><subject>Phenotype</subject><subject>Polyunsaturated Alkamides - pharmacology</subject><subject>Rats, Wistar</subject><subject>Receptors, Chemokine - metabolism</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1v1DAQtRCIbgs_gAvysRx2sZ04icVpW1GKVAmE6NlyxpONlzgOdrYiv4c_Wi9bOCKNNB96782MHiFvONtwxqv3-00L00Yw3mxYDiafkRVv6mItVNU8JyvGWJVrKc7IeUr7Y9tU_CU5KxhTTcHFivz-2pvoDYQh7ByYgbZDgB_GIg0d7cw8L9SAs9R4l2f9YmMYTEJ6ebPd3r6j7ULvv11JVVPnpxgeMFGPPsTMGi2F3oy7PJp7pFOPY5iX6Y9w76YpgPFTXugdxLAbnKEW0-RmpDhnXhgo_ppCOkR8RV50Zkj4-ilfkPubj9-vb9d3Xz59vt7eraFQ1by2rGsqK5iQSlWiLHnZlSBbKxliVSooJYPOgGmKWlS1gBJAybrlTCnbWKiLC3J50s2f_DxgmrV3CXAYzIjhkLRgTS0VayqRofwEzbenFLHTU3TexEVzpo_e6L3O3uijN5rlYDJz3j7JH1qP9h_jrxkZ8OEEwPzkg8OoEzgcAa2LCLO2wf1H_hGtF6EG</recordid><startdate>201811</startdate><enddate>201811</enddate><creator>Rivera, Patricia</creator><creator>Fernández-Arjona, María del Mar</creator><creator>Silva-Peña, Daniel</creator><creator>Blanco, Eduardo</creator><creator>Vargas, Antonio</creator><creator>López-Ávalos, María Dolores</creator><creator>Grondona, Jesús M.</creator><creator>Serrano, Antonia</creator><creator>Pavón, Francisco Javier</creator><creator>Rodríguez de Fonseca, Fernando</creator><creator>Suárez, Juan</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201811</creationdate><title>Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure</title><author>Rivera, Patricia ; Fernández-Arjona, María del Mar ; Silva-Peña, Daniel ; Blanco, Eduardo ; Vargas, Antonio ; López-Ávalos, María Dolores ; Grondona, Jesús M. ; Serrano, Antonia ; Pavón, Francisco Javier ; Rodríguez de Fonseca, Fernando ; Suárez, Juan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-d0f86d202599624414f4c5bd50ee649c450cfaca8372672c4cc957b1099d8dc73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alcohol</topic><topic>Amidohydrolases - antagonists & inhibitors</topic><topic>Animals</topic><topic>Arachidonic Acids - pharmacology</topic><topic>Benzamides - pharmacology</topic><topic>Carbamates - pharmacology</topic><topic>Chemokines - genetics</topic><topic>Chemokines - metabolism</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Dentate Gyrus - drug effects</topic><topic>Endocannabinoids - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Ethanol - toxicity</topic><topic>FAAH</topic><topic>Gene Expression - drug effects</topic><topic>Glial Fibrillary Acidic Protein - analysis</topic><topic>Hippocampus</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - immunology</topic><topic>Male</topic><topic>Memory - drug effects</topic><topic>Memory, Long-Term - drug effects</topic><topic>Memory, microglia</topic><topic>Memory, Short-Term - drug effects</topic><topic>Microglia - cytology</topic><topic>Microglia - drug effects</topic><topic>Microglia - enzymology</topic><topic>Nitric Oxide Synthase Type II - analysis</topic><topic>Phenotype</topic><topic>Polyunsaturated Alkamides - pharmacology</topic><topic>Rats, Wistar</topic><topic>Receptors, Chemokine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rivera, Patricia</creatorcontrib><creatorcontrib>Fernández-Arjona, María del Mar</creatorcontrib><creatorcontrib>Silva-Peña, Daniel</creatorcontrib><creatorcontrib>Blanco, Eduardo</creatorcontrib><creatorcontrib>Vargas, Antonio</creatorcontrib><creatorcontrib>López-Ávalos, María Dolores</creatorcontrib><creatorcontrib>Grondona, Jesús M.</creatorcontrib><creatorcontrib>Serrano, Antonia</creatorcontrib><creatorcontrib>Pavón, Francisco Javier</creatorcontrib><creatorcontrib>Rodríguez de Fonseca, Fernando</creatorcontrib><creatorcontrib>Suárez, Juan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rivera, Patricia</au><au>Fernández-Arjona, María del Mar</au><au>Silva-Peña, Daniel</au><au>Blanco, Eduardo</au><au>Vargas, Antonio</au><au>López-Ávalos, María Dolores</au><au>Grondona, Jesús M.</au><au>Serrano, Antonia</au><au>Pavón, Francisco Javier</au><au>Rodríguez de Fonseca, Fernando</au><au>Suárez, Juan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>2018-11</date><risdate>2018</risdate><volume>157</volume><spage>244</spage><epage>257</epage><pages>244-257</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><abstract>[Display omitted]
Changes in endogenous cannabinoid homeostasis are associated with both ethanol-related neuroinflammation and memory decline. Extensive research is still required to unveil the role of endocannabinoid signaling activation on hippocampal microglial cells after ethanol exposure. Either microglial morphology, phenotype and recruitment may become notably altered after chronic alcohol-related neurodegeneration. Here, we evaluated the pharmacological effects of fatty-acid amide-hydrolase (FAAH) inhibitor URB597 (0.3 mg/kg), oleoylethanolamide (OEA, 10 mg/kg), arachidonoylethanolamide (AEA, 10 mg/kg), the CB1 receptor agonist ACEA (3 mg/kg) and the CB2 receptor agonist JWH133 (0.2 mg/kg) administered for 5 days in a rat model of subchronic (2 weeks) ethanol diet (11% v/v) exposure. URB597 turned to be the most effective treatment. URB597 increased microglial (IBA-1+) cell population, and changed morphometric features (cell area and perimeter, roughness, fractal dimension, lacunarity) associated with activated microglia in the hippocampus of ethanol-exposed rats. Regarding innate immune activity, URB597 specifically increased mRNA levels of toll-like receptor 4 (TLR4), glial fibrillary acidic protein (Gfap) and the chemokine stromal cell-derived factor 1 (SDF-1α/CXCL12), and elevated the cell population expressing the chemokine receptors CX3CR1, CCR2 and CCR4 in the ethanol-exposed rat hippocampus. Contrary to ethanol effect, URB597 reduced mRNA levels of Iba-1, Tnfα, IL-6 and the monocyte chemoattractant protein-1 (MCP-1/CCL2), as well as cell population expressing iNOS. URB597 effects on hippocampal immune system were accompanied by changes in short and long-term visual recognition memory. These results suggest that FAAH inhibition may modulates hippocampal microglial recruitment and activation that can be associated with improved hippocampal-dependent memory despite ethanol exposure.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>30098312</pmid><doi>10.1016/j.bcp.2018.08.005</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alcohol Amidohydrolases - antagonists & inhibitors Animals Arachidonic Acids - pharmacology Benzamides - pharmacology Carbamates - pharmacology Chemokines - genetics Chemokines - metabolism Cytokines - genetics Cytokines - metabolism Dentate Gyrus - drug effects Endocannabinoids - pharmacology Enzyme Inhibitors - pharmacology Ethanol - toxicity FAAH Gene Expression - drug effects Glial Fibrillary Acidic Protein - analysis Hippocampus Hippocampus - cytology Hippocampus - drug effects Hippocampus - immunology Male Memory - drug effects Memory, Long-Term - drug effects Memory, microglia Memory, Short-Term - drug effects Microglia - cytology Microglia - drug effects Microglia - enzymology Nitric Oxide Synthase Type II - analysis Phenotype Polyunsaturated Alkamides - pharmacology Rats, Wistar Receptors, Chemokine - metabolism |
| title | Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure |
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