Acute actions of marine toxin latrunculin A on the electrophysiological properties of cultured dorsal root ganglion neurones

Wael E Houssen, Marcel Jaspars, Kerrie N Wease, Roderick H Scott

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14 Citations (Scopus)

Abstract

The effects of latrunculin A, isolated from the nudibranch Chromodoris sp., on the excitability of neonatal rat cultured dorsal root ganglion neurones were investigated using patch-clamp recording and Ca(2+) imaging techniques. Under current-clamp conditions, acute application of latrunculin A (100 microM) reversibly induced multiple action potential firing and significantly increased action potential duration. No significant effects on action potential peak amplitude, threshold of action potential firing, resting membrane potential and input resistance were observed. Under voltage-clamp conditions, significant and dose-dependent suppression of K(+) current was seen with 10-100 microM latrunculin A. Additionally, a significant difference between inhibition of the current measured at the peak and the end of a 100 ms voltage step was seen with 100 microM latrunculin A. Fura-2 fluorescence Ca(2+) imaging revealed that latrunculin A (100 microM) significantly inhibited Ca(2+) transients evoked by KCl-induced depolarisation in all neurones. In 36% of DRG neurones, latrunculin A alone had no effect on intracellular Ca(2+). In 64% of neurones, latrunculin A alone evoked a transient rise in intracellular Ca(2+). Moreover, latrunculin A (10-100 microM) significantly inhibited the mean high voltage-activated Ca(2+) current. The effects of latrunculin A on action potential firing and K(+) currents were attenuated by intracellular phalloidin, an indication that these effects are mediated through actin disruption.
Original languageEnglish
Pages (from-to)19-29
Number of pages11
JournalComparative Biochemistry and Physiology Part C: Toxicology & Pharmacology
Volume142
Issue number1-2
DOIs
Publication statusPublished - 2006

Keywords

  • action potential
  • potassium current
  • calcium current
  • Chromodoris sp.
  • dorsal root ganglion
  • latrunculin A
  • phalloidin
  • nudibranch chromodoris-hamiltoni
  • calcium-entry
  • cytoskeleton
  • cells
  • channels
  • currents
  • disruption
  • diterpenes
  • activation
  • release

Cite this

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title = "Acute actions of marine toxin latrunculin A on the electrophysiological properties of cultured dorsal root ganglion neurones",
abstract = "The effects of latrunculin A, isolated from the nudibranch Chromodoris sp., on the excitability of neonatal rat cultured dorsal root ganglion neurones were investigated using patch-clamp recording and Ca(2+) imaging techniques. Under current-clamp conditions, acute application of latrunculin A (100 microM) reversibly induced multiple action potential firing and significantly increased action potential duration. No significant effects on action potential peak amplitude, threshold of action potential firing, resting membrane potential and input resistance were observed. Under voltage-clamp conditions, significant and dose-dependent suppression of K(+) current was seen with 10-100 microM latrunculin A. Additionally, a significant difference between inhibition of the current measured at the peak and the end of a 100 ms voltage step was seen with 100 microM latrunculin A. Fura-2 fluorescence Ca(2+) imaging revealed that latrunculin A (100 microM) significantly inhibited Ca(2+) transients evoked by KCl-induced depolarisation in all neurones. In 36{\%} of DRG neurones, latrunculin A alone had no effect on intracellular Ca(2+). In 64{\%} of neurones, latrunculin A alone evoked a transient rise in intracellular Ca(2+). Moreover, latrunculin A (10-100 microM) significantly inhibited the mean high voltage-activated Ca(2+) current. The effects of latrunculin A on action potential firing and K(+) currents were attenuated by intracellular phalloidin, an indication that these effects are mediated through actin disruption.",
keywords = "action potential, potassium current, calcium current, Chromodoris sp., dorsal root ganglion, latrunculin A, phalloidin, nudibranch chromodoris-hamiltoni, calcium-entry, cytoskeleton, cells, channels, currents, disruption, diterpenes, activation, release",
author = "Houssen, {Wael E} and Marcel Jaspars and Wease, {Kerrie N} and Scott, {Roderick H}",
year = "2006",
doi = "10.1016/j.cbpc.2005.09.006",
language = "English",
volume = "142",
pages = "19--29",
journal = "Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology",
issn = "1532-0456",
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number = "1-2",

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TY - JOUR

T1 - Acute actions of marine toxin latrunculin A on the electrophysiological properties of cultured dorsal root ganglion neurones

AU - Houssen, Wael E

AU - Jaspars, Marcel

AU - Wease, Kerrie N

AU - Scott, Roderick H

PY - 2006

Y1 - 2006

N2 - The effects of latrunculin A, isolated from the nudibranch Chromodoris sp., on the excitability of neonatal rat cultured dorsal root ganglion neurones were investigated using patch-clamp recording and Ca(2+) imaging techniques. Under current-clamp conditions, acute application of latrunculin A (100 microM) reversibly induced multiple action potential firing and significantly increased action potential duration. No significant effects on action potential peak amplitude, threshold of action potential firing, resting membrane potential and input resistance were observed. Under voltage-clamp conditions, significant and dose-dependent suppression of K(+) current was seen with 10-100 microM latrunculin A. Additionally, a significant difference between inhibition of the current measured at the peak and the end of a 100 ms voltage step was seen with 100 microM latrunculin A. Fura-2 fluorescence Ca(2+) imaging revealed that latrunculin A (100 microM) significantly inhibited Ca(2+) transients evoked by KCl-induced depolarisation in all neurones. In 36% of DRG neurones, latrunculin A alone had no effect on intracellular Ca(2+). In 64% of neurones, latrunculin A alone evoked a transient rise in intracellular Ca(2+). Moreover, latrunculin A (10-100 microM) significantly inhibited the mean high voltage-activated Ca(2+) current. The effects of latrunculin A on action potential firing and K(+) currents were attenuated by intracellular phalloidin, an indication that these effects are mediated through actin disruption.

AB - The effects of latrunculin A, isolated from the nudibranch Chromodoris sp., on the excitability of neonatal rat cultured dorsal root ganglion neurones were investigated using patch-clamp recording and Ca(2+) imaging techniques. Under current-clamp conditions, acute application of latrunculin A (100 microM) reversibly induced multiple action potential firing and significantly increased action potential duration. No significant effects on action potential peak amplitude, threshold of action potential firing, resting membrane potential and input resistance were observed. Under voltage-clamp conditions, significant and dose-dependent suppression of K(+) current was seen with 10-100 microM latrunculin A. Additionally, a significant difference between inhibition of the current measured at the peak and the end of a 100 ms voltage step was seen with 100 microM latrunculin A. Fura-2 fluorescence Ca(2+) imaging revealed that latrunculin A (100 microM) significantly inhibited Ca(2+) transients evoked by KCl-induced depolarisation in all neurones. In 36% of DRG neurones, latrunculin A alone had no effect on intracellular Ca(2+). In 64% of neurones, latrunculin A alone evoked a transient rise in intracellular Ca(2+). Moreover, latrunculin A (10-100 microM) significantly inhibited the mean high voltage-activated Ca(2+) current. The effects of latrunculin A on action potential firing and K(+) currents were attenuated by intracellular phalloidin, an indication that these effects are mediated through actin disruption.

KW - action potential

KW - potassium current

KW - calcium current

KW - Chromodoris sp.

KW - dorsal root ganglion

KW - latrunculin A

KW - phalloidin

KW - nudibranch chromodoris-hamiltoni

KW - calcium-entry

KW - cytoskeleton

KW - cells

KW - channels

KW - currents

KW - disruption

KW - diterpenes

KW - activation

KW - release

U2 - 10.1016/j.cbpc.2005.09.006

DO - 10.1016/j.cbpc.2005.09.006

M3 - Article

VL - 142

SP - 19

EP - 29

JO - Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

JF - Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

SN - 1532-0456

IS - 1-2

ER -