Opioid inhibition of GABA release from presynaptic terminals of rat hippocampal interneurons
Opiates and the opioid peptide enkephalin can cause indirect excitation of principal cortical neurons by reducing inhibitory synaptic transmission mediated by GABAergic interneurons. The mechanism by which opioids mediate these effects on interneurons is unknown, but enkephalin hyperpolarizes the so...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 1992, Vol.9 (2), p.325-335 |
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| creator | Cohen, Gal A. Doze, Van A. Madison, Daniel V. |
| description | Opiates and the opioid peptide enkephalin can cause indirect excitation of principal cortical neurons by reducing inhibitory synaptic transmission mediated by GABAergic interneurons. The mechanism by which opioids mediate these effects on interneurons is unknown, but enkephalin hyperpolarizes the somatic membrane potential of a variety of neurons in the brain, including hippocampal interneurons. We now report a new, more direct mechanism for the opioid-mediated reduction in synaptic inhibition. The enkephalin analog
d-Ala
2-Met
5-enkeph-alinamide (DALA) decreases the frequency of miniature, action potential-independent, spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) without causing a change in their amplitude. Thus, we conclude that DALA inhibits the action potential—independent release of GABA through a direct action on interneuronal synaptic terminals. In contrast, DALA reduces the amplitude of action potential—evoked, GABA-mediated IPSCs, as well as decreases their frequency. This suggests that the opioid-mediated inhibition of non—action potential—dependent GABA release reveals a mechanism that contributes to reducing action potential—evoked GABA release, thereby decreasing synaptic inhibition. |
| doi_str_mv | 10.1016/0896-6273(92)90171-9 |
| format | Article |
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d-Ala
2-Met
5-enkeph-alinamide (DALA) decreases the frequency of miniature, action potential-independent, spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) without causing a change in their amplitude. Thus, we conclude that DALA inhibits the action potential—independent release of GABA through a direct action on interneuronal synaptic terminals. In contrast, DALA reduces the amplitude of action potential—evoked, GABA-mediated IPSCs, as well as decreases their frequency. This suggests that the opioid-mediated inhibition of non—action potential—dependent GABA release reveals a mechanism that contributes to reducing action potential—evoked GABA release, thereby decreasing synaptic inhibition.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/0896-6273(92)90171-9</identifier><identifier>PMID: 1497896</identifier><identifier>CODEN: NERNET</identifier><language>eng</language><publisher>Cambridge, MA: Elsevier Inc</publisher><subject>Action Potentials - drug effects ; Animals ; Biological and medical sciences ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Electric Conductivity ; Electric Stimulation ; Enkephalin, Methionine - analogs & derivatives ; Enkephalin, Methionine - pharmacology ; Fundamental and applied biological sciences. Psychology ; gamma-Aminobutyric Acid - metabolism ; Hippocampus - cytology ; Hippocampus - physiology ; Interneurons - physiology ; Male ; Molecular Sequence Data ; Naloxone - pharmacology ; Rats ; Rats, Inbred Strains ; Synapses - physiology ; Tetrodotoxin - pharmacology ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuron (Cambridge, Mass.), 1992, Vol.9 (2), p.325-335</ispartof><rights>1992</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c537t-5eff31c9a6d45cc318038f7cf77ec84d6f287a648e7e78e6372dbdf4f8939b563</citedby><cites>FETCH-LOGICAL-c537t-5eff31c9a6d45cc318038f7cf77ec84d6f287a648e7e78e6372dbdf4f8939b563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0896627392901719$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4338410$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1497896$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cohen, Gal A.</creatorcontrib><creatorcontrib>Doze, Van A.</creatorcontrib><creatorcontrib>Madison, Daniel V.</creatorcontrib><title>Opioid inhibition of GABA release from presynaptic terminals of rat hippocampal interneurons</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>Opiates and the opioid peptide enkephalin can cause indirect excitation of principal cortical neurons by reducing inhibitory synaptic transmission mediated by GABAergic interneurons. The mechanism by which opioids mediate these effects on interneurons is unknown, but enkephalin hyperpolarizes the somatic membrane potential of a variety of neurons in the brain, including hippocampal interneurons. We now report a new, more direct mechanism for the opioid-mediated reduction in synaptic inhibition. The enkephalin analog
d-Ala
2-Met
5-enkeph-alinamide (DALA) decreases the frequency of miniature, action potential-independent, spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) without causing a change in their amplitude. Thus, we conclude that DALA inhibits the action potential—independent release of GABA through a direct action on interneuronal synaptic terminals. In contrast, DALA reduces the amplitude of action potential—evoked, GABA-mediated IPSCs, as well as decreases their frequency. This suggests that the opioid-mediated inhibition of non—action potential—dependent GABA release reveals a mechanism that contributes to reducing action potential—evoked GABA release, thereby decreasing synaptic inhibition.</description><subject>Action Potentials - drug effects</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Electric Conductivity</subject><subject>Electric Stimulation</subject><subject>Enkephalin, Methionine - analogs & derivatives</subject><subject>Enkephalin, Methionine - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>gamma-Aminobutyric Acid - metabolism</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - physiology</subject><subject>Interneurons - physiology</subject><subject>Male</subject><subject>Molecular Sequence Data</subject><subject>Naloxone - pharmacology</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Synapses - physiology</subject><subject>Tetrodotoxin - pharmacology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLJDEUhYM4aPv4Bwq1ENFFjUkllcdG6BF1Bhp6M-6EkE7dYKQqKZNqwX8_6elGd67u4nzncPkQOiP4J8GE32CpeM0bQa9Uc60wEaRWe2hGsBI1I0rto9kncoiOcn7FmLBWkQN0QJgSJZuh5-Xoo-8qH178yk8-hiq66nH-a14l6MFkqFyKQzUmyB_BjJO31QRp8MH0eYMmM1UvfhyjNcNo-jJU4gDrFEM-QT9cweB0d4_R08P937vf9WL5-OduvqhtS8VUt-AcJVYZ3rHWWkokptIJ64QAK1nHXSOF4UyCACGBU9F0q84xJxVVq5bTY3S53R1TfFtDnvTgs4W-NwHiOmvCGZaUtQVkW9CmmHMCp8fkB5M-NMF6I1VvjOmNMa0a_V-qVqV2vttfrwbovkpbiyW_2OUmW9O7ZIL1-RNjlEpGcMFutxgUF-8eks7WQ7DQ-QR20l303__xD1UTlBw</recordid><startdate>1992</startdate><enddate>1992</enddate><creator>Cohen, Gal A.</creator><creator>Doze, Van A.</creator><creator>Madison, Daniel V.</creator><general>Elsevier Inc</general><general>Cell Press</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></search><sort><creationdate>1992</creationdate><title>Opioid inhibition of GABA release from presynaptic terminals of rat hippocampal interneurons</title><author>Cohen, Gal A. ; Doze, Van A. ; Madison, Daniel V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c537t-5eff31c9a6d45cc318038f7cf77ec84d6f287a648e7e78e6372dbdf4f8939b563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Action Potentials - drug effects</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Electric Conductivity</topic><topic>Electric Stimulation</topic><topic>Enkephalin, Methionine - analogs & derivatives</topic><topic>Enkephalin, Methionine - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>gamma-Aminobutyric Acid - metabolism</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - physiology</topic><topic>Interneurons - physiology</topic><topic>Male</topic><topic>Molecular Sequence Data</topic><topic>Naloxone - pharmacology</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Synapses - physiology</topic><topic>Tetrodotoxin - pharmacology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cohen, Gal A.</creatorcontrib><creatorcontrib>Doze, Van A.</creatorcontrib><creatorcontrib>Madison, Daniel V.</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><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cohen, Gal A.</au><au>Doze, Van A.</au><au>Madison, Daniel V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Opioid inhibition of GABA release from presynaptic terminals of rat hippocampal interneurons</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>1992</date><risdate>1992</risdate><volume>9</volume><issue>2</issue><spage>325</spage><epage>335</epage><pages>325-335</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><coden>NERNET</coden><abstract>Opiates and the opioid peptide enkephalin can cause indirect excitation of principal cortical neurons by reducing inhibitory synaptic transmission mediated by GABAergic interneurons. The mechanism by which opioids mediate these effects on interneurons is unknown, but enkephalin hyperpolarizes the somatic membrane potential of a variety of neurons in the brain, including hippocampal interneurons. We now report a new, more direct mechanism for the opioid-mediated reduction in synaptic inhibition. The enkephalin analog
d-Ala
2-Met
5-enkeph-alinamide (DALA) decreases the frequency of miniature, action potential-independent, spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) without causing a change in their amplitude. Thus, we conclude that DALA inhibits the action potential—independent release of GABA through a direct action on interneuronal synaptic terminals. In contrast, DALA reduces the amplitude of action potential—evoked, GABA-mediated IPSCs, as well as decreases their frequency. This suggests that the opioid-mediated inhibition of non—action potential—dependent GABA release reveals a mechanism that contributes to reducing action potential—evoked GABA release, thereby decreasing synaptic inhibition.</abstract><cop>Cambridge, MA</cop><pub>Elsevier Inc</pub><pmid>1497896</pmid><doi>10.1016/0896-6273(92)90171-9</doi><tpages>11</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Action Potentials - drug effects Animals Biological and medical sciences Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Electric Conductivity Electric Stimulation Enkephalin, Methionine - analogs & derivatives Enkephalin, Methionine - pharmacology Fundamental and applied biological sciences. Psychology gamma-Aminobutyric Acid - metabolism Hippocampus - cytology Hippocampus - physiology Interneurons - physiology Male Molecular Sequence Data Naloxone - pharmacology Rats Rats, Inbred Strains Synapses - physiology Tetrodotoxin - pharmacology Vertebrates: nervous system and sense organs |
| title | Opioid inhibition of GABA release from presynaptic terminals of rat hippocampal interneurons |
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