Enhancement of cyclic AMP-dependent sodium current by the convulsant drug pentylenetetrazol

Catherine R. McCrohan; Rhanor Gillette

doi:10.1016/0006-8993(88)90004-2

Enhancement of cyclic AMP-dependent sodium current by the convulsant drug pentylenetetrazol

Catherine R. McCrohan, Rhanor Gillette

Research output: Contribution to journal › Article › peer-review

Abstract

The convulsant drug pentylenetetrazol (PTZ) causes paroxysmal depolarizing shifts (PDS) and bursting in molluscan neurons. PDS has been found to be accompanied by increased levels of cyclic AMP (cAMP) and supported by persistent Na⁺ current. In neurons of the snailLymnaea stagnalis the blocker of cAMP degradation isobutylmethylxanthine (IBMX) mimicks PTZ action. Na⁺ dependence of PTZ-induced inward shift in holding current in voltage-clamped cells supports the potential Na⁺ current origin of PDS. Intracellular cAMP injection elicits a transient Na⁺ current whose amplitude and duration are enhanced by both PTZ and IBMX. PTZ may cause PDS partly through slowing cAMP degradation, thus enhancing the cAMP-dependent Na⁺ current. PDS-generated bursts cause partial inactivation of the Na⁺ current, which may contribute towards burst termination.

Original language	English (US)
Pages (from-to)	21-27
Number of pages	7
Journal	Brain Research
Volume	452
Issue number	1-2
DOIs	https://doi.org/10.1016/0006-8993(88)90004-2
State	Published - Jun 14 1988

Keywords

Cyclic adenosine monophosphate (cAMP)
Molluscan neuron
Pentylenetetrazol
Phosphodiesterase
Sodium current

ASJC Scopus subject areas

General Neuroscience
Molecular Biology
Clinical Neurology
Developmental Biology

Online availability

10.1016/0006-8993(88)90004-2

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title = "Enhancement of cyclic AMP-dependent sodium current by the convulsant drug pentylenetetrazol",

abstract = "The convulsant drug pentylenetetrazol (PTZ) causes paroxysmal depolarizing shifts (PDS) and bursting in molluscan neurons. PDS has been found to be accompanied by increased levels of cyclic AMP (cAMP) and supported by persistent Na+ current. In neurons of the snailLymnaea stagnalis the blocker of cAMP degradation isobutylmethylxanthine (IBMX) mimicks PTZ action. Na+ dependence of PTZ-induced inward shift in holding current in voltage-clamped cells supports the potential Na+ current origin of PDS. Intracellular cAMP injection elicits a transient Na+ current whose amplitude and duration are enhanced by both PTZ and IBMX. PTZ may cause PDS partly through slowing cAMP degradation, thus enhancing the cAMP-dependent Na+ current. PDS-generated bursts cause partial inactivation of the Na+ current, which may contribute towards burst termination.",

keywords = "Cyclic adenosine monophosphate (cAMP), Molluscan neuron, Pentylenetetrazol, Phosphodiesterase, Sodium current",

author = "McCrohan, {Catherine R.} and Rhanor Gillette",

year = "1988",

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AU - McCrohan, Catherine R.

AU - Gillette, Rhanor

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Y1 - 1988/6/14

N2 - The convulsant drug pentylenetetrazol (PTZ) causes paroxysmal depolarizing shifts (PDS) and bursting in molluscan neurons. PDS has been found to be accompanied by increased levels of cyclic AMP (cAMP) and supported by persistent Na+ current. In neurons of the snailLymnaea stagnalis the blocker of cAMP degradation isobutylmethylxanthine (IBMX) mimicks PTZ action. Na+ dependence of PTZ-induced inward shift in holding current in voltage-clamped cells supports the potential Na+ current origin of PDS. Intracellular cAMP injection elicits a transient Na+ current whose amplitude and duration are enhanced by both PTZ and IBMX. PTZ may cause PDS partly through slowing cAMP degradation, thus enhancing the cAMP-dependent Na+ current. PDS-generated bursts cause partial inactivation of the Na+ current, which may contribute towards burst termination.

AB - The convulsant drug pentylenetetrazol (PTZ) causes paroxysmal depolarizing shifts (PDS) and bursting in molluscan neurons. PDS has been found to be accompanied by increased levels of cyclic AMP (cAMP) and supported by persistent Na+ current. In neurons of the snailLymnaea stagnalis the blocker of cAMP degradation isobutylmethylxanthine (IBMX) mimicks PTZ action. Na+ dependence of PTZ-induced inward shift in holding current in voltage-clamped cells supports the potential Na+ current origin of PDS. Intracellular cAMP injection elicits a transient Na+ current whose amplitude and duration are enhanced by both PTZ and IBMX. PTZ may cause PDS partly through slowing cAMP degradation, thus enhancing the cAMP-dependent Na+ current. PDS-generated bursts cause partial inactivation of the Na+ current, which may contribute towards burst termination.

KW - Cyclic adenosine monophosphate (cAMP)

KW - Molluscan neuron

KW - Pentylenetetrazol

KW - Phosphodiesterase

KW - Sodium current

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Enhancement of cyclic AMP-dependent sodium current by the convulsant drug pentylenetetrazol

Abstract

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