Contribution of the hyperpolarization-activated current to the resting membrane potential of rat nodose sensory neurons
The voltage- and time-dependent characteristics of the hyperpolarization-activated current ( I H ) and its contribution to the resting membrane potential of neonatal rat nodose sensory neurons were investigated using the whole-cell tight seal method of voltage and current clamp recording. I H was fo...
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| Veröffentlicht in: | The Journal of physiology 1999-01, Vol.514 (1), p.125-138 |
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| description | The voltage- and time-dependent characteristics of the hyperpolarization-activated current ( I H ) and its contribution to the resting membrane potential of neonatal rat nodose sensory neurons were investigated using the
whole-cell tight seal method of voltage and current clamp recording.
I H was found in all neonatal nodose neurons in vitro , contrary to previous reports where its presence was particular for A-type neurons. We used the presence of both tetrodotoxin-sensitive
(TTX-S) and tetrodotoxin-resistant (TTX-R) sodium currents to distinguish C- from A-type neurons (TTX-S only). We obtained
further support for the presence of I H in C-type neurons with experiments in which I H was demonstrated in a subset of neurons sensitive to capsaicin.
In both groups I H activated at potentials negative to â50 mV, developed slowly with time and was inhibited by 1â5 m m extracellular caesium. At â120 mV, I H activated with a fast time constant of 73 ± 3 ms in A-type neurons and 163 ± 37 ms in C-type neurons ( P < 0.05). A second, slower time constant of 682 ± 83 ms was observed in A-type neurons and 957 ± 122 ms in C-type neurons.
A- and C-type neurons differed in the amplitude of I H . The mean magnitude of I H at â110 mV was â2338 ± 258 pA in A-type neurons but only -241 ± 40 pA ( P < 0.001) in C-type neurons. This disparity persisted when currents were normalized for capacitance. The reversal potentials
for I H were â39 ± 4 mV for A-type neurons and â37 ± 5 mV for C-type neurons ( P > 0.05).
During current clamp recording I H caused time-dependent rectification in response to hyperpolarizing current injections from the resting membrane potential.
CsCl abolished the rectification and hyperpolarized the resting potential of A-type neurons from â55 ± 3 mV to â61 ± 4 mV
and C-type neurons from â62 ± 2 mV to â71 ± 3 mV. Taken together, the results in these studies indicate that I H contributes to the resting membrane potential in all nodose neurons. |
| doi_str_mv | 10.1111/j.1469-7793.1999.125af.x |
| format | Article |
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whole-cell tight seal method of voltage and current clamp recording.
I H was found in all neonatal nodose neurons in vitro , contrary to previous reports where its presence was particular for A-type neurons. We used the presence of both tetrodotoxin-sensitive
(TTX-S) and tetrodotoxin-resistant (TTX-R) sodium currents to distinguish C- from A-type neurons (TTX-S only). We obtained
further support for the presence of I H in C-type neurons with experiments in which I H was demonstrated in a subset of neurons sensitive to capsaicin.
In both groups I H activated at potentials negative to â50 mV, developed slowly with time and was inhibited by 1â5 m m extracellular caesium. At â120 mV, I H activated with a fast time constant of 73 ± 3 ms in A-type neurons and 163 ± 37 ms in C-type neurons ( P < 0.05). A second, slower time constant of 682 ± 83 ms was observed in A-type neurons and 957 ± 122 ms in C-type neurons.
A- and C-type neurons differed in the amplitude of I H . The mean magnitude of I H at â110 mV was â2338 ± 258 pA in A-type neurons but only -241 ± 40 pA ( P < 0.001) in C-type neurons. This disparity persisted when currents were normalized for capacitance. The reversal potentials
for I H were â39 ± 4 mV for A-type neurons and â37 ± 5 mV for C-type neurons ( P > 0.05).
During current clamp recording I H caused time-dependent rectification in response to hyperpolarizing current injections from the resting membrane potential.
CsCl abolished the rectification and hyperpolarized the resting potential of A-type neurons from â55 ± 3 mV to â61 ± 4 mV
and C-type neurons from â62 ± 2 mV to â71 ± 3 mV. Taken together, the results in these studies indicate that I H contributes to the resting membrane potential in all nodose neurons.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1111/j.1469-7793.1999.125af.x</identifier><identifier>PMID: 9831721</identifier><language>eng</language><publisher>Oxford, UK: The Physiological Society</publisher><subject>Animals ; Capsaicin - pharmacology ; Cells, Cultured ; Gluconates - pharmacology ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Neurons, Afferent - cytology ; Neurons, Afferent - physiology ; Nodose Ganglion - cytology ; Nodose Ganglion - physiology ; Patch-Clamp Techniques ; Potassium - pharmacokinetics ; Rats ; Rats, Sprague-Dawley ; Research Papers ; Sodium - pharmacokinetics ; Tetrodotoxin - pharmacology</subject><ispartof>The Journal of physiology, 1999-01, Vol.514 (1), p.125-138</ispartof><rights>1999 The Journal of Physiology © 1999 The Physiological Society</rights><rights>The Physiological Society 1999 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5995-52feb9321c9bf5afb19eef148000b6be8f79b1dac9b043bfb9b61f7a4f72f4c83</citedby><cites>FETCH-LOGICAL-c5995-52feb9321c9bf5afb19eef148000b6be8f79b1dac9b043bfb9b61f7a4f72f4c83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2269051/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2269051/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9831721$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Doan, T. N.</creatorcontrib><creatorcontrib>Kunze, D. L.</creatorcontrib><title>Contribution of the hyperpolarization-activated current to the resting membrane potential of rat nodose sensory neurons</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>The voltage- and time-dependent characteristics of the hyperpolarization-activated current ( I H ) and its contribution to the resting membrane potential of neonatal rat nodose sensory neurons were investigated using the
whole-cell tight seal method of voltage and current clamp recording.
I H was found in all neonatal nodose neurons in vitro , contrary to previous reports where its presence was particular for A-type neurons. We used the presence of both tetrodotoxin-sensitive
(TTX-S) and tetrodotoxin-resistant (TTX-R) sodium currents to distinguish C- from A-type neurons (TTX-S only). We obtained
further support for the presence of I H in C-type neurons with experiments in which I H was demonstrated in a subset of neurons sensitive to capsaicin.
In both groups I H activated at potentials negative to â50 mV, developed slowly with time and was inhibited by 1â5 m m extracellular caesium. At â120 mV, I H activated with a fast time constant of 73 ± 3 ms in A-type neurons and 163 ± 37 ms in C-type neurons ( P < 0.05). A second, slower time constant of 682 ± 83 ms was observed in A-type neurons and 957 ± 122 ms in C-type neurons.
A- and C-type neurons differed in the amplitude of I H . The mean magnitude of I H at â110 mV was â2338 ± 258 pA in A-type neurons but only -241 ± 40 pA ( P < 0.001) in C-type neurons. This disparity persisted when currents were normalized for capacitance. The reversal potentials
for I H were â39 ± 4 mV for A-type neurons and â37 ± 5 mV for C-type neurons ( P > 0.05).
During current clamp recording I H caused time-dependent rectification in response to hyperpolarizing current injections from the resting membrane potential.
CsCl abolished the rectification and hyperpolarized the resting potential of A-type neurons from â55 ± 3 mV to â61 ± 4 mV
and C-type neurons from â62 ± 2 mV to â71 ± 3 mV. Taken together, the results in these studies indicate that I H contributes to the resting membrane potential in all nodose neurons.</description><subject>Animals</subject><subject>Capsaicin - pharmacology</subject><subject>Cells, Cultured</subject><subject>Gluconates - pharmacology</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Neurons, Afferent - cytology</subject><subject>Neurons, Afferent - physiology</subject><subject>Nodose Ganglion - cytology</subject><subject>Nodose Ganglion - physiology</subject><subject>Patch-Clamp Techniques</subject><subject>Potassium - pharmacokinetics</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Research Papers</subject><subject>Sodium - pharmacokinetics</subject><subject>Tetrodotoxin - pharmacology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUuLFDEUhYMoYzv6E4TsdFNlknoGRJBmfDGgi3EdkuqbrjRVSZmkpqf89aamm0Z3ZpPAd8_JPRyEMCU5TefdIadlzbOm4UVOOec5ZZXU-cMTtLmAp2hDCGNZ0VT0OXoRwoEQWhDOr9AVbwvaMLpBx62z0Rs1R-MsdhrHHnC_TOAnN0hvfssVZLKL5l5G2OFu9h5sxNE9jnoI0dg9HmFUXlrAk4sJGzmsZl5GbN3OBcABbHB-wRZm72x4iZ5pOQR4db6v0c9PN3fbL9nt989ftx9vs67ivMoqpkHxgtGOK50SKsoBNC1bQoiqFbS64YruZMKkLJRWXNVUN7LUDdNl1xbX6MPJd5rVCLsu7eblICZvRukX4aQR_xJrerF394KxmpOKJoO3ZwPvfs0prRhN6GAYUlg3B0GbqmVlXdUkjban0c67EDzoyzeUiLU2cRBrO2JtR6y1icfaxEOSvv57zYvw3FPi70_8aAZY_ttX3H37kZ5J_uYk782-PxoPYuqXYFxwnYG4iIqWgq6i4g8Wm7sC</recordid><startdate>19990101</startdate><enddate>19990101</enddate><creator>Doan, T. N.</creator><creator>Kunze, D. L.</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Blackwell Science Inc</general><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>5PM</scope></search><sort><creationdate>19990101</creationdate><title>Contribution of the hyperpolarization-activated current to the resting membrane potential of rat nodose sensory neurons</title><author>Doan, T. N. ; Kunze, D. L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5995-52feb9321c9bf5afb19eef148000b6be8f79b1dac9b043bfb9b61f7a4f72f4c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Capsaicin - pharmacology</topic><topic>Cells, Cultured</topic><topic>Gluconates - pharmacology</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>Neurons, Afferent - cytology</topic><topic>Neurons, Afferent - physiology</topic><topic>Nodose Ganglion - cytology</topic><topic>Nodose Ganglion - physiology</topic><topic>Patch-Clamp Techniques</topic><topic>Potassium - pharmacokinetics</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Research Papers</topic><topic>Sodium - pharmacokinetics</topic><topic>Tetrodotoxin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Doan, T. N.</creatorcontrib><creatorcontrib>Kunze, D. L.</creatorcontrib><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>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Doan, T. N.</au><au>Kunze, D. L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contribution of the hyperpolarization-activated current to the resting membrane potential of rat nodose sensory neurons</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1999-01-01</date><risdate>1999</risdate><volume>514</volume><issue>1</issue><spage>125</spage><epage>138</epage><pages>125-138</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>The voltage- and time-dependent characteristics of the hyperpolarization-activated current ( I H ) and its contribution to the resting membrane potential of neonatal rat nodose sensory neurons were investigated using the
whole-cell tight seal method of voltage and current clamp recording.
I H was found in all neonatal nodose neurons in vitro , contrary to previous reports where its presence was particular for A-type neurons. We used the presence of both tetrodotoxin-sensitive
(TTX-S) and tetrodotoxin-resistant (TTX-R) sodium currents to distinguish C- from A-type neurons (TTX-S only). We obtained
further support for the presence of I H in C-type neurons with experiments in which I H was demonstrated in a subset of neurons sensitive to capsaicin.
In both groups I H activated at potentials negative to â50 mV, developed slowly with time and was inhibited by 1â5 m m extracellular caesium. At â120 mV, I H activated with a fast time constant of 73 ± 3 ms in A-type neurons and 163 ± 37 ms in C-type neurons ( P < 0.05). A second, slower time constant of 682 ± 83 ms was observed in A-type neurons and 957 ± 122 ms in C-type neurons.
A- and C-type neurons differed in the amplitude of I H . The mean magnitude of I H at â110 mV was â2338 ± 258 pA in A-type neurons but only -241 ± 40 pA ( P < 0.001) in C-type neurons. This disparity persisted when currents were normalized for capacitance. The reversal potentials
for I H were â39 ± 4 mV for A-type neurons and â37 ± 5 mV for C-type neurons ( P > 0.05).
During current clamp recording I H caused time-dependent rectification in response to hyperpolarizing current injections from the resting membrane potential.
CsCl abolished the rectification and hyperpolarized the resting potential of A-type neurons from â55 ± 3 mV to â61 ± 4 mV
and C-type neurons from â62 ± 2 mV to â71 ± 3 mV. Taken together, the results in these studies indicate that I H contributes to the resting membrane potential in all nodose neurons.</abstract><cop>Oxford, UK</cop><pub>The Physiological Society</pub><pmid>9831721</pmid><doi>10.1111/j.1469-7793.1999.125af.x</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Capsaicin - pharmacology Cells, Cultured Gluconates - pharmacology Membrane Potentials - drug effects Membrane Potentials - physiology Neurons, Afferent - cytology Neurons, Afferent - physiology Nodose Ganglion - cytology Nodose Ganglion - physiology Patch-Clamp Techniques Potassium - pharmacokinetics Rats Rats, Sprague-Dawley Research Papers Sodium - pharmacokinetics Tetrodotoxin - pharmacology |
| title | Contribution of the hyperpolarization-activated current to the resting membrane potential of rat nodose sensory neurons |
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