Programming of neural cells by (endo)cannabinoids: from physiological rules to emerging therapies
Key Points Cannabinoid receptor diversity and signalling in the immature brain are vastly different from those in the adult nervous system. These include the differential localization of, and signal transduction by, cannabinoid receptors and the enzymes that limit endocannabinoid bioavailability. CB...
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Veröffentlicht in: | Nature reviews. Neuroscience 2014-12, Vol.15 (12), p.786-801 |
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description | Key Points
Cannabinoid receptor diversity and signalling in the immature brain are vastly different from those in the adult nervous system. These include the differential localization of, and signal transduction by, cannabinoid receptors and the enzymes that limit endocannabinoid bioavailability. CB1 and CB2 cannabinoid receptors signal neural progenitor proliferation in the developing brain, including gliogenesis, by coupling to mitogenic pathways such as PI3K and ERK.
Endocannabinoid hot spots can facilitate the directional migration of postmitotic neurons in the foetal nervous system, as well as of neuroblasts in neurogenic areas of the adult mammalian brain.
CB1 cannabinoid receptors, and probably CB2 and TRPV1 receptors, in growth cones signal to modulate steering decisions during directional axonal growth. In part, autocrine signalling by endocannabinoids mediates neurite elongation.
Diacylgycerol lipase-dependent endocannabainoid signalling regulates neurogenesis in the adult hippocampus and subventricular zone.
Δ
9
-THC affects neuronal development via CB1 cannabinoid receptor-mediated mechanisms, disrupting cytoskeletal integrity, axonal growth and synaptogenesis. Therefore, THC exposure is adverse in developmental contexts.
Preclinical evidence suggests that pharmacological activation of cannabinoid receptors might be exploited therapeutically to inhibit tumor growth in glioma patients.
Endocannabinoids are involved in regulating neural progenitor cell proliferation, as well as neuronal and glial differentiation. In this Review, Maccarrone, Harkany and colleagues discuss mechanisms of endocannabinoid signalling, the action of plant cannabinoids in the foetal brain, and their exploitation to modulate diseases associated with defective cell cycle control, particularly cancer.
Among the many signalling lipids, endocannabinoids are increasingly recognized for their important roles in neuronal and glial development. Recent experimental evidence suggests that, during neuronal differentiation, endocannabinoid signalling undergoes a fundamental switch from the prenatal determination of cell fate to the homeostatic regulation of synaptic neurotransmission and bioenergetics in the mature nervous system. These studies also offer novel insights into neuropsychiatric disease mechanisms and contribute to the public debate about the benefits and the risks of cannabis use during pregnancy and in adolescence. |
doi_str_mv | 10.1038/nrn3846 |
format | Article |
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Cannabinoid receptor diversity and signalling in the immature brain are vastly different from those in the adult nervous system. These include the differential localization of, and signal transduction by, cannabinoid receptors and the enzymes that limit endocannabinoid bioavailability. CB1 and CB2 cannabinoid receptors signal neural progenitor proliferation in the developing brain, including gliogenesis, by coupling to mitogenic pathways such as PI3K and ERK.
Endocannabinoid hot spots can facilitate the directional migration of postmitotic neurons in the foetal nervous system, as well as of neuroblasts in neurogenic areas of the adult mammalian brain.
CB1 cannabinoid receptors, and probably CB2 and TRPV1 receptors, in growth cones signal to modulate steering decisions during directional axonal growth. In part, autocrine signalling by endocannabinoids mediates neurite elongation.
Diacylgycerol lipase-dependent endocannabainoid signalling regulates neurogenesis in the adult hippocampus and subventricular zone.
Δ
9
-THC affects neuronal development via CB1 cannabinoid receptor-mediated mechanisms, disrupting cytoskeletal integrity, axonal growth and synaptogenesis. Therefore, THC exposure is adverse in developmental contexts.
Preclinical evidence suggests that pharmacological activation of cannabinoid receptors might be exploited therapeutically to inhibit tumor growth in glioma patients.
Endocannabinoids are involved in regulating neural progenitor cell proliferation, as well as neuronal and glial differentiation. In this Review, Maccarrone, Harkany and colleagues discuss mechanisms of endocannabinoid signalling, the action of plant cannabinoids in the foetal brain, and their exploitation to modulate diseases associated with defective cell cycle control, particularly cancer.
Among the many signalling lipids, endocannabinoids are increasingly recognized for their important roles in neuronal and glial development. Recent experimental evidence suggests that, during neuronal differentiation, endocannabinoid signalling undergoes a fundamental switch from the prenatal determination of cell fate to the homeostatic regulation of synaptic neurotransmission and bioenergetics in the mature nervous system. These studies also offer novel insights into neuropsychiatric disease mechanisms and contribute to the public debate about the benefits and the risks of cannabis use during pregnancy and in adolescence.</description><identifier>ISSN: 1471-003X</identifier><identifier>ISSN: 1471-0048</identifier><identifier>EISSN: 1471-0048</identifier><identifier>EISSN: 1469-3178</identifier><identifier>DOI: 10.1038/nrn3846</identifier><identifier>PMID: 25409697</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/44 ; 13/51 ; 14/19 ; 14/28 ; 14/34 ; 631/136/368 ; 631/378/1595 ; 631/378/2571 ; 631/378/2571/2577 ; 631/80/84 ; Animal Genetics and Genomics ; Animals ; Axons ; Behavioral Sciences ; Biological Techniques ; Biomedicine ; Cannabis - adverse effects ; Cell differentiation ; Cell Differentiation - drug effects ; Cell Differentiation - physiology ; Cell growth ; Cellular signal transduction ; Endocannabinoids ; Endocannabinoids - metabolism ; Fatty acids ; Female ; Growth ; Humans ; Lipids ; Medicin och hälsovetenskap ; Metabolism ; Nervous system ; Neurobiology ; Neurogenesis - drug effects ; Neurogenesis - physiology ; Neurons - cytology ; Neurons - drug effects ; Neurons - metabolism ; Neurosciences ; Observations ; Physiological aspects ; Physiology ; Pregnancy ; review-article ; Tetrahydrocannabinol ; THC</subject><ispartof>Nature reviews. Neuroscience, 2014-12, Vol.15 (12), p.786-801</ispartof><rights>Springer Nature Limited 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c629t-cee2ef8563a2f281a1eea2dec0edd83f6c06312310e677f8f9b226fd06ea0e73</citedby><cites>FETCH-LOGICAL-c629t-cee2ef8563a2f281a1eea2dec0edd83f6c06312310e677f8f9b226fd06ea0e73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,552,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25409697$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:130212727$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Maccarrone, Mauro</creatorcontrib><creatorcontrib>Guzmán, Manuel</creatorcontrib><creatorcontrib>Mackie, Ken</creatorcontrib><creatorcontrib>Doherty, Patrick</creatorcontrib><creatorcontrib>Harkany, Tibor</creatorcontrib><title>Programming of neural cells by (endo)cannabinoids: from physiological rules to emerging therapies</title><title>Nature reviews. Neuroscience</title><addtitle>Nat Rev Neurosci</addtitle><addtitle>Nat Rev Neurosci</addtitle><description>Key Points
Cannabinoid receptor diversity and signalling in the immature brain are vastly different from those in the adult nervous system. These include the differential localization of, and signal transduction by, cannabinoid receptors and the enzymes that limit endocannabinoid bioavailability. CB1 and CB2 cannabinoid receptors signal neural progenitor proliferation in the developing brain, including gliogenesis, by coupling to mitogenic pathways such as PI3K and ERK.
Endocannabinoid hot spots can facilitate the directional migration of postmitotic neurons in the foetal nervous system, as well as of neuroblasts in neurogenic areas of the adult mammalian brain.
CB1 cannabinoid receptors, and probably CB2 and TRPV1 receptors, in growth cones signal to modulate steering decisions during directional axonal growth. In part, autocrine signalling by endocannabinoids mediates neurite elongation.
Diacylgycerol lipase-dependent endocannabainoid signalling regulates neurogenesis in the adult hippocampus and subventricular zone.
Δ
9
-THC affects neuronal development via CB1 cannabinoid receptor-mediated mechanisms, disrupting cytoskeletal integrity, axonal growth and synaptogenesis. Therefore, THC exposure is adverse in developmental contexts.
Preclinical evidence suggests that pharmacological activation of cannabinoid receptors might be exploited therapeutically to inhibit tumor growth in glioma patients.
Endocannabinoids are involved in regulating neural progenitor cell proliferation, as well as neuronal and glial differentiation. In this Review, Maccarrone, Harkany and colleagues discuss mechanisms of endocannabinoid signalling, the action of plant cannabinoids in the foetal brain, and their exploitation to modulate diseases associated with defective cell cycle control, particularly cancer.
Among the many signalling lipids, endocannabinoids are increasingly recognized for their important roles in neuronal and glial development. Recent experimental evidence suggests that, during neuronal differentiation, endocannabinoid signalling undergoes a fundamental switch from the prenatal determination of cell fate to the homeostatic regulation of synaptic neurotransmission and bioenergetics in the mature nervous system. These studies also offer novel insights into neuropsychiatric disease mechanisms and contribute to the public debate about the benefits and the risks of cannabis use during pregnancy and in adolescence.</description><subject>13/44</subject><subject>13/51</subject><subject>14/19</subject><subject>14/28</subject><subject>14/34</subject><subject>631/136/368</subject><subject>631/378/1595</subject><subject>631/378/2571</subject><subject>631/378/2571/2577</subject><subject>631/80/84</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Axons</subject><subject>Behavioral Sciences</subject><subject>Biological Techniques</subject><subject>Biomedicine</subject><subject>Cannabis - adverse effects</subject><subject>Cell differentiation</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - physiology</subject><subject>Cell growth</subject><subject>Cellular signal transduction</subject><subject>Endocannabinoids</subject><subject>Endocannabinoids - 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adverse effects</topic><topic>Cell differentiation</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - physiology</topic><topic>Cell growth</topic><topic>Cellular signal transduction</topic><topic>Endocannabinoids</topic><topic>Endocannabinoids - metabolism</topic><topic>Fatty acids</topic><topic>Female</topic><topic>Growth</topic><topic>Humans</topic><topic>Lipids</topic><topic>Medicin och hälsovetenskap</topic><topic>Metabolism</topic><topic>Nervous system</topic><topic>Neurobiology</topic><topic>Neurogenesis - drug effects</topic><topic>Neurogenesis - physiology</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>Observations</topic><topic>Physiological aspects</topic><topic>Physiology</topic><topic>Pregnancy</topic><topic>review-article</topic><topic>Tetrahydrocannabinol</topic><topic>THC</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maccarrone, Mauro</creatorcontrib><creatorcontrib>Guzmán, Manuel</creatorcontrib><creatorcontrib>Mackie, Ken</creatorcontrib><creatorcontrib>Doherty, Patrick</creatorcontrib><creatorcontrib>Harkany, Tibor</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>Nature reviews. Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maccarrone, Mauro</au><au>Guzmán, Manuel</au><au>Mackie, Ken</au><au>Doherty, Patrick</au><au>Harkany, Tibor</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Programming of neural cells by (endo)cannabinoids: from physiological rules to emerging therapies</atitle><jtitle>Nature reviews. Neuroscience</jtitle><stitle>Nat Rev Neurosci</stitle><addtitle>Nat Rev Neurosci</addtitle><date>2014-12-01</date><risdate>2014</risdate><volume>15</volume><issue>12</issue><spage>786</spage><epage>801</epage><pages>786-801</pages><issn>1471-003X</issn><issn>1471-0048</issn><eissn>1471-0048</eissn><eissn>1469-3178</eissn><abstract>Key Points
Cannabinoid receptor diversity and signalling in the immature brain are vastly different from those in the adult nervous system. These include the differential localization of, and signal transduction by, cannabinoid receptors and the enzymes that limit endocannabinoid bioavailability. CB1 and CB2 cannabinoid receptors signal neural progenitor proliferation in the developing brain, including gliogenesis, by coupling to mitogenic pathways such as PI3K and ERK.
Endocannabinoid hot spots can facilitate the directional migration of postmitotic neurons in the foetal nervous system, as well as of neuroblasts in neurogenic areas of the adult mammalian brain.
CB1 cannabinoid receptors, and probably CB2 and TRPV1 receptors, in growth cones signal to modulate steering decisions during directional axonal growth. In part, autocrine signalling by endocannabinoids mediates neurite elongation.
Diacylgycerol lipase-dependent endocannabainoid signalling regulates neurogenesis in the adult hippocampus and subventricular zone.
Δ
9
-THC affects neuronal development via CB1 cannabinoid receptor-mediated mechanisms, disrupting cytoskeletal integrity, axonal growth and synaptogenesis. Therefore, THC exposure is adverse in developmental contexts.
Preclinical evidence suggests that pharmacological activation of cannabinoid receptors might be exploited therapeutically to inhibit tumor growth in glioma patients.
Endocannabinoids are involved in regulating neural progenitor cell proliferation, as well as neuronal and glial differentiation. In this Review, Maccarrone, Harkany and colleagues discuss mechanisms of endocannabinoid signalling, the action of plant cannabinoids in the foetal brain, and their exploitation to modulate diseases associated with defective cell cycle control, particularly cancer.
Among the many signalling lipids, endocannabinoids are increasingly recognized for their important roles in neuronal and glial development. Recent experimental evidence suggests that, during neuronal differentiation, endocannabinoid signalling undergoes a fundamental switch from the prenatal determination of cell fate to the homeostatic regulation of synaptic neurotransmission and bioenergetics in the mature nervous system. These studies also offer novel insights into neuropsychiatric disease mechanisms and contribute to the public debate about the benefits and the risks of cannabis use during pregnancy and in adolescence.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25409697</pmid><doi>10.1038/nrn3846</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13/44 13/51 14/19 14/28 14/34 631/136/368 631/378/1595 631/378/2571 631/378/2571/2577 631/80/84 Animal Genetics and Genomics Animals Axons Behavioral Sciences Biological Techniques Biomedicine Cannabis - adverse effects Cell differentiation Cell Differentiation - drug effects Cell Differentiation - physiology Cell growth Cellular signal transduction Endocannabinoids Endocannabinoids - metabolism Fatty acids Female Growth Humans Lipids Medicin och hälsovetenskap Metabolism Nervous system Neurobiology Neurogenesis - drug effects Neurogenesis - physiology Neurons - cytology Neurons - drug effects Neurons - metabolism Neurosciences Observations Physiological aspects Physiology Pregnancy review-article Tetrahydrocannabinol THC |
title | Programming of neural cells by (endo)cannabinoids: from physiological rules to emerging therapies |
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