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L-type calcium channels and NMDA receptors: a determinant duo for short-term nociceptive plasticity.

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Title: L-type calcium channels and NMDA receptors: a determinant duo for short-term nociceptive plasticity.
Authors: Fossat, Pascal (AUTHOR), Sibon, Igor (AUTHOR), Le Masson, Gwendal (AUTHOR), Landry, Marc (AUTHOR), Nagy, Frédéric (AUTHOR)
Source: European Journal of Neuroscience. Jan2007, Vol. 25 Issue 1, p127-135. 9p.
Subjects: Neuroplasticity, Calcium channels, Methyl aspartate, Pain, Spinal cord, Rats
Abstract: In the dorsal horn of the spinal cord, pain-transmitting neurons exhibit action potential windup, a form of short-term plasticity, which consists of a progressive increase in neuronal response during repetitive stimulation of nociceptive input fibers. Windup depends on N-methyl-d-aspartate (NMDA) receptor activation, but previous in vitro studies indicated that windup also relies on intrinsic plateau properties of spinal neurons. In the present study, we considered the possible involvement of these properties in windup in vivo. For this purpose, we first studied a nociceptive flexion reflex in the rat. We showed that windup of the reflex is actually suppressed by blockers ofL-type calcium current and Ca2+-activated non-specific cationic current (Ican), the two main depolarizing conductances of plateau potentials. We further showed that, during windup, NMDA receptors provide a critical excitatory component in a dynamic balance of excitatory and inhibitory inputs which ultimately activatesL-type calcium channels. The nociceptive reflex involves at least two neuronal groups, which may express intrinsic amplification properties, motor neurons and dorsal horn neurons. By means of extracellular recordings in the dorsal horn, we showed that windup of dorsal horn neuron discharge was sensitive to the modulators ofL-type calcium current. Altogether, our results suggest that, in vivo, windup also depends on the amplification properties of spinal neurons, the triggering of which requires previous activation of NMDA receptors. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: L-type calcium channels and NMDA receptors: a determinant duo for short-term nociceptive plasticity.
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  Data: <searchLink fieldCode="AR" term="%22Fossat%2C+Pascal%22">Fossat, Pascal</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Sibon%2C+Igor%22">Sibon, Igor</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Le+Masson%2C+Gwendal%22">Le Masson, Gwendal</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Landry%2C+Marc%22">Landry, Marc</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Nagy%2C+Frédéric%22">Nagy, Frédéric</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Jan2007, Vol. 25 Issue 1, p127-135. 9p.
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  Data: <searchLink fieldCode="DE" term="%22Neuroplasticity%22">Neuroplasticity</searchLink><br /><searchLink fieldCode="DE" term="%22Calcium+channels%22">Calcium channels</searchLink><br /><searchLink fieldCode="DE" term="%22Methyl+aspartate%22">Methyl aspartate</searchLink><br /><searchLink fieldCode="DE" term="%22Pain%22">Pain</searchLink><br /><searchLink fieldCode="DE" term="%22Spinal+cord%22">Spinal cord</searchLink><br /><searchLink fieldCode="DE" term="%22Rats%22">Rats</searchLink>
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  Label: Abstract
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  Data: In the dorsal horn of the spinal cord, pain-transmitting neurons exhibit action potential windup, a form of short-term plasticity, which consists of a progressive increase in neuronal response during repetitive stimulation of nociceptive input fibers. Windup depends on N-methyl-d-aspartate (NMDA) receptor activation, but previous in vitro studies indicated that windup also relies on intrinsic plateau properties of spinal neurons. In the present study, we considered the possible involvement of these properties in windup in vivo. For this purpose, we first studied a nociceptive flexion reflex in the rat. We showed that windup of the reflex is actually suppressed by blockers ofL-type calcium current and Ca2+-activated non-specific cationic current (Ican), the two main depolarizing conductances of plateau potentials. We further showed that, during windup, NMDA receptors provide a critical excitatory component in a dynamic balance of excitatory and inhibitory inputs which ultimately activatesL-type calcium channels. The nociceptive reflex involves at least two neuronal groups, which may express intrinsic amplification properties, motor neurons and dorsal horn neurons. By means of extracellular recordings in the dorsal horn, we showed that windup of dorsal horn neuron discharge was sensitive to the modulators ofL-type calcium current. Altogether, our results suggest that, in vivo, windup also depends on the amplification properties of spinal neurons, the triggering of which requires previous activation of NMDA receptors. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/j.1460-9568.2006.05256.x
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        Text: English
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              Text: Jan2007
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