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Transient gain adjustment in the inferior colliculus is serotonin- and calcium-dependent
In the inferior colliculus (IC), a brief period of acoustic conditioning can transiently enhance evoked discharge rate. The cellular basis of this phenomenon was assessed with whole cell current-clamp recordings in a gerbil IC brain slice preparation. The current needed to elicit a single action pot...
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Published in: | Hearing research 2009-05, Vol.251 (1), p.39-50 |
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description | In the inferior colliculus (IC), a brief period of acoustic conditioning can transiently enhance evoked discharge rate. The cellular basis of this phenomenon was assessed with whole cell current-clamp recordings in a gerbil IC brain slice preparation. The current needed to elicit a single action potential was first established for each neuron. A 5s synaptic stimulus train was delivered to the lateral lemniscus (LL), and followed immediately by the initial current pulse to assess a change in postsynaptic gain. The majority of IC neurons (66%) displayed an increase in current-evoked action potentials (Positive Gain). Despite the blockade of ionotropic glutamate receptors, this effect was correlated with membrane depolarization that occurred during the synaptic train. The postsynaptic mechanism for positive gain was examined by selective blockade of specific neurotransmitter receptors. Gain in action potentials was enhanced by antagonists of metabotropic glutamate, acetylcholine, GABA
A and glycine receptors. In contrast, the gain was blocked or reduced by an antagonist to ionotropic serotonin receptors (5-HT
3R). Blocking voltage-activated calcium channels with verapamil also reduced the effect. These results suggest that 5-HT
3R activation, coupled with increased intracellular calcium, can transiently alter postsynaptic excitability in IC neurons. |
doi_str_mv | 10.1016/j.heares.2009.02.003 |
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A and glycine receptors. In contrast, the gain was blocked or reduced by an antagonist to ionotropic serotonin receptors (5-HT
3R). Blocking voltage-activated calcium channels with verapamil also reduced the effect. These results suggest that 5-HT
3R activation, coupled with increased intracellular calcium, can transiently alter postsynaptic excitability in IC neurons.</description><identifier>ISSN: 0378-5955</identifier><identifier>EISSN: 1878-5891</identifier><identifier>DOI: 10.1016/j.heares.2009.02.003</identifier><identifier>PMID: 19232535</identifier><identifier>CODEN: HERED3</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>5-HT 3 receptor ; Action Potentials - drug effects ; Action Potentials - physiology ; Anesthetics. Neuromuscular blocking agents ; Animals ; Bicuculline - pharmacology ; Biological and medical sciences ; Calcium - physiology ; Calcium Channel Blockers - pharmacology ; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation ; Excitatory Amino Acid Antagonists - pharmacology ; Fundamental and applied biological sciences. Psychology ; GABA Antagonists - pharmacology ; GABA-A Receptor Antagonists ; Gerbillinae ; Inferior Colliculi - cytology ; Inferior Colliculi - physiology ; Inferior colliculus ; Medical sciences ; Neurons - physiology ; Neuropharmacology ; Organ Culture Techniques ; Patch-Clamp Techniques ; Pharmacology. Drug treatments ; Quinoxalines - pharmacology ; Receptors, GABA-A - physiology ; Receptors, Glutamate - physiology ; Receptors, Glycine - antagonists & inhibitors ; Receptors, Glycine - physiology ; Receptors, Serotonin, 5-HT3 - physiology ; Serotonin ; Serotonin - physiology ; Serotonin 5-HT3 Receptor Antagonists ; Serotonin Antagonists - pharmacology ; Synaptic plasticity ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>Hearing research, 2009-05, Vol.251 (1), p.39-50</ispartof><rights>2009 Elsevier B.V.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c522t-6564727df4753bb72ea16e6362a47ac4d869b6a2044f6449a9a352946ed464c73</citedby><cites>FETCH-LOGICAL-c522t-6564727df4753bb72ea16e6362a47ac4d869b6a2044f6449a9a352946ed464c73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21452319$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19232535$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miko, Ilona J.</creatorcontrib><creatorcontrib>Sanes, Dan H.</creatorcontrib><title>Transient gain adjustment in the inferior colliculus is serotonin- and calcium-dependent</title><title>Hearing research</title><addtitle>Hear Res</addtitle><description>In the inferior colliculus (IC), a brief period of acoustic conditioning can transiently enhance evoked discharge rate. The cellular basis of this phenomenon was assessed with whole cell current-clamp recordings in a gerbil IC brain slice preparation. The current needed to elicit a single action potential was first established for each neuron. A 5s synaptic stimulus train was delivered to the lateral lemniscus (LL), and followed immediately by the initial current pulse to assess a change in postsynaptic gain. The majority of IC neurons (66%) displayed an increase in current-evoked action potentials (Positive Gain). Despite the blockade of ionotropic glutamate receptors, this effect was correlated with membrane depolarization that occurred during the synaptic train. The postsynaptic mechanism for positive gain was examined by selective blockade of specific neurotransmitter receptors. Gain in action potentials was enhanced by antagonists of metabotropic glutamate, acetylcholine, GABA
A and glycine receptors. In contrast, the gain was blocked or reduced by an antagonist to ionotropic serotonin receptors (5-HT
3R). Blocking voltage-activated calcium channels with verapamil also reduced the effect. These results suggest that 5-HT
3R activation, coupled with increased intracellular calcium, can transiently alter postsynaptic excitability in IC neurons.</description><subject>5-HT 3 receptor</subject><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Anesthetics. Neuromuscular blocking agents</subject><subject>Animals</subject><subject>Bicuculline - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Calcium - physiology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GABA Antagonists - pharmacology</subject><subject>GABA-A Receptor Antagonists</subject><subject>Gerbillinae</subject><subject>Inferior Colliculi - cytology</subject><subject>Inferior Colliculi - physiology</subject><subject>Inferior colliculus</subject><subject>Medical sciences</subject><subject>Neurons - physiology</subject><subject>Neuropharmacology</subject><subject>Organ Culture Techniques</subject><subject>Patch-Clamp Techniques</subject><subject>Pharmacology. Drug treatments</subject><subject>Quinoxalines - pharmacology</subject><subject>Receptors, GABA-A - physiology</subject><subject>Receptors, Glutamate - physiology</subject><subject>Receptors, Glycine - antagonists & inhibitors</subject><subject>Receptors, Glycine - physiology</subject><subject>Receptors, Serotonin, 5-HT3 - physiology</subject><subject>Serotonin</subject><subject>Serotonin - physiology</subject><subject>Serotonin 5-HT3 Receptor Antagonists</subject><subject>Serotonin Antagonists - pharmacology</subject><subject>Synaptic plasticity</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0378-5955</issn><issn>1878-5891</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNqFkUtr3DAUhUVpaKZp_0Ep3rQ7O3rL2hRK6AsC2STQndBI1xkNtjSV7ED-fWVmSNpNu7q66Jyrq_Mh9I7gjmAiL_fdDmyG0lGMdYdphzF7gTakV30rek1eog1m61kLcY5el7LHmAjG6St0TjRlVDCxQT9vs40lQJybextiY_1-KfO09rWbd1DLADmk3Lg0jsEt41KaUJoCOc0phtg2NvrG2dGFZWo9HCD6an-DzgY7Fnh7qhfo7uuX26vv7fXNtx9Xn69bJyidWykkV1T5gSvBtltFwRIJkklqubKO-17qrbQUcz5IzrXVlgmquQTPJXeKXaBPx7mHZTuBd_XpbEdzyGGy-dEkG8zfNzHszH16MFQqrDmtAz6eBuT0a4EymykUB-NoI6SlGKkIk1rJ_worh54zsgr5UehyKiXD8LQNwWZlZ_bmyG71aIOpqeyq7f2fP3k2nWBVwYeTwJaa91DJuVCedJRwQRnRz5FAzf0hQDbFVcIOfMjgZuNT-PcmvwE_3rqk</recordid><startdate>20090501</startdate><enddate>20090501</enddate><creator>Miko, Ilona J.</creator><creator>Sanes, Dan H.</creator><general>Elsevier B.V</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>7QP</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090501</creationdate><title>Transient gain adjustment in the inferior colliculus is serotonin- and calcium-dependent</title><author>Miko, Ilona J. ; Sanes, Dan H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c522t-6564727df4753bb72ea16e6362a47ac4d869b6a2044f6449a9a352946ed464c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>5-HT 3 receptor</topic><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Anesthetics. Neuromuscular blocking agents</topic><topic>Animals</topic><topic>Bicuculline - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Calcium - physiology</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GABA Antagonists - pharmacology</topic><topic>GABA-A Receptor Antagonists</topic><topic>Gerbillinae</topic><topic>Inferior Colliculi - cytology</topic><topic>Inferior Colliculi - physiology</topic><topic>Inferior colliculus</topic><topic>Medical sciences</topic><topic>Neurons - physiology</topic><topic>Neuropharmacology</topic><topic>Organ Culture Techniques</topic><topic>Patch-Clamp Techniques</topic><topic>Pharmacology. Drug treatments</topic><topic>Quinoxalines - pharmacology</topic><topic>Receptors, GABA-A - physiology</topic><topic>Receptors, Glutamate - physiology</topic><topic>Receptors, Glycine - antagonists & inhibitors</topic><topic>Receptors, Glycine - physiology</topic><topic>Receptors, Serotonin, 5-HT3 - physiology</topic><topic>Serotonin</topic><topic>Serotonin - physiology</topic><topic>Serotonin 5-HT3 Receptor Antagonists</topic><topic>Serotonin Antagonists - pharmacology</topic><topic>Synaptic plasticity</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miko, Ilona J.</creatorcontrib><creatorcontrib>Sanes, Dan H.</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Hearing research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miko, Ilona J.</au><au>Sanes, Dan H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transient gain adjustment in the inferior colliculus is serotonin- and calcium-dependent</atitle><jtitle>Hearing research</jtitle><addtitle>Hear Res</addtitle><date>2009-05-01</date><risdate>2009</risdate><volume>251</volume><issue>1</issue><spage>39</spage><epage>50</epage><pages>39-50</pages><issn>0378-5955</issn><eissn>1878-5891</eissn><coden>HERED3</coden><abstract>In the inferior colliculus (IC), a brief period of acoustic conditioning can transiently enhance evoked discharge rate. The cellular basis of this phenomenon was assessed with whole cell current-clamp recordings in a gerbil IC brain slice preparation. The current needed to elicit a single action potential was first established for each neuron. A 5s synaptic stimulus train was delivered to the lateral lemniscus (LL), and followed immediately by the initial current pulse to assess a change in postsynaptic gain. The majority of IC neurons (66%) displayed an increase in current-evoked action potentials (Positive Gain). Despite the blockade of ionotropic glutamate receptors, this effect was correlated with membrane depolarization that occurred during the synaptic train. The postsynaptic mechanism for positive gain was examined by selective blockade of specific neurotransmitter receptors. Gain in action potentials was enhanced by antagonists of metabotropic glutamate, acetylcholine, GABA
A and glycine receptors. In contrast, the gain was blocked or reduced by an antagonist to ionotropic serotonin receptors (5-HT
3R). Blocking voltage-activated calcium channels with verapamil also reduced the effect. These results suggest that 5-HT
3R activation, coupled with increased intracellular calcium, can transiently alter postsynaptic excitability in IC neurons.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>19232535</pmid><doi>10.1016/j.heares.2009.02.003</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 5-HT 3 receptor Action Potentials - drug effects Action Potentials - physiology Anesthetics. Neuromuscular blocking agents Animals Bicuculline - pharmacology Biological and medical sciences Calcium - physiology Calcium Channel Blockers - pharmacology Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation Excitatory Amino Acid Antagonists - pharmacology Fundamental and applied biological sciences. Psychology GABA Antagonists - pharmacology GABA-A Receptor Antagonists Gerbillinae Inferior Colliculi - cytology Inferior Colliculi - physiology Inferior colliculus Medical sciences Neurons - physiology Neuropharmacology Organ Culture Techniques Patch-Clamp Techniques Pharmacology. Drug treatments Quinoxalines - pharmacology Receptors, GABA-A - physiology Receptors, Glutamate - physiology Receptors, Glycine - antagonists & inhibitors Receptors, Glycine - physiology Receptors, Serotonin, 5-HT3 - physiology Serotonin Serotonin - physiology Serotonin 5-HT3 Receptor Antagonists Serotonin Antagonists - pharmacology Synaptic plasticity Synaptic Transmission - drug effects Synaptic Transmission - physiology Vertebrates: nervous system and sense organs |
title | Transient gain adjustment in the inferior colliculus is serotonin- and calcium-dependent |
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