Cannabinoids attenuate norepinephrine‐induced melatonin biosynthesis in the rat pineal gland by reducing arylalkylamine N‐acetyltransferase activity without involvement of cannabinoid receptors
Cannabinoids modulate neuronal and neuroendocrine circuits by binding to cannabinoid receptors acting upon cAMP/Ca2+‐mediated intracellular signaling cascades. The rat pineal represents an established model to investigate intracellular signaling processes because a well defined input, the neurotrans...
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| Veröffentlicht in: | Journal of neurochemistry 2006-07, Vol.98 (1), p.267-278 |
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| creator | Koch, Marco Dehghani, Faramarz Habazettl, Iris Schomerus, Christof Korf, Horst‐Werner |
| description | Cannabinoids modulate neuronal and neuroendocrine circuits by binding to cannabinoid receptors acting upon cAMP/Ca2+‐mediated intracellular signaling cascades. The rat pineal represents an established model to investigate intracellular signaling processes because a well defined input, the neurotransmitter norepinephrine, is transformed via cAMP/Ca2+‐dependent mechanisms into an easily detectable output signal, the biosynthesis of melatonin. Here we investigated the impact of cannabinoids on norepinephrine‐regulated melatonin biosynthesis in the rat pineal. We demonstrated that treatment of cultured rat pineals with 9‐carboxy‐11‐nor‐delta‐9‐tetrahydrocannabinol (THC), cannabidiol or cannabinol significantly reduced norepinephrine‐induced arylalkylamine N‐acetyltransferase (AANAT) activity and melatonin biosynthesis. These effects were not mimicked by the cannabinoid receptor agonist WIN55,212–2 and were not blocked by cannabinoid 1 and 2 receptor antagonists. The cannabinoids used did not affect norepinephrine‐induced increases in cAMP/Ca2+ levels. Notably, cannabinoids were found to directly inhibit AANAT activity in lysates of the pineal gland. This effect was specific in so far as cannabinoids did not influence the activity of hydroxyindole‐O‐methyltransferase (HIOMT), the last enzyme in melatonin biosynthesis. Taken together, our data strongly suggest that cannabinoids inhibit AANAT activity and attenuate melatonin biosynthesis through intracellular actions without involvement of classical cannabinoid receptor‐dependent signaling cascades. |
| doi_str_mv | 10.1111/j.1471-4159.2006.03873.x |
| format | Article |
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The rat pineal represents an established model to investigate intracellular signaling processes because a well defined input, the neurotransmitter norepinephrine, is transformed via cAMP/Ca2+‐dependent mechanisms into an easily detectable output signal, the biosynthesis of melatonin. Here we investigated the impact of cannabinoids on norepinephrine‐regulated melatonin biosynthesis in the rat pineal. We demonstrated that treatment of cultured rat pineals with 9‐carboxy‐11‐nor‐delta‐9‐tetrahydrocannabinol (THC), cannabidiol or cannabinol significantly reduced norepinephrine‐induced arylalkylamine N‐acetyltransferase (AANAT) activity and melatonin biosynthesis. These effects were not mimicked by the cannabinoid receptor agonist WIN55,212–2 and were not blocked by cannabinoid 1 and 2 receptor antagonists. The cannabinoids used did not affect norepinephrine‐induced increases in cAMP/Ca2+ levels. Notably, cannabinoids were found to directly inhibit AANAT activity in lysates of the pineal gland. This effect was specific in so far as cannabinoids did not influence the activity of hydroxyindole‐O‐methyltransferase (HIOMT), the last enzyme in melatonin biosynthesis. Taken together, our data strongly suggest that cannabinoids inhibit AANAT activity and attenuate melatonin biosynthesis through intracellular actions without involvement of classical cannabinoid receptor‐dependent signaling cascades.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2006.03873.x</identifier><identifier>PMID: 16805813</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Area Under Curve ; Arylalkylamine N-Acetyltransferase - metabolism ; arylalkylamine N‐acetyltransferase ; Biological and medical sciences ; cannabidiol ; cannabinoid system ; Cannabinoids - pharmacology ; cannabinol ; Cells, Cultured ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Cyclic AMP - metabolism ; Cyclic AMP Response Element-Binding Protein - metabolism ; delta‐9‐tetrahydrocannabinol ; Dose-Response Relationship, Drug ; Drug Interactions ; Endocrine system ; Enzyme Activation - drug effects ; Enzyme Inhibitors - pharmacology ; Enzymes ; Fundamental and applied biological sciences. Psychology ; Hormones and neuropeptides. Regulation ; Hypothalamus. Hypophysis. Epiphysis. Urophysis ; Immunohistochemistry - methods ; Male ; Melatonin - biosynthesis ; Neurons ; Norepinephrine - pharmacology ; Organ Culture Techniques ; Pineal Gland - cytology ; Pineal Gland - drug effects ; Radiometry - methods ; Rats ; Rats, Wistar ; Receptors, Cannabinoid - physiology ; Rodents ; Vertebrates: endocrinology ; Vertebrates: nervous system and sense organs</subject><ispartof>Journal of neurochemistry, 2006-07, Vol.98 (1), p.267-278</ispartof><rights>2006 INIST-CNRS</rights><rights>2006 The Authors Journal Compilation 2006 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5053-2a12f6d528b5998d27ea2e757aa5a7755306ed786528f1ebfb67fe41476c15b93</citedby><cites>FETCH-LOGICAL-c5053-2a12f6d528b5998d27ea2e757aa5a7755306ed786528f1ebfb67fe41476c15b93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2006.03873.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2006.03873.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17848383$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16805813$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koch, Marco</creatorcontrib><creatorcontrib>Dehghani, Faramarz</creatorcontrib><creatorcontrib>Habazettl, Iris</creatorcontrib><creatorcontrib>Schomerus, Christof</creatorcontrib><creatorcontrib>Korf, Horst‐Werner</creatorcontrib><title>Cannabinoids attenuate norepinephrine‐induced melatonin biosynthesis in the rat pineal gland by reducing arylalkylamine N‐acetyltransferase activity without involvement of cannabinoid receptors</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Cannabinoids modulate neuronal and neuroendocrine circuits by binding to cannabinoid receptors acting upon cAMP/Ca2+‐mediated intracellular signaling cascades. The rat pineal represents an established model to investigate intracellular signaling processes because a well defined input, the neurotransmitter norepinephrine, is transformed via cAMP/Ca2+‐dependent mechanisms into an easily detectable output signal, the biosynthesis of melatonin. Here we investigated the impact of cannabinoids on norepinephrine‐regulated melatonin biosynthesis in the rat pineal. We demonstrated that treatment of cultured rat pineals with 9‐carboxy‐11‐nor‐delta‐9‐tetrahydrocannabinol (THC), cannabidiol or cannabinol significantly reduced norepinephrine‐induced arylalkylamine N‐acetyltransferase (AANAT) activity and melatonin biosynthesis. These effects were not mimicked by the cannabinoid receptor agonist WIN55,212–2 and were not blocked by cannabinoid 1 and 2 receptor antagonists. The cannabinoids used did not affect norepinephrine‐induced increases in cAMP/Ca2+ levels. Notably, cannabinoids were found to directly inhibit AANAT activity in lysates of the pineal gland. This effect was specific in so far as cannabinoids did not influence the activity of hydroxyindole‐O‐methyltransferase (HIOMT), the last enzyme in melatonin biosynthesis. Taken together, our data strongly suggest that cannabinoids inhibit AANAT activity and attenuate melatonin biosynthesis through intracellular actions without involvement of classical cannabinoid receptor‐dependent signaling cascades.</description><subject>Animals</subject><subject>Area Under Curve</subject><subject>Arylalkylamine N-Acetyltransferase - metabolism</subject><subject>arylalkylamine N‐acetyltransferase</subject><subject>Biological and medical sciences</subject><subject>cannabidiol</subject><subject>cannabinoid system</subject><subject>Cannabinoids - pharmacology</subject><subject>cannabinol</subject><subject>Cells, Cultured</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Cyclic AMP - metabolism</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>delta‐9‐tetrahydrocannabinol</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Interactions</subject><subject>Endocrine system</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Enzymes</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hormones and neuropeptides. Regulation</subject><subject>Hypothalamus. Hypophysis. Epiphysis. Urophysis</subject><subject>Immunohistochemistry - methods</subject><subject>Male</subject><subject>Melatonin - biosynthesis</subject><subject>Neurons</subject><subject>Norepinephrine - pharmacology</subject><subject>Organ Culture Techniques</subject><subject>Pineal Gland - cytology</subject><subject>Pineal Gland - drug effects</subject><subject>Radiometry - methods</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Cannabinoid - physiology</subject><subject>Rodents</subject><subject>Vertebrates: endocrinology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc-u1CAUxhuj8Y5XX8EQE911BFooXbgwE__m5rrRNaH09A4jhRHo3Nudj-BL-SI-idSZOIkrWcAh_L4vh_MVBSJ4TfJ6uVuTuiFlTVi7phjzNa5EU63v7hWrvw_3ixXGlJYVrulF8SjGHcaE15w8LC4IF5gJUq2KnxvlnOqM86aPSKUEblIJkPMB9sbBfhvy_uv7D-P6SUOPRrAqeWcc6oyPs0tbiCaifM8VCiqhRaYsurHK9aibUYCsNO4GqTBbZb_mbcwIus6uSkOabQrKxQGCioCUTuZg0oxuTdr6KWXng7cHGMEl5Aekz_1mZw375EN8XDwYlI3w5HReFl_evvm8eV9efXr3YfP6qtQMs6qkitCB94yKjrWt6GkDikLDGqWYahrGKsyhbwTPxECgGzreDFDnkXJNWNdWl8WLo-8--G8TxCRHEzXY_FXwU5Skpa3AnGbw2T_gzk_B5d4kxZzVom5ZhsQR0sHHGGCQ-2DGPCVJsFxylju5xCmXOOWSs_yTs7zL0qcn_6kboT8LT8Fm4PkJUFErO-QJaxPPXCNqUYmFe3Xkbo2F-b8bkB-vN0tV_Qa8i8vb</recordid><startdate>200607</startdate><enddate>200607</enddate><creator>Koch, Marco</creator><creator>Dehghani, Faramarz</creator><creator>Habazettl, Iris</creator><creator>Schomerus, Christof</creator><creator>Korf, Horst‐Werner</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7QP</scope></search><sort><creationdate>200607</creationdate><title>Cannabinoids attenuate norepinephrine‐induced melatonin biosynthesis in the rat pineal gland by reducing arylalkylamine N‐acetyltransferase activity without involvement of cannabinoid receptors</title><author>Koch, Marco ; Dehghani, Faramarz ; Habazettl, Iris ; Schomerus, Christof ; Korf, Horst‐Werner</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5053-2a12f6d528b5998d27ea2e757aa5a7755306ed786528f1ebfb67fe41476c15b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Area Under Curve</topic><topic>Arylalkylamine N-Acetyltransferase - metabolism</topic><topic>arylalkylamine N‐acetyltransferase</topic><topic>Biological and medical sciences</topic><topic>cannabidiol</topic><topic>cannabinoid system</topic><topic>Cannabinoids - pharmacology</topic><topic>cannabinol</topic><topic>Cells, Cultured</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Cyclic AMP - metabolism</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>delta‐9‐tetrahydrocannabinol</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Interactions</topic><topic>Endocrine system</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Enzymes</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hormones and neuropeptides. Regulation</topic><topic>Hypothalamus. Hypophysis. Epiphysis. Urophysis</topic><topic>Immunohistochemistry - methods</topic><topic>Male</topic><topic>Melatonin - biosynthesis</topic><topic>Neurons</topic><topic>Norepinephrine - pharmacology</topic><topic>Organ Culture Techniques</topic><topic>Pineal Gland - cytology</topic><topic>Pineal Gland - drug effects</topic><topic>Radiometry - methods</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Cannabinoid - physiology</topic><topic>Rodents</topic><topic>Vertebrates: endocrinology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koch, Marco</creatorcontrib><creatorcontrib>Dehghani, Faramarz</creatorcontrib><creatorcontrib>Habazettl, Iris</creatorcontrib><creatorcontrib>Schomerus, Christof</creatorcontrib><creatorcontrib>Korf, Horst‐Werner</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koch, Marco</au><au>Dehghani, Faramarz</au><au>Habazettl, Iris</au><au>Schomerus, Christof</au><au>Korf, Horst‐Werner</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cannabinoids attenuate norepinephrine‐induced melatonin biosynthesis in the rat pineal gland by reducing arylalkylamine N‐acetyltransferase activity without involvement of cannabinoid receptors</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2006-07</date><risdate>2006</risdate><volume>98</volume><issue>1</issue><spage>267</spage><epage>278</epage><pages>267-278</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>Cannabinoids modulate neuronal and neuroendocrine circuits by binding to cannabinoid receptors acting upon cAMP/Ca2+‐mediated intracellular signaling cascades. The rat pineal represents an established model to investigate intracellular signaling processes because a well defined input, the neurotransmitter norepinephrine, is transformed via cAMP/Ca2+‐dependent mechanisms into an easily detectable output signal, the biosynthesis of melatonin. Here we investigated the impact of cannabinoids on norepinephrine‐regulated melatonin biosynthesis in the rat pineal. We demonstrated that treatment of cultured rat pineals with 9‐carboxy‐11‐nor‐delta‐9‐tetrahydrocannabinol (THC), cannabidiol or cannabinol significantly reduced norepinephrine‐induced arylalkylamine N‐acetyltransferase (AANAT) activity and melatonin biosynthesis. These effects were not mimicked by the cannabinoid receptor agonist WIN55,212–2 and were not blocked by cannabinoid 1 and 2 receptor antagonists. The cannabinoids used did not affect norepinephrine‐induced increases in cAMP/Ca2+ levels. Notably, cannabinoids were found to directly inhibit AANAT activity in lysates of the pineal gland. This effect was specific in so far as cannabinoids did not influence the activity of hydroxyindole‐O‐methyltransferase (HIOMT), the last enzyme in melatonin biosynthesis. Taken together, our data strongly suggest that cannabinoids inhibit AANAT activity and attenuate melatonin biosynthesis through intracellular actions without involvement of classical cannabinoid receptor‐dependent signaling cascades.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16805813</pmid><doi>10.1111/j.1471-4159.2006.03873.x</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Area Under Curve Arylalkylamine N-Acetyltransferase - metabolism arylalkylamine N‐acetyltransferase Biological and medical sciences cannabidiol cannabinoid system Cannabinoids - pharmacology cannabinol Cells, Cultured Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cyclic AMP - metabolism Cyclic AMP Response Element-Binding Protein - metabolism delta‐9‐tetrahydrocannabinol Dose-Response Relationship, Drug Drug Interactions Endocrine system Enzyme Activation - drug effects Enzyme Inhibitors - pharmacology Enzymes Fundamental and applied biological sciences. Psychology Hormones and neuropeptides. Regulation Hypothalamus. Hypophysis. Epiphysis. Urophysis Immunohistochemistry - methods Male Melatonin - biosynthesis Neurons Norepinephrine - pharmacology Organ Culture Techniques Pineal Gland - cytology Pineal Gland - drug effects Radiometry - methods Rats Rats, Wistar Receptors, Cannabinoid - physiology Rodents Vertebrates: endocrinology Vertebrates: nervous system and sense organs |
| title | Cannabinoids attenuate norepinephrine‐induced melatonin biosynthesis in the rat pineal gland by reducing arylalkylamine N‐acetyltransferase activity without involvement of cannabinoid receptors |
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