Membrane Ionic Currents and Electrical Excitability in Barnacle Neurons. PREMACK, B. A. Ph.D. Thesis, University of Alberta (Canada), Canada, 1987. ![Membrane Ionic Currents and Electrical Excitability in Barnacle Neurons [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper abstract bibtex Neurons in the ventral ganglion of the barnacle, Balanus nubilus were studied under either voltage or current clamp conditions in order to describe the membrane ionic currents and relate these to membrane excitability. Neurons were clamped at the soma using two microelectrodes and conventional voltage and current measuring circuitry. Five distinct ionic currents were identified, and the voltage dependence and kinetics of each described. These were: a fast Na${\}sp +$ current, $I{\}sb\{{\}rm Na\}$; a slow Ca${\}sp\{2+\}$ current, $I{\}sb\{{\}rm Ca\}$; a transient K${\}sp +$ current, $I{\}sb\{{\}rm A\}$; a delayed K${\}sp +$ current, $I{\}sb\{{\}rm K\}$; and a slowly activating Ca${\}sp\{2+\}$-dependent current, $I{\}sb\{{\}rm K(Ca)\}$. This ensemble of ionic currents is quite typical of many neuronal somata, but barnacle neurons were found to differ in that much of the total outward current was Ca${\}sp\{2+\}$-dependent. A very rapidly activating fraction of $I{\}sb\{{\}rm A\}$ appeared to be Ca${\}sp\{2+\}$-dependent, and was eliminated when Ca${\}sp\{2+\}$ influx was blocked by Co${\}sp\{2+\}$ or Mn${\}sp\{2+\}$. The possibility that the reduction in $I{\}sb\{{\}rm A\}$ resulted from an alteration in the surface potential was examined, but found not to account for the observed Ca${\}sp\{2+\}$-dependence. The major functions of both components of $I{\}sb\{{\}rm A\}$ were: regulation of the response time at the onset of a stimulus, repolarization of the action potential, and control of low frequency repetitive firing. A numerical simulation based on the voltage clamp data, using modified Hodgkin-Huxley formulations, indicates that the above physiological roles are consistent with the measured voltage dependence and kinetics of $I{\}sb\{{\}rm A\}$. The adenylate cyclase activator forskolin accelerated the inactivation kinetics of $I{\}sb\{{\}rm A\}$, and increased the excitability of neurons in current clamp. However, some of the evidence indicates that this effect may not be mediated by a rise in cAMP. The other Ca${\}sp\{2+\}$-dependent K${\}sp +$ current, $I{\}sb\{{\}rm K(Ca)\}$ appeared to be important in causing adaptation of the action potential frequency during maintained current stimuli. Elimination of Ca${\}sp\{2+\}$ influx reduced adaptation, as did intracellular iontophoresis of the Ca${\}sp\{2+\}$ chelator EGTA. Intracellular iontophoresis of Ca${\}sp\{2+\}$ augmented the rate of adaptation and, in voltage clamp, activated $I{\}sb\{{\}rm K(Ca)\}$. When activated by Ca${\}sp\{2+\}$ iontophoresis $I{\}sb\{{\}rm K(Ca)\}$ was weakly voltage dependent, showed no voltage threshold, and therefore could be activated at any physiological voltage. However, when activated by depolarization, the effective voltage dependence of $I{\}sb\{{\}rm K(Ca)\}$ was much steeper, and was almost identical to that of $I{\}sb\{{\}rm Ca\}$, suggesting that voltage-dependent Ca${\}sp\{2+\}$ influx normally regulates $I{\}sb\{{\}rm K(Ca)\}.$
@phdthesis{premack_membrane_1987,
address = {Canada},
type = {Ph.{D}.},
title = {Membrane {Ionic} {Currents} and {Electrical} {Excitability} in {Barnacle} {Neurons}},
copyright = {Database copyright ProQuest LLC; ProQuest does not claim copyright in the individual underlying works.},
url = {http://search.proquest.com.ezproxy.library.ubc.ca/pqdtglobal/docview/251600536/abstract/44F6649723EB4803PQ/1},
abstract = {Neurons in the ventral ganglion of the barnacle, Balanus nubilus were studied under either voltage or current clamp conditions in order to describe the membrane ionic currents and relate these to membrane excitability. Neurons were clamped at the soma using two microelectrodes and conventional voltage and current measuring circuitry. Five distinct ionic currents were identified, and the voltage dependence and kinetics of each described. These were: a fast Na\${\textbackslash}sp +\$ current, \$I{\textbackslash}sb\{{\textbackslash}rm Na\}\$; a slow Ca\${\textbackslash}sp\{2+\}\$ current, \$I{\textbackslash}sb\{{\textbackslash}rm Ca\}\$; a transient K\${\textbackslash}sp +\$ current, \$I{\textbackslash}sb\{{\textbackslash}rm A\}\$; a delayed K\${\textbackslash}sp +\$ current, \$I{\textbackslash}sb\{{\textbackslash}rm K\}\$; and a slowly activating Ca\${\textbackslash}sp\{2+\}\$-dependent current, \$I{\textbackslash}sb\{{\textbackslash}rm K(Ca)\}\$. This ensemble of ionic currents is quite typical of many neuronal somata, but barnacle neurons were found to differ in that much of the total outward current was Ca\${\textbackslash}sp\{2+\}\$-dependent.
A very rapidly activating fraction of \$I{\textbackslash}sb\{{\textbackslash}rm A\}\$ appeared to be Ca\${\textbackslash}sp\{2+\}\$-dependent, and was eliminated when Ca\${\textbackslash}sp\{2+\}\$ influx was blocked by Co\${\textbackslash}sp\{2+\}\$ or Mn\${\textbackslash}sp\{2+\}\$. The possibility that the reduction in \$I{\textbackslash}sb\{{\textbackslash}rm A\}\$ resulted from an alteration in the surface potential was examined, but found not to account for the observed Ca\${\textbackslash}sp\{2+\}\$-dependence. The major functions of both components of \$I{\textbackslash}sb\{{\textbackslash}rm A\}\$ were: regulation of the response time at the onset of a stimulus, repolarization of the action potential, and control of low frequency repetitive firing. A numerical simulation based on the voltage clamp data, using modified Hodgkin-Huxley formulations, indicates that the above physiological roles are consistent with the measured voltage dependence and kinetics of \$I{\textbackslash}sb\{{\textbackslash}rm A\}\$. The adenylate cyclase activator forskolin accelerated the inactivation kinetics of \$I{\textbackslash}sb\{{\textbackslash}rm A\}\$, and increased the excitability of neurons in current clamp. However, some of the evidence indicates that this effect may not be mediated by a rise in cAMP.
The other Ca\${\textbackslash}sp\{2+\}\$-dependent K\${\textbackslash}sp +\$ current, \$I{\textbackslash}sb\{{\textbackslash}rm K(Ca)\}\$ appeared to be important in causing adaptation of the action potential frequency during maintained current stimuli. Elimination of Ca\${\textbackslash}sp\{2+\}\$ influx reduced adaptation, as did intracellular iontophoresis of the Ca\${\textbackslash}sp\{2+\}\$ chelator EGTA. Intracellular iontophoresis of Ca\${\textbackslash}sp\{2+\}\$ augmented the rate of adaptation and, in voltage clamp, activated \$I{\textbackslash}sb\{{\textbackslash}rm K(Ca)\}\$. When activated by Ca\${\textbackslash}sp\{2+\}\$ iontophoresis \$I{\textbackslash}sb\{{\textbackslash}rm K(Ca)\}\$ was weakly voltage dependent, showed no voltage threshold, and therefore could be activated at any physiological voltage. However, when activated by depolarization, the effective voltage dependence of \$I{\textbackslash}sb\{{\textbackslash}rm K(Ca)\}\$ was much steeper, and was almost identical to that of \$I{\textbackslash}sb\{{\textbackslash}rm Ca\}\$, suggesting that voltage-dependent Ca\${\textbackslash}sp\{2+\}\$ influx normally regulates \$I{\textbackslash}sb\{{\textbackslash}rm K(Ca)\}.\$},
language = {English},
urldate = {2016-06-09},
school = {University of Alberta (Canada)},
author = {PREMACK, BRETT ANTHONY},
year = {1987},
keywords = {Balanus nubilus},
}
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{"_id":"BaCDokJ2gQd4WMoZC","bibbaseid":"premack-membraneioniccurrentsandelectricalexcitabilityinbarnacleneurons-1987","downloads":0,"creationDate":"2016-06-09T22:02:48.270Z","title":"Membrane Ionic Currents and Electrical Excitability in Barnacle Neurons","author_short":["PREMACK, B. A."],"year":1987,"bibtype":"phdthesis","biburl":"http://bibbase.org/zotero/BMSC","bibdata":{"bibtype":"phdthesis","type":"Ph.D.","address":"Canada","title":"Membrane Ionic Currents and Electrical Excitability in Barnacle Neurons","copyright":"Database copyright ProQuest LLC; ProQuest does not claim copyright in the individual underlying works.","url":"http://search.proquest.com.ezproxy.library.ubc.ca/pqdtglobal/docview/251600536/abstract/44F6649723EB4803PQ/1","abstract":"Neurons in the ventral ganglion of the barnacle, Balanus nubilus were studied under either voltage or current clamp conditions in order to describe the membrane ionic currents and relate these to membrane excitability. Neurons were clamped at the soma using two microelectrodes and conventional voltage and current measuring circuitry. Five distinct ionic currents were identified, and the voltage dependence and kinetics of each described. These were: a fast Na${\\}sp +$ current, $I{\\}sb\\{{\\}rm Na\\}$; a slow Ca${\\}sp\\{2+\\}$ current, $I{\\}sb\\{{\\}rm Ca\\}$; a transient K${\\}sp +$ current, $I{\\}sb\\{{\\}rm A\\}$; a delayed K${\\}sp +$ current, $I{\\}sb\\{{\\}rm K\\}$; and a slowly activating Ca${\\}sp\\{2+\\}$-dependent current, $I{\\}sb\\{{\\}rm K(Ca)\\}$. This ensemble of ionic currents is quite typical of many neuronal somata, but barnacle neurons were found to differ in that much of the total outward current was Ca${\\}sp\\{2+\\}$-dependent. A very rapidly activating fraction of $I{\\}sb\\{{\\}rm A\\}$ appeared to be Ca${\\}sp\\{2+\\}$-dependent, and was eliminated when Ca${\\}sp\\{2+\\}$ influx was blocked by Co${\\}sp\\{2+\\}$ or Mn${\\}sp\\{2+\\}$. The possibility that the reduction in $I{\\}sb\\{{\\}rm A\\}$ resulted from an alteration in the surface potential was examined, but found not to account for the observed Ca${\\}sp\\{2+\\}$-dependence. The major functions of both components of $I{\\}sb\\{{\\}rm A\\}$ were: regulation of the response time at the onset of a stimulus, repolarization of the action potential, and control of low frequency repetitive firing. A numerical simulation based on the voltage clamp data, using modified Hodgkin-Huxley formulations, indicates that the above physiological roles are consistent with the measured voltage dependence and kinetics of $I{\\}sb\\{{\\}rm A\\}$. The adenylate cyclase activator forskolin accelerated the inactivation kinetics of $I{\\}sb\\{{\\}rm A\\}$, and increased the excitability of neurons in current clamp. However, some of the evidence indicates that this effect may not be mediated by a rise in cAMP. The other Ca${\\}sp\\{2+\\}$-dependent K${\\}sp +$ current, $I{\\}sb\\{{\\}rm K(Ca)\\}$ appeared to be important in causing adaptation of the action potential frequency during maintained current stimuli. Elimination of Ca${\\}sp\\{2+\\}$ influx reduced adaptation, as did intracellular iontophoresis of the Ca${\\}sp\\{2+\\}$ chelator EGTA. Intracellular iontophoresis of Ca${\\}sp\\{2+\\}$ augmented the rate of adaptation and, in voltage clamp, activated $I{\\}sb\\{{\\}rm K(Ca)\\}$. When activated by Ca${\\}sp\\{2+\\}$ iontophoresis $I{\\}sb\\{{\\}rm K(Ca)\\}$ was weakly voltage dependent, showed no voltage threshold, and therefore could be activated at any physiological voltage. However, when activated by depolarization, the effective voltage dependence of $I{\\}sb\\{{\\}rm K(Ca)\\}$ was much steeper, and was almost identical to that of $I{\\}sb\\{{\\}rm Ca\\}$, suggesting that voltage-dependent Ca${\\}sp\\{2+\\}$ influx normally regulates $I{\\}sb\\{{\\}rm K(Ca)\\}.$","language":"English","urldate":"2016-06-09","school":"University of Alberta (Canada)","author":[{"propositions":[],"lastnames":["PREMACK"],"firstnames":["BRETT","ANTHONY"],"suffixes":[]}],"year":"1987","keywords":"Balanus nubilus","bibtex":"@phdthesis{premack_membrane_1987,\n\taddress = {Canada},\n\ttype = {Ph.{D}.},\n\ttitle = {Membrane {Ionic} {Currents} and {Electrical} {Excitability} in {Barnacle} {Neurons}},\n\tcopyright = {Database copyright ProQuest LLC; ProQuest does not claim copyright in the individual underlying works.},\n\turl = {http://search.proquest.com.ezproxy.library.ubc.ca/pqdtglobal/docview/251600536/abstract/44F6649723EB4803PQ/1},\n\tabstract = {Neurons in the ventral ganglion of the barnacle, Balanus nubilus were studied under either voltage or current clamp conditions in order to describe the membrane ionic currents and relate these to membrane excitability. Neurons were clamped at the soma using two microelectrodes and conventional voltage and current measuring circuitry. Five distinct ionic currents were identified, and the voltage dependence and kinetics of each described. These were: a fast Na\\${\\textbackslash}sp +\\$ current, \\$I{\\textbackslash}sb\\{{\\textbackslash}rm Na\\}\\$; a slow Ca\\${\\textbackslash}sp\\{2+\\}\\$ current, \\$I{\\textbackslash}sb\\{{\\textbackslash}rm Ca\\}\\$; a transient K\\${\\textbackslash}sp +\\$ current, \\$I{\\textbackslash}sb\\{{\\textbackslash}rm A\\}\\$; a delayed K\\${\\textbackslash}sp +\\$ current, \\$I{\\textbackslash}sb\\{{\\textbackslash}rm K\\}\\$; and a slowly activating Ca\\${\\textbackslash}sp\\{2+\\}\\$-dependent current, \\$I{\\textbackslash}sb\\{{\\textbackslash}rm K(Ca)\\}\\$. This ensemble of ionic currents is quite typical of many neuronal somata, but barnacle neurons were found to differ in that much of the total outward current was Ca\\${\\textbackslash}sp\\{2+\\}\\$-dependent.\nA very rapidly activating fraction of \\$I{\\textbackslash}sb\\{{\\textbackslash}rm A\\}\\$ appeared to be Ca\\${\\textbackslash}sp\\{2+\\}\\$-dependent, and was eliminated when Ca\\${\\textbackslash}sp\\{2+\\}\\$ influx was blocked by Co\\${\\textbackslash}sp\\{2+\\}\\$ or Mn\\${\\textbackslash}sp\\{2+\\}\\$. The possibility that the reduction in \\$I{\\textbackslash}sb\\{{\\textbackslash}rm A\\}\\$ resulted from an alteration in the surface potential was examined, but found not to account for the observed Ca\\${\\textbackslash}sp\\{2+\\}\\$-dependence. The major functions of both components of \\$I{\\textbackslash}sb\\{{\\textbackslash}rm A\\}\\$ were: regulation of the response time at the onset of a stimulus, repolarization of the action potential, and control of low frequency repetitive firing. A numerical simulation based on the voltage clamp data, using modified Hodgkin-Huxley formulations, indicates that the above physiological roles are consistent with the measured voltage dependence and kinetics of \\$I{\\textbackslash}sb\\{{\\textbackslash}rm A\\}\\$. The adenylate cyclase activator forskolin accelerated the inactivation kinetics of \\$I{\\textbackslash}sb\\{{\\textbackslash}rm A\\}\\$, and increased the excitability of neurons in current clamp. However, some of the evidence indicates that this effect may not be mediated by a rise in cAMP.\nThe other Ca\\${\\textbackslash}sp\\{2+\\}\\$-dependent K\\${\\textbackslash}sp +\\$ current, \\$I{\\textbackslash}sb\\{{\\textbackslash}rm K(Ca)\\}\\$ appeared to be important in causing adaptation of the action potential frequency during maintained current stimuli. Elimination of Ca\\${\\textbackslash}sp\\{2+\\}\\$ influx reduced adaptation, as did intracellular iontophoresis of the Ca\\${\\textbackslash}sp\\{2+\\}\\$ chelator EGTA. Intracellular iontophoresis of Ca\\${\\textbackslash}sp\\{2+\\}\\$ augmented the rate of adaptation and, in voltage clamp, activated \\$I{\\textbackslash}sb\\{{\\textbackslash}rm K(Ca)\\}\\$. When activated by Ca\\${\\textbackslash}sp\\{2+\\}\\$ iontophoresis \\$I{\\textbackslash}sb\\{{\\textbackslash}rm K(Ca)\\}\\$ was weakly voltage dependent, showed no voltage threshold, and therefore could be activated at any physiological voltage. However, when activated by depolarization, the effective voltage dependence of \\$I{\\textbackslash}sb\\{{\\textbackslash}rm K(Ca)\\}\\$ was much steeper, and was almost identical to that of \\$I{\\textbackslash}sb\\{{\\textbackslash}rm Ca\\}\\$, suggesting that voltage-dependent Ca\\${\\textbackslash}sp\\{2+\\}\\$ influx normally regulates \\$I{\\textbackslash}sb\\{{\\textbackslash}rm K(Ca)\\}.\\$},\n\tlanguage = {English},\n\turldate = {2016-06-09},\n\tschool = {University of Alberta (Canada)},\n\tauthor = {PREMACK, BRETT ANTHONY},\n\tyear = {1987},\n\tkeywords = {Balanus nubilus},\n}\n\n\n\n","author_short":["PREMACK, B. 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