Differential cannabinoid-induced electrophysiological effects in rat ventral tegmentum
Cannabinoids are known to exert mainly excitatory effects on dopaminergic cells of the ventral tegmental area (VTA). We have utilized an in vivo multiple-single unit electrophysiological approach to assess different neuronal contributions that may ultimately lead to excitation in this area. Baseline...
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| Veröffentlicht in: | Neuropharmacology 2003-04, Vol.44 (5), p.633-641 |
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| creator | Cheer, J.F. Kendall, D.A. Mason, R. Marsden, C.A. |
| description | Cannabinoids are known to exert mainly excitatory effects on dopaminergic cells of the ventral tegmental area (VTA). We have utilized an in vivo multiple-single unit electrophysiological approach to assess different neuronal contributions that may ultimately lead to excitation in this area. Baseline neuron recordings, using low impedance microwires, showed a variety of waveforms with a wide range of durations (0.8–3.2 ms). In the first experiment systemic injection of the potent cannabinoid agonist HU210 (100 μg/kg, i.p.) led predominantly to an increase in firing rate (~214%, compared to pre-drug) in slowly firing cells with broad action potentials, possibly driven by a majority of presumed dopaminergic neurons (
n = 31). However, the firing rate of some units was either unaffected ( |
| doi_str_mv | 10.1016/S0028-3908(03)00029-7 |
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n = 31). However, the firing rate of some units was either unaffected (<25%,
n = 9) or even decreased (~67%,
n = 9) following cannabinoid injection concomitantly with excitation. Apomorphine (75 μg/kg, i.p.) injected following HU210 produced a marked inhibition of both responses (~76%) in 39 out of 49 cells. The second group of animals was treated with the CB
1 receptor antagonist SR141716A (1 mg/kg, i.p.), which had no effect when injected alone but prevented all HU210-evoked changes in firing rate suggesting that cannabinoid receptors mediated the observed responses (
n = 39). Taken together, the present results suggest that the observed actions of cannabinoids may involve complex neurotransmitter interactions leading to differential effects on dopamine release. These heterogeneous neuronal responses are likely to underly the behavioural discrepancies reported in animal models of cannabinoid reinforcement.</description><identifier>ISSN: 0028-3908</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/S0028-3908(03)00029-7</identifier><identifier>PMID: 12668049</identifier><identifier>CODEN: NEPHBW</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Action Potentials - drug effects ; Action Potentials - physiology ; Animals ; Biological and medical sciences ; Cannabinoids - pharmacology ; Dopamine ; Dronabinol - analogs & derivatives ; Dronabinol - pharmacology ; Electrophysiology ; Ensemble recording ; HU210 ; Male ; Medical sciences ; Piperidines - pharmacology ; Pyrazoles - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Cannabinoid ; Receptors, Drug - agonists ; Receptors, Drug - antagonists & inhibitors ; Receptors, Drug - physiology ; Reinforcement ; Rimonabant ; Ventral Tegmental Area - drug effects ; Ventral Tegmental Area - physiology ; VTA</subject><ispartof>Neuropharmacology, 2003-04, Vol.44 (5), p.633-641</ispartof><rights>2003 Elsevier Science Ltd</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-615986503b46a84f75ab0b853493bfb96fcc5c078db80c970923bcaee74d44893</citedby><cites>FETCH-LOGICAL-c474t-615986503b46a84f75ab0b853493bfb96fcc5c078db80c970923bcaee74d44893</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0028-3908(03)00029-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14642069$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12668049$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheer, J.F.</creatorcontrib><creatorcontrib>Kendall, D.A.</creatorcontrib><creatorcontrib>Mason, R.</creatorcontrib><creatorcontrib>Marsden, C.A.</creatorcontrib><title>Differential cannabinoid-induced electrophysiological effects in rat ventral tegmentum</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>Cannabinoids are known to exert mainly excitatory effects on dopaminergic cells of the ventral tegmental area (VTA). We have utilized an in vivo multiple-single unit electrophysiological approach to assess different neuronal contributions that may ultimately lead to excitation in this area. Baseline neuron recordings, using low impedance microwires, showed a variety of waveforms with a wide range of durations (0.8–3.2 ms). In the first experiment systemic injection of the potent cannabinoid agonist HU210 (100 μg/kg, i.p.) led predominantly to an increase in firing rate (~214%, compared to pre-drug) in slowly firing cells with broad action potentials, possibly driven by a majority of presumed dopaminergic neurons (
n = 31). However, the firing rate of some units was either unaffected (<25%,
n = 9) or even decreased (~67%,
n = 9) following cannabinoid injection concomitantly with excitation. Apomorphine (75 μg/kg, i.p.) injected following HU210 produced a marked inhibition of both responses (~76%) in 39 out of 49 cells. The second group of animals was treated with the CB
1 receptor antagonist SR141716A (1 mg/kg, i.p.), which had no effect when injected alone but prevented all HU210-evoked changes in firing rate suggesting that cannabinoid receptors mediated the observed responses (
n = 39). Taken together, the present results suggest that the observed actions of cannabinoids may involve complex neurotransmitter interactions leading to differential effects on dopamine release. These heterogeneous neuronal responses are likely to underly the behavioural discrepancies reported in animal models of cannabinoid reinforcement.</description><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cannabinoids - pharmacology</subject><subject>Dopamine</subject><subject>Dronabinol - analogs & derivatives</subject><subject>Dronabinol - pharmacology</subject><subject>Electrophysiology</subject><subject>Ensemble recording</subject><subject>HU210</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Piperidines - pharmacology</subject><subject>Pyrazoles - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Cannabinoid</subject><subject>Receptors, Drug - agonists</subject><subject>Receptors, Drug - antagonists & inhibitors</subject><subject>Receptors, Drug - physiology</subject><subject>Reinforcement</subject><subject>Rimonabant</subject><subject>Ventral Tegmental Area - drug effects</subject><subject>Ventral Tegmental Area - physiology</subject><subject>VTA</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1P3DAQhi3UCrZbfgJVLkXtIXQcO_44IURbioTUQz-ulu1MqFHiLHaCxL-vl13BkZPt0fN6Rs8QckLhjAIVX34BNKpmGtQnYJ-hvHQtD8iKKslqCYK_Iatn5Ii8y_muQFxRdUiOaCOEAq5X5O_X0PeYMM7BDpW3MVoX4hS6OsRu8dhVOKCf07T595jDNEy3wRcQS8jPuQqxSnauHko-lfKMt2O5LuN78ra3Q8bj_bkmf75_-335o775eXV9eXFTey75XAvaaiVaYI4Lq3gvW-vAqZZxzVzvtOi9bz1I1TkFXkvQDXPeIkreca40W5PT3b-bNN0vmGczhuxxGGzEaclGMsqE4K-DRVvDBOcFbHegT1POCXuzSWG06dFQMFvz5sm82Wo1wMyT-dJnTT7sGyxuxO4ltVddgI97wOaisE82-pBfOC54A2LLne84LN4eAiaTfcBYVhFScW66Kbwyyn8lnaCL</recordid><startdate>20030401</startdate><enddate>20030401</enddate><creator>Cheer, J.F.</creator><creator>Kendall, D.A.</creator><creator>Mason, R.</creator><creator>Marsden, C.A.</creator><general>Elsevier Ltd</general><general>Elsevier</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20030401</creationdate><title>Differential cannabinoid-induced electrophysiological effects in rat ventral tegmentum</title><author>Cheer, J.F. ; Kendall, D.A. ; Mason, R. ; Marsden, C.A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-615986503b46a84f75ab0b853493bfb96fcc5c078db80c970923bcaee74d44893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cannabinoids - pharmacology</topic><topic>Dopamine</topic><topic>Dronabinol - analogs & derivatives</topic><topic>Dronabinol - pharmacology</topic><topic>Electrophysiology</topic><topic>Ensemble recording</topic><topic>HU210</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Piperidines - pharmacology</topic><topic>Pyrazoles - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Cannabinoid</topic><topic>Receptors, Drug - agonists</topic><topic>Receptors, Drug - antagonists & inhibitors</topic><topic>Receptors, Drug - physiology</topic><topic>Reinforcement</topic><topic>Rimonabant</topic><topic>Ventral Tegmental Area - drug effects</topic><topic>Ventral Tegmental Area - physiology</topic><topic>VTA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheer, J.F.</creatorcontrib><creatorcontrib>Kendall, D.A.</creatorcontrib><creatorcontrib>Mason, R.</creatorcontrib><creatorcontrib>Marsden, C.A.</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheer, J.F.</au><au>Kendall, D.A.</au><au>Mason, R.</au><au>Marsden, C.A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential cannabinoid-induced electrophysiological effects in rat ventral tegmentum</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>2003-04-01</date><risdate>2003</risdate><volume>44</volume><issue>5</issue><spage>633</spage><epage>641</epage><pages>633-641</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><coden>NEPHBW</coden><abstract>Cannabinoids are known to exert mainly excitatory effects on dopaminergic cells of the ventral tegmental area (VTA). We have utilized an in vivo multiple-single unit electrophysiological approach to assess different neuronal contributions that may ultimately lead to excitation in this area. Baseline neuron recordings, using low impedance microwires, showed a variety of waveforms with a wide range of durations (0.8–3.2 ms). In the first experiment systemic injection of the potent cannabinoid agonist HU210 (100 μg/kg, i.p.) led predominantly to an increase in firing rate (~214%, compared to pre-drug) in slowly firing cells with broad action potentials, possibly driven by a majority of presumed dopaminergic neurons (
n = 31). However, the firing rate of some units was either unaffected (<25%,
n = 9) or even decreased (~67%,
n = 9) following cannabinoid injection concomitantly with excitation. Apomorphine (75 μg/kg, i.p.) injected following HU210 produced a marked inhibition of both responses (~76%) in 39 out of 49 cells. The second group of animals was treated with the CB
1 receptor antagonist SR141716A (1 mg/kg, i.p.), which had no effect when injected alone but prevented all HU210-evoked changes in firing rate suggesting that cannabinoid receptors mediated the observed responses (
n = 39). Taken together, the present results suggest that the observed actions of cannabinoids may involve complex neurotransmitter interactions leading to differential effects on dopamine release. These heterogeneous neuronal responses are likely to underly the behavioural discrepancies reported in animal models of cannabinoid reinforcement.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>12668049</pmid><doi>10.1016/S0028-3908(03)00029-7</doi><tpages>9</tpages></addata></record> |
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| subjects | Action Potentials - drug effects Action Potentials - physiology Animals Biological and medical sciences Cannabinoids - pharmacology Dopamine Dronabinol - analogs & derivatives Dronabinol - pharmacology Electrophysiology Ensemble recording HU210 Male Medical sciences Piperidines - pharmacology Pyrazoles - pharmacology Rats Rats, Sprague-Dawley Receptors, Cannabinoid Receptors, Drug - agonists Receptors, Drug - antagonists & inhibitors Receptors, Drug - physiology Reinforcement Rimonabant Ventral Tegmental Area - drug effects Ventral Tegmental Area - physiology VTA |
| title | Differential cannabinoid-induced electrophysiological effects in rat ventral tegmentum |
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