Dendritically released transmitters cooperate via autocrine and retrograde actions to inhibit afferent excitation in rat brain
Oxytocin is released from supraoptic magnocellular neurones and is thought to act at presynaptic receptors to inhibit transmitter release. We now show that this effect is mediated by endocannabinoids, but that oxytocin nonetheless plays an important role in endocannabinoid signalling. WIN55,212-2, a...
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| Veröffentlicht in: | The Journal of physiology 2004-09, Vol.559 (2), p.611-624 |
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| creator | Hirasawa, Michiru Schwab, Yannick Natah, Sirajedin Hillard, Cecilia J. Mackie, Ken Sharkey, Keith A. Pittman, Quentin J. |
| description | Oxytocin is released from supraoptic magnocellular neurones and is thought to act at presynaptic receptors to inhibit transmitter
release. We now show that this effect is mediated by endocannabinoids, but that oxytocin nonetheless plays an important role
in endocannabinoid signalling. WIN55,212-2, a cannabinoid receptor agonist, mimicked the action of oxytocin and occluded oxytocin-induced
presynaptic inhibition. The cannabinoid action is at the presynaptic terminal as shown by alteration in paired pulse ratio,
a reduction in miniature EPSC frequency and immunohistochemical localization of CB 1 receptors on presynaptic terminals. AM251, a CB 1 receptor antagonist, blocked both the WIN55,212-2 and the oxytocin-induced presynaptic inhibition of EPSCs. Depolarization
of postsynaptic magnocellular neurones (which contain fatty acid amide hydrolase, a cannabinoid catabolic enzyme) caused a
transient inhibition of EPSCs that could be blocked by both the AM251 and Manning compound, an oxytocin/vasopressin receptor
antagonist. This indicates that somatodendritic peptide release and action on previously identified autoreceptors facilitates
the release of endocannabinoids that act as mediators of presynaptic inhibition. |
| doi_str_mv | 10.1113/jphysiol.2004.066159 |
| format | Article |
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release. We now show that this effect is mediated by endocannabinoids, but that oxytocin nonetheless plays an important role
in endocannabinoid signalling. WIN55,212-2, a cannabinoid receptor agonist, mimicked the action of oxytocin and occluded oxytocin-induced
presynaptic inhibition. The cannabinoid action is at the presynaptic terminal as shown by alteration in paired pulse ratio,
a reduction in miniature EPSC frequency and immunohistochemical localization of CB 1 receptors on presynaptic terminals. AM251, a CB 1 receptor antagonist, blocked both the WIN55,212-2 and the oxytocin-induced presynaptic inhibition of EPSCs. Depolarization
of postsynaptic magnocellular neurones (which contain fatty acid amide hydrolase, a cannabinoid catabolic enzyme) caused a
transient inhibition of EPSCs that could be blocked by both the AM251 and Manning compound, an oxytocin/vasopressin receptor
antagonist. This indicates that somatodendritic peptide release and action on previously identified autoreceptors facilitates
the release of endocannabinoids that act as mediators of presynaptic inhibition.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2004.066159</identifier><identifier>PMID: 15254151</identifier><language>eng</language><publisher>9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society</publisher><subject>Animals ; Autocrine Communication - drug effects ; Autocrine Communication - physiology ; Benzoxazines ; Biochemistry, Molecular Biology ; Brain - drug effects ; Brain - metabolism ; Cannabinoid Receptor Modulators - metabolism ; Dendrites - drug effects ; Dendrites - metabolism ; In Vitro Techniques ; Life Sciences ; Male ; Morpholines - pharmacology ; Naphthalenes - pharmacology ; Neurons, Afferent - drug effects ; Neurons, Afferent - metabolism ; Neurotransmitter Agents - metabolism ; Nifedipine - pharmacology ; Rats ; Rats, Sprague-Dawley ; Research Papers</subject><ispartof>The Journal of physiology, 2004-09, Vol.559 (2), p.611-624</ispartof><rights>2004 The Journal of Physiology © 2004 The Physiological Society</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>The Physiological Society 2004 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5484-b5b2db69aada489561b5a5c0ae2c8074710474bf8ce551666d6cb78fb038edc43</citedby><cites>FETCH-LOGICAL-c5484-b5b2db69aada489561b5a5c0ae2c8074710474bf8ce551666d6cb78fb038edc43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665137/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665137/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15254151$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04125181$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirasawa, Michiru</creatorcontrib><creatorcontrib>Schwab, Yannick</creatorcontrib><creatorcontrib>Natah, Sirajedin</creatorcontrib><creatorcontrib>Hillard, Cecilia J.</creatorcontrib><creatorcontrib>Mackie, Ken</creatorcontrib><creatorcontrib>Sharkey, Keith A.</creatorcontrib><creatorcontrib>Pittman, Quentin J.</creatorcontrib><title>Dendritically released transmitters cooperate via autocrine and retrograde actions to inhibit afferent excitation in rat brain</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Oxytocin is released from supraoptic magnocellular neurones and is thought to act at presynaptic receptors to inhibit transmitter
release. We now show that this effect is mediated by endocannabinoids, but that oxytocin nonetheless plays an important role
in endocannabinoid signalling. WIN55,212-2, a cannabinoid receptor agonist, mimicked the action of oxytocin and occluded oxytocin-induced
presynaptic inhibition. The cannabinoid action is at the presynaptic terminal as shown by alteration in paired pulse ratio,
a reduction in miniature EPSC frequency and immunohistochemical localization of CB 1 receptors on presynaptic terminals. AM251, a CB 1 receptor antagonist, blocked both the WIN55,212-2 and the oxytocin-induced presynaptic inhibition of EPSCs. Depolarization
of postsynaptic magnocellular neurones (which contain fatty acid amide hydrolase, a cannabinoid catabolic enzyme) caused a
transient inhibition of EPSCs that could be blocked by both the AM251 and Manning compound, an oxytocin/vasopressin receptor
antagonist. This indicates that somatodendritic peptide release and action on previously identified autoreceptors facilitates
the release of endocannabinoids that act as mediators of presynaptic inhibition.</description><subject>Animals</subject><subject>Autocrine Communication - drug effects</subject><subject>Autocrine Communication - physiology</subject><subject>Benzoxazines</subject><subject>Biochemistry, Molecular Biology</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Cannabinoid Receptor Modulators - metabolism</subject><subject>Dendrites - drug effects</subject><subject>Dendrites - metabolism</subject><subject>In Vitro Techniques</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Morpholines - pharmacology</subject><subject>Naphthalenes - pharmacology</subject><subject>Neurons, Afferent - drug effects</subject><subject>Neurons, Afferent - metabolism</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Nifedipine - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Research Papers</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkkuP0zAUhSMEYsrAP0DIK0YsWuzEr2yQRsNjQJVgMaytG-em9SiNi-12yIbfjqOU5wZWln3P-Xx9fYriKaMrxlj18na_HaPz_aqklK-olEzU94oF47JeKlVX94sFpWW5rJRgZ8WjGG8pZRWt64fFGROl4EywRfHtNQ5tcMlZ6PuRBOwRIrYkBRjizqWEIRLr_R4DJCRHBwQOydvgBiQwtNmRgt8EaPPWJueHSJInbti6xiUCXYcBh0Twq3UJpnqukcwiTQA3PC4edNBHfHJaz4vPb9_cXF0v1x_fvb-6XC-t4JovG9GUbSNrgBa4roVkjQBhKWBpNVVcMcoVbzptUQgmpWylbZTuGlppbC2vzotXM3d_aHb5JLcUoDf74HYQRuPBmT8rg9uajT-aDBOsUhnwYgZs_7JdX67NdEY5KwXT7Miy9vnpsuC_HDAms3PRYt_DgP4QjZS6UlqX_xQyTStVq4nIZ6ENPsaA3c8WGDVTGsyPNJgpDWZOQ7Y9-_3Vv0yn788CPQvuXI_jf0HNzYdPvJomenEaiNts71xAM4ujtw7TaESWlkZmzHdEG9aV</recordid><startdate>200409</startdate><enddate>200409</enddate><creator>Hirasawa, Michiru</creator><creator>Schwab, Yannick</creator><creator>Natah, Sirajedin</creator><creator>Hillard, Cecilia J.</creator><creator>Mackie, Ken</creator><creator>Sharkey, Keith A.</creator><creator>Pittman, Quentin J.</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Wiley</general><general>Blackwell Science 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>7TK</scope><scope>7X8</scope><scope>1XC</scope><scope>5PM</scope></search><sort><creationdate>200409</creationdate><title>Dendritically released transmitters cooperate via autocrine and retrograde actions to inhibit afferent excitation in rat brain</title><author>Hirasawa, Michiru ; 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release. We now show that this effect is mediated by endocannabinoids, but that oxytocin nonetheless plays an important role
in endocannabinoid signalling. WIN55,212-2, a cannabinoid receptor agonist, mimicked the action of oxytocin and occluded oxytocin-induced
presynaptic inhibition. The cannabinoid action is at the presynaptic terminal as shown by alteration in paired pulse ratio,
a reduction in miniature EPSC frequency and immunohistochemical localization of CB 1 receptors on presynaptic terminals. AM251, a CB 1 receptor antagonist, blocked both the WIN55,212-2 and the oxytocin-induced presynaptic inhibition of EPSCs. Depolarization
of postsynaptic magnocellular neurones (which contain fatty acid amide hydrolase, a cannabinoid catabolic enzyme) caused a
transient inhibition of EPSCs that could be blocked by both the AM251 and Manning compound, an oxytocin/vasopressin receptor
antagonist. This indicates that somatodendritic peptide release and action on previously identified autoreceptors facilitates
the release of endocannabinoids that act as mediators of presynaptic inhibition.</abstract><cop>9600 Garsington Road , Oxford , OX4 2DQ , UK</cop><pub>The Physiological Society</pub><pmid>15254151</pmid><doi>10.1113/jphysiol.2004.066159</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 2004-09, Vol.559 (2), p.611-624 |
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| source | Wiley Free Content; MEDLINE; IngentaConnect Free/Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals Autocrine Communication - drug effects Autocrine Communication - physiology Benzoxazines Biochemistry, Molecular Biology Brain - drug effects Brain - metabolism Cannabinoid Receptor Modulators - metabolism Dendrites - drug effects Dendrites - metabolism In Vitro Techniques Life Sciences Male Morpholines - pharmacology Naphthalenes - pharmacology Neurons, Afferent - drug effects Neurons, Afferent - metabolism Neurotransmitter Agents - metabolism Nifedipine - pharmacology Rats Rats, Sprague-Dawley Research Papers |
| title | Dendritically released transmitters cooperate via autocrine and retrograde actions to inhibit afferent excitation in rat brain |
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