Characterization of a depolarizing dopamine response in a vertebrate neuronal somatic cell hybrid
The physiology and pharmacology of a depolarizing dopamine response was studied in the vertebrate neuronal somatic cell hybrid TCX11. The average resting membrane potential was −50 mV (S.D. = ±7) with a membrane resistance of 40.5 mOhms (S.D. = ±8) as determined from intracellular recordings. Depola...
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| Veröffentlicht in: | Journal of cellular physiology 1977-04, Vol.91 (1), p.103-118 |
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| creator | Myers, Paul R. Livengood, David R. Shain, William |
| description | The physiology and pharmacology of a depolarizing dopamine response was studied in the vertebrate neuronal somatic cell hybrid TCX11. The average resting membrane potential was −50 mV (S.D. = ±7) with a membrane resistance of 40.5 mOhms (S.D. = ±8) as determined from intracellular recordings. Depolarizing current pulses did not elicit an action potential. Cells displayed a linear current‐voltage relationship when artificially depolarized up to +30 mV. Iontophoretically applied dopamine elicited a depolarizing response with a conductance increase and a reversal potential of −15 mV (S.D. = ±4.7). Experiments altering medium ion concentrations demonstrated the conductance increase was to sodium and most likely potassium. The dopamine agonist ET495 (Piribedil) and the analogue epinine mimicked dopamine, while closely related biogenic amines, with the exception of noradrenaline, elicited no response. Apomorphine also elicited a depolarizing response but was much less efficacious than Piribedil. Noradrenaline was less potent than dopamine and appeared to act at the dopamine receptor. Methylation (3‐methoxytyramine) or absence of the 3‐hydroxy group (tyramine) of dopamine resulted in total loss of activity. The dopamine antagonists chlorpromazine, trifluoperazine, promazine, and bulbocapnine reversibly blocked the response to dopamine at medium concentrations less than 5 μM. The adrenergic antagonist phentolamine blocked the response while phenoxybenzamine only reduced the response at higher concentrations. The acetylcholine antagonists α‐bungarotoxin, hexamethonium, and scopolamine did not block the dopamine response. Both d‐tubocurarine and atropine acted as antagonists.
Collectively, these results demonstrate the presence of a receptor on a cultured cell line that is specific for dopamine, mediates a depolarizing and conductance increase response to dopamine, and displays the pharmacology most closely associated with dopamine receptors. |
| doi_str_mv | 10.1002/jcp.1040910111 |
| format | Article |
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Collectively, these results demonstrate the presence of a receptor on a cultured cell line that is specific for dopamine, mediates a depolarizing and conductance increase response to dopamine, and displays the pharmacology most closely associated with dopamine receptors.</description><subject>Acetylcholine - antagonists & inhibitors</subject><subject>Chlorides - metabolism</subject><subject>Dopamine - pharmacology</subject><subject>Dopamine Antagonists</subject><subject>Electric Conductivity</subject><subject>Hybrid Cells - drug effects</subject><subject>Hybrid Cells - physiology</subject><subject>Membrane Potentials - drug effects</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Norepinephrine - pharmacology</subject><subject>Phentolamine - pharmacology</subject><subject>Potassium - metabolism</subject><subject>Receptors, Dopamine</subject><subject>Serotonin - pharmacology</subject><subject>Sodium - metabolism</subject><subject>Temperature</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1977</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1P3DAURS1UaIePLasuvGIXsMdJHC-rqANFo4LESCytF_sFTJM4tTOl01-PURBVV13Zeu_eI_sQcsrZOWdsefFkxnTJmeKMc75HFpwpmeVlsfxAFinAM1Xk_BM5jPGJMaaUEB_JQVWUlagWBOpHCGAmDO4PTM4P1LcUqMXRd5Bmbnig1o_QuwFpwDj6ISJ1Q8r8wjBhE2BCOuA2-AE6Gn2fKIYa7Dr6uGuCs8dkv4Uu4snbeUQ2q6-b-ipb31x-q7-sMyOk5Bm3TWUroaBVjZTCNpAGbS4LvrS2yFu0ADbHvCm5gEqhaK0EZoxpZWO4EkfkbMaOwf_cYpx07-LrM2BAv406_VaJpCMFz-egCT7GgK0eg-sh7DRn-tWoTkb1X6Op8PmNvG16tO_xWWFaq3n97Drc_Qemr-vbf9DZ3HVxwt_vXQg_dCmFLPT990td35d5Ka7v9Eq8APblk-8</recordid><startdate>197704</startdate><enddate>197704</enddate><creator>Myers, Paul R.</creator><creator>Livengood, David R.</creator><creator>Shain, William</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>197704</creationdate><title>Characterization of a depolarizing dopamine response in a vertebrate neuronal somatic cell hybrid</title><author>Myers, Paul R. ; Livengood, David R. ; Shain, William</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3771-1db8d839af9b773dbadb8f47512dd54fedaad4e4b613a89e3fd7a0cccf7bc193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1977</creationdate><topic>Acetylcholine - antagonists & inhibitors</topic><topic>Chlorides - metabolism</topic><topic>Dopamine - pharmacology</topic><topic>Dopamine Antagonists</topic><topic>Electric Conductivity</topic><topic>Hybrid Cells - drug effects</topic><topic>Hybrid Cells - physiology</topic><topic>Membrane Potentials - drug effects</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Norepinephrine - pharmacology</topic><topic>Phentolamine - pharmacology</topic><topic>Potassium - metabolism</topic><topic>Receptors, Dopamine</topic><topic>Serotonin - pharmacology</topic><topic>Sodium - metabolism</topic><topic>Temperature</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Myers, Paul R.</creatorcontrib><creatorcontrib>Livengood, David R.</creatorcontrib><creatorcontrib>Shain, William</creatorcontrib><collection>Istex</collection><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>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Myers, Paul R.</au><au>Livengood, David R.</au><au>Shain, William</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of a depolarizing dopamine response in a vertebrate neuronal somatic cell hybrid</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J. Cell. Physiol</addtitle><date>1977-04</date><risdate>1977</risdate><volume>91</volume><issue>1</issue><spage>103</spage><epage>118</epage><pages>103-118</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>The physiology and pharmacology of a depolarizing dopamine response was studied in the vertebrate neuronal somatic cell hybrid TCX11. The average resting membrane potential was −50 mV (S.D. = ±7) with a membrane resistance of 40.5 mOhms (S.D. = ±8) as determined from intracellular recordings. Depolarizing current pulses did not elicit an action potential. Cells displayed a linear current‐voltage relationship when artificially depolarized up to +30 mV. Iontophoretically applied dopamine elicited a depolarizing response with a conductance increase and a reversal potential of −15 mV (S.D. = ±4.7). Experiments altering medium ion concentrations demonstrated the conductance increase was to sodium and most likely potassium. The dopamine agonist ET495 (Piribedil) and the analogue epinine mimicked dopamine, while closely related biogenic amines, with the exception of noradrenaline, elicited no response. Apomorphine also elicited a depolarizing response but was much less efficacious than Piribedil. Noradrenaline was less potent than dopamine and appeared to act at the dopamine receptor. Methylation (3‐methoxytyramine) or absence of the 3‐hydroxy group (tyramine) of dopamine resulted in total loss of activity. The dopamine antagonists chlorpromazine, trifluoperazine, promazine, and bulbocapnine reversibly blocked the response to dopamine at medium concentrations less than 5 μM. The adrenergic antagonist phentolamine blocked the response while phenoxybenzamine only reduced the response at higher concentrations. The acetylcholine antagonists α‐bungarotoxin, hexamethonium, and scopolamine did not block the dopamine response. Both d‐tubocurarine and atropine acted as antagonists.
Collectively, these results demonstrate the presence of a receptor on a cultured cell line that is specific for dopamine, mediates a depolarizing and conductance increase response to dopamine, and displays the pharmacology most closely associated with dopamine receptors.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>856838</pmid><doi>10.1002/jcp.1040910111</doi><tpages>16</tpages></addata></record> |
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| subjects | Acetylcholine - antagonists & inhibitors Chlorides - metabolism Dopamine - pharmacology Dopamine Antagonists Electric Conductivity Hybrid Cells - drug effects Hybrid Cells - physiology Membrane Potentials - drug effects Neurons - drug effects Neurons - physiology Norepinephrine - pharmacology Phentolamine - pharmacology Potassium - metabolism Receptors, Dopamine Serotonin - pharmacology Sodium - metabolism Temperature |
| title | Characterization of a depolarizing dopamine response in a vertebrate neuronal somatic cell hybrid |
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