Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus
Neurons in the ventral partition of the medial geniculate body are able to fire high-threshold Ca 2+-spikes. The neurons normally discharge such spikes on low-threshold Ca 2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold C...
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| Veröffentlicht in: | Neuroscience 1998-04, Vol.83 (4), p.1063-1073 |
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| description | Neurons in the ventral partition of the medial geniculate body are able to fire high-threshold Ca
2+-spikes. The neurons normally discharge such spikes on low-threshold Ca
2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca
2+-spikes, using whole-cell recording techniques in a slice preparation of rat thalamus. A subthreshold (persistent) Na
+-conductance amplified depolarizing inputs, enhancing membrane excitability in the tonic firing mode and amplifying the low-threshold Ca
2+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold Ca
2+-spike firing. A slowly inactivating K
+ conductance, sensitive to blockade with 4-aminopyridine (50–100 μM), but not tetraethylammonium (2–10 mM), appeared to suppress excitability and high-threshold Ca
2+-spike firing. Application of 4-aminopyridine increased the low-threshold Ca
2+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca
2+-spike into a plateau potential. Application of the Ca
2+-channel blocker Cd
2+ (50 μM), reduced or eliminated this plateau potential. The tetrodotoxin sensitive, persistent Na
+-conductance also sustained plateau potentials, triggered after 4-aminopyridine application on depolarization by current pulses.
Our results suggest that high-threshold Ca
2+-spike firing, and a short-term influx of Ca
2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K
+-conductance may reduce high-threshold Ca
2+-spike firing and shorten high-threshold Ca
2+-spike duration. A persistent Na
+-conductance promotes coupling of the low-threshold Ca
2+-spike to a high-threshold Ca
2+-spike.
Thus, the activation of both voltage-dependent conductances would affect Ca
2+ influx into ventral medial geniculate neurons. This would alter the quality of the different signals transmitted in the thalamocortical system during wakefulness, sleep and pathological states. |
| doi_str_mv | 10.1016/S0306-4522(97)00458-2 |
| format | Article |
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2+-spikes. The neurons normally discharge such spikes on low-threshold Ca
2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca
2+-spikes, using whole-cell recording techniques in a slice preparation of rat thalamus. A subthreshold (persistent) Na
+-conductance amplified depolarizing inputs, enhancing membrane excitability in the tonic firing mode and amplifying the low-threshold Ca
2+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold Ca
2+-spike firing. A slowly inactivating K
+ conductance, sensitive to blockade with 4-aminopyridine (50–100 μM), but not tetraethylammonium (2–10 mM), appeared to suppress excitability and high-threshold Ca
2+-spike firing. Application of 4-aminopyridine increased the low-threshold Ca
2+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca
2+-spike into a plateau potential. Application of the Ca
2+-channel blocker Cd
2+ (50 μM), reduced or eliminated this plateau potential. The tetrodotoxin sensitive, persistent Na
+-conductance also sustained plateau potentials, triggered after 4-aminopyridine application on depolarization by current pulses.
Our results suggest that high-threshold Ca
2+-spike firing, and a short-term influx of Ca
2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K
+-conductance may reduce high-threshold Ca
2+-spike firing and shorten high-threshold Ca
2+-spike duration. A persistent Na
+-conductance promotes coupling of the low-threshold Ca
2+-spike to a high-threshold Ca
2+-spike.
Thus, the activation of both voltage-dependent conductances would affect Ca
2+ influx into ventral medial geniculate neurons. This would alter the quality of the different signals transmitted in the thalamocortical system during wakefulness, sleep and pathological states.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/S0306-4522(97)00458-2</identifier><identifier>PMID: 9502246</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>4-Aminopyridine - pharmacology ; Animals ; Auditory Pathways - physiology ; auditory system ; Biological and medical sciences ; Cadmium - pharmacology ; Calcium - metabolism ; Calcium Channel Blockers - pharmacology ; Calcium Channels - physiology ; calcium spikes ; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation ; Evoked Potentials - drug effects ; Evoked Potentials - physiology ; Fundamental and applied biological sciences. Psychology ; In Vitro Techniques ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Neurons - drug effects ; Neurons - physiology ; Patch-Clamp Techniques ; persistent sodium current ; Potassium Channels - physiology ; rat ; Rats ; Rats, Sprague-Dawley ; Reaction Time ; Tetraethylammonium - pharmacology ; Tetrodotoxin - pharmacology ; thalamus ; Thalamus - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 1998-04, Vol.83 (4), p.1063-1073</ispartof><rights>1998 IBRO. Published by Elsevier Science Ltd</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-6f9d4b06a3794ceebcdecb8fe0fc13204ba59136c1a5d1f16466e7e859e65bed3</citedby><cites>FETCH-LOGICAL-c472t-6f9d4b06a3794ceebcdecb8fe0fc13204ba59136c1a5d1f16466e7e859e65bed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0306452297004582$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2149504$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9502246$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tennigkeit, F.</creatorcontrib><creatorcontrib>Schwarz, D.W.F.</creatorcontrib><creatorcontrib>Puil, E.</creatorcontrib><title>Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Neurons in the ventral partition of the medial geniculate body are able to fire high-threshold Ca
2+-spikes. The neurons normally discharge such spikes on low-threshold Ca
2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca
2+-spikes, using whole-cell recording techniques in a slice preparation of rat thalamus. A subthreshold (persistent) Na
+-conductance amplified depolarizing inputs, enhancing membrane excitability in the tonic firing mode and amplifying the low-threshold Ca
2+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold Ca
2+-spike firing. A slowly inactivating K
+ conductance, sensitive to blockade with 4-aminopyridine (50–100 μM), but not tetraethylammonium (2–10 mM), appeared to suppress excitability and high-threshold Ca
2+-spike firing. Application of 4-aminopyridine increased the low-threshold Ca
2+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca
2+-spike into a plateau potential. Application of the Ca
2+-channel blocker Cd
2+ (50 μM), reduced or eliminated this plateau potential. The tetrodotoxin sensitive, persistent Na
+-conductance also sustained plateau potentials, triggered after 4-aminopyridine application on depolarization by current pulses.
Our results suggest that high-threshold Ca
2+-spike firing, and a short-term influx of Ca
2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K
+-conductance may reduce high-threshold Ca
2+-spike firing and shorten high-threshold Ca
2+-spike duration. A persistent Na
+-conductance promotes coupling of the low-threshold Ca
2+-spike to a high-threshold Ca
2+-spike.
Thus, the activation of both voltage-dependent conductances would affect Ca
2+ influx into ventral medial geniculate neurons. This would alter the quality of the different signals transmitted in the thalamocortical system during wakefulness, sleep and pathological states.</description><subject>4-Aminopyridine - pharmacology</subject><subject>Animals</subject><subject>Auditory Pathways - physiology</subject><subject>auditory system</subject><subject>Biological and medical sciences</subject><subject>Cadmium - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channels - physiology</subject><subject>calcium spikes</subject><subject>Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation</subject><subject>Evoked Potentials - drug effects</subject><subject>Evoked Potentials - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>In Vitro Techniques</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Patch-Clamp Techniques</subject><subject>persistent sodium current</subject><subject>Potassium Channels - physiology</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reaction Time</subject><subject>Tetraethylammonium - pharmacology</subject><subject>Tetrodotoxin - pharmacology</subject><subject>thalamus</subject><subject>Thalamus - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFu1DAQhi1EVZbCI1TyAaFyCLUd20lOqKoKRWrFoXDhYjn2hBiSePHYSH17st3VXjuXOcz3z4w-Qs45-8gZ15cPrGa6kkqIi675wJhUbSVekA1vm7pqlJQvyeaIvCKvEX-ztZSsT8lpp5gQUm_Iz_voy2RziAuNA-1LwozULp6O4ddY5TEBjnHy1NnJhTJT3IY_gDQsdIGS4oK7WLKZ2uJDjumR5tFOdi74hpwMdkJ4e-hn5Mfnm-_Xt9Xdty9fr6_uKicbkSs9dF72TNu66aQD6J0H17cDsMHxWjDZW9XxWjtulecD11JraKBVHWjVg6_PyPv93m2KfwtgNnNAB9NkF4gFDdeKtVrwFVR70KWImGAw2xRmmx4NZ2bn1Dw5NTthpmvMk1Mj1tz54UDpZ_DH1EHiOn93mFtcNQ3JLi7gERNcrqRcsU97DFYZ_wIkgy7A4sCHBC4bH8Mzj_wHGh2Ugg</recordid><startdate>19980401</startdate><enddate>19980401</enddate><creator>Tennigkeit, F.</creator><creator>Schwarz, D.W.F.</creator><creator>Puil, E.</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>7QP</scope><scope>7TK</scope></search><sort><creationdate>19980401</creationdate><title>Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus</title><author>Tennigkeit, F. ; Schwarz, D.W.F. ; Puil, E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-6f9d4b06a3794ceebcdecb8fe0fc13204ba59136c1a5d1f16466e7e859e65bed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>Animals</topic><topic>Auditory Pathways - physiology</topic><topic>auditory system</topic><topic>Biological and medical sciences</topic><topic>Cadmium - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channels - physiology</topic><topic>calcium spikes</topic><topic>Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation</topic><topic>Evoked Potentials - drug effects</topic><topic>Evoked Potentials - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>In Vitro Techniques</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Patch-Clamp Techniques</topic><topic>persistent sodium current</topic><topic>Potassium Channels - physiology</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reaction Time</topic><topic>Tetraethylammonium - pharmacology</topic><topic>Tetrodotoxin - pharmacology</topic><topic>thalamus</topic><topic>Thalamus - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tennigkeit, F.</creatorcontrib><creatorcontrib>Schwarz, D.W.F.</creatorcontrib><creatorcontrib>Puil, E.</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><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tennigkeit, F.</au><au>Schwarz, D.W.F.</au><au>Puil, E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>1998-04-01</date><risdate>1998</risdate><volume>83</volume><issue>4</issue><spage>1063</spage><epage>1073</epage><pages>1063-1073</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Neurons in the ventral partition of the medial geniculate body are able to fire high-threshold Ca
2+-spikes. The neurons normally discharge such spikes on low-threshold Ca
2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca
2+-spikes, using whole-cell recording techniques in a slice preparation of rat thalamus. A subthreshold (persistent) Na
+-conductance amplified depolarizing inputs, enhancing membrane excitability in the tonic firing mode and amplifying the low-threshold Ca
2+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold Ca
2+-spike firing. A slowly inactivating K
+ conductance, sensitive to blockade with 4-aminopyridine (50–100 μM), but not tetraethylammonium (2–10 mM), appeared to suppress excitability and high-threshold Ca
2+-spike firing. Application of 4-aminopyridine increased the low-threshold Ca
2+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca
2+-spike into a plateau potential. Application of the Ca
2+-channel blocker Cd
2+ (50 μM), reduced or eliminated this plateau potential. The tetrodotoxin sensitive, persistent Na
+-conductance also sustained plateau potentials, triggered after 4-aminopyridine application on depolarization by current pulses.
Our results suggest that high-threshold Ca
2+-spike firing, and a short-term influx of Ca
2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K
+-conductance may reduce high-threshold Ca
2+-spike firing and shorten high-threshold Ca
2+-spike duration. A persistent Na
+-conductance promotes coupling of the low-threshold Ca
2+-spike to a high-threshold Ca
2+-spike.
Thus, the activation of both voltage-dependent conductances would affect Ca
2+ influx into ventral medial geniculate neurons. This would alter the quality of the different signals transmitted in the thalamocortical system during wakefulness, sleep and pathological states.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>9502246</pmid><doi>10.1016/S0306-4522(97)00458-2</doi><tpages>11</tpages></addata></record> |
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| ispartof | Neuroscience, 1998-04, Vol.83 (4), p.1063-1073 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | 4-Aminopyridine - pharmacology Animals Auditory Pathways - physiology auditory system Biological and medical sciences Cadmium - pharmacology Calcium - metabolism Calcium Channel Blockers - pharmacology Calcium Channels - physiology calcium spikes Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation Evoked Potentials - drug effects Evoked Potentials - physiology Fundamental and applied biological sciences. Psychology In Vitro Techniques Membrane Potentials - drug effects Membrane Potentials - physiology Neurons - drug effects Neurons - physiology Patch-Clamp Techniques persistent sodium current Potassium Channels - physiology rat Rats Rats, Sprague-Dawley Reaction Time Tetraethylammonium - pharmacology Tetrodotoxin - pharmacology thalamus Thalamus - physiology Vertebrates: nervous system and sense organs |
| title | Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus |
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